We report differences in ( Ca2+ ) i requirement for NF-kB activation in thymocytes as compared to mature T cells .

We report differences in ( Ca2+ ) i requirement for <protein>NF-kB</protein> activation in <cell_type>thymocytes</cell_type> as compared to mature <cell_type>T cells</cell_type> .


Furthermore , our results indicated that thymocytes have a constitutively active form of NF-kB , suggesting that they are activated in vivo .

Furthermore , our results indicated that <cell_type>thymocytes</cell_type> have a <protein>constitutively active form</protein> of <protein>NF-kB</protein> , suggesting that they are activated in vivo .


TCF-1 , a T cell-specific transcription factor of the HMG box family , interacts with sequence motifs in the TCR beta and TCR delta enhancers .

<protein>TCF-1</protein> , a <protein>T cell-specific transcription factor</protein> of the <protein>HMG box family</protein> , interacts with <dna>sequence motifs</dna> in the <dna>TCR beta and TCR delta enhancers</dna> .


We have recently identified and cloned TCF-1 , a T cell-specific transcription factor with specificity for the AACAAAG motif in the CD3 epsilon enhancer and for the TTCAAAG motif in the TCR alpha enhancer .

We have recently identified and cloned <protein>TCF-1</protein> , a <protein>T cell-specific transcription factor</protein> with specificity for the AACAAAG motif in the CD3 epsilon enhancer and for the <dna>TTCAAAG motif</dna> in the <dna>TCR alpha enhancer</dna> .


TCF-1 belongs to the family of transcription-regulating proteins which share a region of homology termed the HMG-box .

<protein>TCF-1</protein> belongs to the family of <protein>transcription-regulating proteins</protein> which share a region of homology termed the <protein>HMG-box</protein> .


Here , we show by gel retardation analysis that TCF-1 specifically recognizes the T beta 5 element of the TCR beta enhancer and the T delta 7 element of the TCR delta enhancer .

Here , we show by gel retardation analysis that <protein>TCF-1</protein> specifically recognizes the <dna>T beta 5 element</dna> of the <dna>TCR beta enhancer</dna> and the <dna>T delta 7 element</dna> of the <dna>TCR delta enhancer</dna> .


Comparison of the sequences of all elements recognized by TCF-1 defines a consensus motif A/T A/T C A A/G A G .

Comparison of the sequences of all <dna>elements</dna> recognized by <protein>TCF-1</protein> defines a <dna>consensus motif</dna> <dna>A/T A/T C A A/G A G</dna> .


These observations imply that TCF-1 is involved in the control of several T cell-specific genes and might thus play an important role in the establishment and maintenance of the mature T cell phenotype .

These observations imply that <protein>TCF-1</protein> is involved in the control of several <dna>T cell-specific genes</dna> and might thus play an important role in the establishment and maintenance of the <cell_type>mature T cell phenotype</cell_type> .


[ Regulatory effect of insulin on glucocorticoid receptor in human peripheral leukocytes ]

[ Regulatory effect of <protein>insulin</protein> on <protein>glucocorticoid receptor</protein> in <cell_type>human peripheral leukocytes</cell_type> ]


The regulatory effect of insulin on the specific binding power of glucocorticoid receptor ( GR ) of human leukocytes was assessed by the unoccupied receptor sites capable of combining with [ 3H ] labelled dexamethasone measured at 3 and 24 h after incubation with various concentrations of insulin added to the medium .

The regulatory effect of <protein>insulin</protein> on the specific binding power of <protein>glucocorticoid receptor</protein> ( <protein>GR</protein> ) of <cell_type>human leukocytes</cell_type> was assessed by the <protein>unoccupied receptor sites</protein> capable of combining with [ 3H ] labelled dexamethasone measured at 3 and 24 h after incubation with various concentrations of <protein>insulin</protein> added to the medium .


After 3 h incubation the specific binding power with [ 3H ] Dex was decreased by 23.3 +/- 10.0 , 32.2 +/- 13.2 and 54.3 +/- 9.2 % ( P greater than 0.05 , P greater than 0.05 and P less than 0.01 as compared with the control value of 100 in the absence of insulin ) respectively in the presence of 20 mU/L ( physiological testing concentration ) , 200 mU/L ( physiological upper limit ) and 2 , 000 mU/L ( pharmacological concentration ) insulin in the incubation medium .

After 3 h incubation the specific binding power with [ 3H ] Dex was decreased by 23.3 +/- 10.0 , 32.2 +/- 13.2 and 54.3 +/- 9.2 % ( P greater than 0.05 , P greater than 0.05 and P less than 0.01 as compared with the control value of 100 in the absence of <protein>insulin</protein> ) respectively in the presence of 20 mU/L ( physiological testing concentration ) , 200 mU/L ( physiological upper limit ) and 2 , 000 mU/L ( pharmacological concentration ) <protein>insulin</protein> in the incubation medium .


After 24 h incubation the decrease of these values increased respectively to 43.5 +/- 19.0 , 56.1 +/- 20.7 and 80.2 +/- 15.5 ( P less than 0.05 , P less than 0.01 and P less than 0.01 compared with control ) .


Thus the inhibitory effect of insulin on the GR binding power is both dose- and time-dependent , which strongly suggests that GR is tonically controlled by insulin concentration change under physiological conditions .

Thus the inhibitory effect of <protein>insulin</protein> on the <protein>GR</protein> binding power is both dose- and time-dependent , which strongly suggests that <protein>GR</protein> is tonically controlled by <protein>insulin</protein> concentration change under physiological conditions .


The effect of toremifene therapy on serum immunoglobulin levels in breast cancer .

The effect of toremifene therapy on <protein>serum immunoglobulin</protein> levels in breast cancer .


Estrogens and anti-estrogens enhance the number of immunoglobulin ( Ig ) -secreting cells in pokeweed mitogen ( PWM ) -stimulated lymphocyte cultures .

Estrogens and anti-estrogens enhance the number of <cell_type>immunoglobulin ( Ig ) -secreting cells</cell_type> in <cell_line>pokeweed mitogen ( PWM ) -stimulated lymphocyte cultures</cell_line> .


Lymphocytes from patients who have received anti-estrogen therapy show similar enhancement of Ig-secreting cells after PWM stimulation .

<cell_type>Lymphocytes</cell_type> from patients who have received anti-estrogen therapy show similar enhancement of <cell_type>Ig-secreting cells</cell_type> after <protein>PWM</protein> stimulation .


In this study the effect of anti-estrogen ( toremifene ) therapy on serum immunoglobulin ( IgA , IgM , IgG ) levels in breast cancer patients was investigated .

In this study the effect of anti-estrogen ( toremifene ) therapy on <protein>serum immunoglobulin</protein> ( <protein>IgA</protein> , <protein>IgM</protein> , <protein>IgG</protein> ) levels in breast cancer patients was investigated .


Serum Ig levels were followed up to two years after or during the therapy .


An unexpected finding was that the Ig levels decreased during the follow-up period .


This decrease was seen in patients who responded to the therapy as well as in those who did not .


Human erythroid 5-aminolevulinate synthase : promoter analysis and identification of an iron-responsive element in the mRNA .

<protein>Human erythroid 5-aminolevulinate synthase</protein> : <dna>promoter</dna> analysis and identification of an <dna>iron-responsive element</dna> in the <rna>mRNA</rna> .


5-Aminolevulinate synthase ( ALAS ) catalyzes the first step of the heme biosynthetic pathway .

<protein>5-Aminolevulinate synthase</protein> ( <protein>ALAS</protein> ) catalyzes the first step of the <protein>heme</protein> biosynthetic pathway .


cDNA clones for the human erythroid ALAS isozyme were isolated from a fetal liver library .

<dna>cDNA clones</dna> for the <protein>human erythroid ALAS isozyme</protein> were isolated from a fetal liver library .


It can be deduced that the erythroid ALAS precursor protein has a molecular weight of 64.6 kd , and is similar in size to the previously isolated human housekeeping ALAS precursor of molecular weight 70.6 kd .

It can be deduced that the <protein>erythroid ALAS precursor protein</protein> has a molecular weight of 64.6 kd , and is similar in size to the previously isolated <protein>human housekeeping ALAS precursor</protein> of molecular weight 70.6 kd .


The mature mitochondrial forms of the erythroid and housekeeping ALAS isozymes are predicted to have molecular weights of 59.5 kd and 64.6 kd , respectively .

The mature mitochondrial forms of the erythroid and <protein>housekeeping ALAS isozymes</protein> are predicted to have molecular weights of 59.5 kd and 64.6 kd , respectively .


The two isozymes show little amino acid identity in their N-terminal signal sequences but have considerable sequence identity in the C-terminal two-thirds of their proteins .

The two <protein>isozymes</protein> show little amino acid identity in their <protein>N-terminal signal sequences</protein> but have considerable sequence identity in the <protein>C-terminal two-thirds</protein> of their proteins .


An analysis of the immediate promoter of the human erythroid ALAS gene revealed several putative erythroid-specific cis-acting elements including both a GATA-1 and an NF-E2 binding site .

An analysis of the <dna>immediate promoter</dna> of the <dna>human erythroid ALAS gene</dna> revealed several putative <dna>erythroid-specific cis-acting elements</dna> including both a <dna>GATA-1</dna> and an <dna>NF-E2 binding site</dna> .


An iron-responsive element ( IRE ) motif has been identified in the 5'-untranslated region of the human erythroid ALAS mRNA , but is not present in the housekeeping ALAS mRNA .

An <rna>iron-responsive element ( IRE ) motif</rna> has been identified in the 5'-untranslated region of the <rna>human erythroid ALAS mRNA</rna> , but is not present in the <rna>housekeeping ALAS mRNA</rna> .


Gel retardation experiments established that this IRE motif formed a protein - RNA complex with cytosolic extracts from human K562 cells and this binding was strongly competed with IRE transcripts from ferritin or transferrin receptor mRNAs .

Gel retardation experiments established that this <rna>IRE motif</rna> formed a <protein>protein - RNA complex</protein> with cytosolic extracts from <cell_line>human K562 cells</cell_line> and this binding was strongly competed with <rna>IRE transcripts</rna> from <rna>ferritin or transferrin receptor mRNAs</rna> .


A transcript of the ALAS IRE , mutated in the conserved loop of the IRE , did not readily form this protein - RNA complex .

A transcript of the <dna>ALAS IRE</dna> , mutated in the conserved loop of the <dna>IRE</dna> , did not readily form this <protein>protein - RNA complex</protein> .


These results suggest that the IRE motif in the ALAS mRNA is functional and imply that translation of the mRNA is controlled by cellular iron availability during erythropoiesis .

These results suggest that the <rna>IRE motif</rna> in the <rna>ALAS mRNA</rna> is functional and imply that translation of the <rna>mRNA</rna> is controlled by cellular iron availability during erythropoiesis .


Regulation of jun and fos gene expression in human monocytes by the macrophage colony-stimulating factor .

Regulation of jun and fos gene expression in <cell_type>human monocytes</cell_type> by the <protein>macrophage colony-stimulating factor</protein> .


The macrophage colony-stimulating factor ( M-CSF ) is required for the growth and differentiation of mononuclear phagocytes .

The <protein>macrophage colony-stimulating factor</protein> ( <protein>M-CSF</protein> ) is required for the growth and differentiation of <cell_type>mononuclear phagocytes</cell_type> .


However , the signaling events responsible for these effects remain unclear .


The present studies have examined the effects of M-CSF on potential signaling pathways involving expression of the jun and fos early response genes .

The present studies have examined the effects of <protein>M-CSF</protein> on potential signaling pathways involving expression of the <dna>jun and fos early response genes</dna> .


Low levels of c-jun transcripts were detectable in resting human peripheral blood monocytes .

Low levels of <protein>c-jun transcripts</protein> were detectable in <cell_type>resting human peripheral blood monocytes</cell_type> .


Treatment of these cells with 10 ( 3 ) units/ml human recombinant M-CSF was associated with rapid and transient increases in c-jun mRNA levels .

Treatment of these cells with 10 ( 3 ) units/ml <protein>human recombinant M-CSF</protein> was associated with rapid and transient increases in <rna>c-jun mRNA</rna> levels .


Nuclear run-on assays and mRNA stability studies demonstrated that M-CSF regulates c-jun expression by both an increase in transcription rate and a prolongation in the half-life of c-jun transcripts .

Nuclear run-on assays and mRNA stability studies demonstrated that <protein>M-CSF</protein> regulates <dna>c-jun</dna> expression by both an increase in transcription rate and a prolongation in the half-life of <rna>c-jun transcripts</rna> .


M-CSF treatment was also associated with a rapid induction of the jun-B gene , although expression of this gene was prolonged compared to that of c-jun .

<protein>M-CSF</protein> treatment was also associated with a rapid induction of the <dna>jun-B gene</dna> , although expression of this gene was prolonged compared to that of <dna>c-jun</dna> .


We further demonstrate that M-CSF increases c-fos mRNA levels in human monocytes through control at both the transcriptional and posttranscriptional levels .

We further demonstrate that <protein>M-CSF</protein> increases <rna>c-fos mRNA</rna> levels in <cell_type>human monocytes</cell_type> through control at both the transcriptional and posttranscriptional levels .


Maximal induction of the c-fos gene was followed by that for the fos-B gene .

Maximal induction of the <dna>c-fos gene</dna> was followed by that for the <dna>fos-B gene</dna> .


Moreover , M-CSF -induced expression of the fos-related gene , fra-1 , was delayed compared to that for both c-fos and fos-B .

Moreover , <protein>M-CSF</protein> -induced expression of the <dna>fos-related gene</dna> , <dna>fra-1</dna> , was delayed compared to that for both <dna>c-fos</dna> and <dna>fos-B</dna> .


Taken together , the results indicate that M-CSF treatment is associated with differential activation of multiple members of the jun/fos family and that expression of these genes could contribute to nuclear signaling mechanisms that regulate a specific program of monocyte differentiation .

Taken together , the results indicate that <protein>M-CSF</protein> treatment is associated with differential activation of multiple members of the <dna>jun/fos family</dna> and that expression of these genes could contribute to nuclear signaling mechanisms that regulate a specific program of monocyte differentiation .


Glucocorticoid receptors in systemic lupus erythematosus .

<protein>Glucocorticoid receptors</protein> in systemic lupus erythematosus .


Glucocorticosteroids remain the major treatment modality for systemic lupus erythematosus ( SLE ) , but their mechanism of action is unclear .


Over the past decade it has become clear that glucocorticosteroid receptors play a significant role in the mechanism of glucocorticosteroid action .

Over the past decade it has become clear that <protein>glucocorticosteroid receptors</protein> play a significant role in the mechanism of glucocorticosteroid action .


We studied glucocorticosteroid receptor density and affinity on peripheral blood mononuclear cells by the glucocorticosteroid binding assay in 33 patients with SLE who had taken no glucocorticosteroid for the previous 6 months and in 32 healthy controls .

We studied <protein>glucocorticosteroid receptor</protein> density and affinity on <cell_type>peripheral blood mononuclear cells</cell_type> by the glucocorticosteroid binding assay in 33 patients with SLE who had taken no glucocorticosteroid for the previous 6 months and in 32 healthy controls .


Patients ' disease activity was measured by the SLE Disease Activity Index ( SLEDAI ) .


Glucocorticosteroid receptors on leukocytes of patients with SLE were significantly higher than in healthy controls ( 4419 +/- 306 vs 3369 +/- 196 , p less than 0.005 ) .

<protein>Glucocorticosteroid receptors</protein> on <cell_type>leukocytes</cell_type> of patients with SLE were significantly higher than in healthy controls ( 4419 +/- 306 vs 3369 +/- 196 , p less than 0.005 ) .


The binding affinity was not different between patients and controls .


There was no correlation between glucocorticosteroid receptor number and SLE disease activity .

There was no correlation between <protein>glucocorticosteroid receptor</protein> number and SLE disease activity .


Kappa B binding proteins are constitutively expressed in an IL-2 autocrine human T cell line .

<protein>Kappa B binding proteins</protein> are constitutively expressed in an <cell_line>IL-2 autocrine human T cell line</cell_line> .


The IL-2 and the IL-2-R alpha genes are both expressed transiently in normal T lymphocytes after Ag or mitogen activation .

The <dna>IL-2 and the IL-2-R alpha genes</dna> are both expressed transiently in <cell_type>normal T lymphocytes</cell_type> after Ag or mitogen activation .


In contrast , the human T cell line , IARC 301 , expresses these two genes constitutively and we have previously demonstrated that its growth depends on the autocrine production of this T cell growth factor and high affinity IL-2R .

In contrast , the <cell_line>human T cell line</cell_line> , <cell_line>IARC 301</cell_line> , expresses these two genes constitutively and we have previously demonstrated that its growth depends on the autocrine production of this <protein>T cell growth factor</protein> and <protein>high affinity IL-2R</protein> .


To dissect the molecular basis for the unusual persistent expression of the IL-2 and IL-2-R alpha genes in these IARC 301 T cells , we have analyzed the interactions of constitutively expressed nuclear proteins with the 5 ' flanking regions of the IL-2 and IL-2-R alpha genes using both DNase I footprinting and gel retardation techniques .

To dissect the molecular basis for the unusual persistent expression of the <dna>IL-2 and IL-2-R alpha genes</dna> in these <cell_line>IARC 301</cell_line> <cell_type>T cells</cell_type> , we have analyzed the interactions of <protein>constitutively expressed nuclear proteins</protein> with the <dna>5 ' flanking regions</dna> of the <dna>IL-2 and IL-2-R alpha genes</dna> using both <protein>DNase I</protein> footprinting and gel retardation techniques .


We have found that a region in both genes ( -276 to -250 for IL-2-R alpha and -203 to -183 for IL-2 ) , which corresponds to a kappa B enhancer element , is specifically protected by nuclear proteins from IARC 301 .

We have found that a region in both genes ( -276 to -250 for <dna>IL-2-R alpha</dna> and -203 to -183 for <dna>IL-2</dna> ) , which corresponds to a <dna>kappa B enhancer element ,</dna> is specifically protected by <protein>nuclear proteins</protein> from <cell_line>IARC 301</cell_line> .


In agreement with this finding , both the IL-2 and IL-2-R alpha promoters are active in transient transfection assays in IARC 301 cells .

In agreement with this finding , both the <dna>IL-2 and IL-2-R alpha promoters</dna> are active in transient transfection assays in <cell_line>IARC 301 cells</cell_line> .


In contrast , mutation of the kappa B enhancer results in markedly attenuated activities of both promoters .

In contrast , mutation of the <protein>kappa B enhancer</protein> results in markedly attenuated activities of both <dna>promoters</dna> .


Two proteins binding the kappa B sequence , NF-kappa B and KBF1 , are constitutively expressed in IARC 301 nuclei and induced by PMA and PHA in Jurkat .

Two proteins binding the <dna>kappa B sequence</dna> , <protein>NF-kappa B</protein> and <protein>KBF1</protein> , are constitutively expressed in <cell_line>IARC 301</cell_line> nuclei and induced by PMA and <protein>PHA</protein> in <cell_line>Jurkat</cell_line> .


They bind to the kappa B motifs with different relative affinities that may reflect their different contribution in the expression of various promoters .

They bind to the <dna>kappa B motifs</dna> with different relative affinities that may reflect their different contribution in the expression of various <dna>promoters</dna> .


HIV1 infection of human monocytes and macrophages promotes induction or translocation of NF-KB-related factors .

HIV1 infection of <cell_type>human monocytes</cell_type> and <cell_type>macrophages</cell_type> promotes induction or translocation of <protein>NF-KB-related factors</protein> .


In 1991 , we demonstrated , using electrophoretic mobility shift assays , that 3 different factors ( termed B1 , B2 and B3 ) with affinity for the KB-enhancer target sequence were specifically detected in nuclear extracts from HIV1-infected monocytes and macrophages .

In 1991 , we demonstrated , using electrophoretic mobility shift assays , that 3 different factors ( termed <protein>B1</protein> , <protein>B2</protein> and <protein>B3</protein> ) with affinity for the <dna>KB-enhancer target sequence</dna> were specifically detected in nuclear extracts from <cell_type>HIV1-infected monocytes</cell_type> and <cell_type>macrophages</cell_type> .


The B2 factor was induced in the nuclei of these cells only upon HIV1 infection .

The <protein>B2 factor</protein> was induced in the nuclei of these cells only upon HIV1 infection .


The B3 factor was only slightly evident in nuclei of uninfected cells but was readily detectable in nuclei of infected monocytes .

The <protein>B3 factor</protein> was only slightly evident in nuclei of <cell_type>uninfected cells</cell_type> but was readily detectable in nuclei of <cell_type>infected monocytes</cell_type> .


Its expression remained very low in nuclei of HIV1-infected macrophages .

Its expression remained very low in nuclei of <cell_type>HIV1-infected macrophages</cell_type> .


In this paper , we demonstrate that the B2 factor is expressed in the cytosol of monocytes and macrophages as a DNA-binding protein , indicating that it is not associated with an inhibitor ( IKB ) .

In this paper , we demonstrate that the <protein>B2 factor</protein> is expressed in the cytosol of <cell_type>monocytes</cell_type> and <cell_type>macrophages</cell_type> as a <protein>DNA-binding protein</protein> , indicating that it is not associated with an inhibitor ( IKB ) .


This factor remained clustered in the cytosol and was translocated to the nuclei only after HIV1 infection .


The B3 factor is detected in the cytosol only when cells are HIV1-infected .

The <protein>B3 factor</protein> is detected in the cytosol only when cells are HIV1-infected .


The role of HIV1 infection in the expression and the translocation of these factors is discussed .


Identification and cloning of TCF-1 , a T lymphocyte-specific transcription factor containing a sequence-specific HMG box .

Identification and cloning of <protein>TCF-1</protein> , a <protein>T lymphocyte-specific transcription factor</protein> containing a <protein>sequence-specific HMG box</protein> .


CD3 -epsilon expression is controlled by a downstream T lymphocyte-specific enhancer element .

<protein>CD3</protein> -epsilon expression is controlled by a <dna>downstream T lymphocyte-specific enhancer element</dna> .


We report the identification of a T cell-specific transcription factor , TCF-1 , binding to this element .

We report the identification of a <protein>T cell-specific transcription factor</protein> , <protein>TCF-1</protein> , binding to this element .


The multimerized recognition motif of TCF-1 constituted a T cell-specific enhancer .

The <protein>multimerized recognition motif</protein> of <protein>TCF-1</protein> constituted a T cell-specific enhancer .


Subsequent cloning of TCF-1 identified three splice alternatives .

Subsequent cloning of <protein>TCF-1</protein> identified three <protein>splice alternatives</protein> .


TCF-1 contained a single DNA-binding HMG box most closely related to similar boxes in the putative mammalian sex-determining gene SRY and in the Schizosaccharomyces pombe Mc mating type gene .

<protein>TCF-1</protein> contained a single <protein>DNA-binding HMG box</protein> most closely related to similar boxes in the <dna>putative mammalian sex-determining gene</dna> <dna>SRY</dna> and in the <dna>Schizosaccharomyces pombe Mc mating type gene</dna> .


TCF-1 mRNA was expressed uniquely in T lymphocytes .

<rna>TCF-1 mRNA</rna> was expressed uniquely in <cell_type>T lymphocytes</cell_type> .


Upon cotransfection into non-T cells , TCF-1 could transactivate through its cognate motif .

Upon cotransfection into <cell_type>non-T cells</cell_type> , <protein>TCF-1</protein> could transactivate through its cognate motif .


These results identify TCF-1 as a T cell-specific transcription factor , which might play a role in the establishment of the mature T cell phenotype .

These results identify <protein>TCF-1</protein> as a <protein>T cell-specific transcription factor</protein> , which might play a role in the establishment of the <cell_type>mature T cell phenotype</cell_type> .


Identification of transcriptional suppressor proteins that bind to the negative regulatory element of the human immunodeficiency virus type 1 .

Identification of <protein>transcriptional suppressor proteins</protein> that bind to the <dna>negative regulatory element</dna> of the human immunodeficiency virus type 1 .


Two different proteins which independently bound to neighboring sequences within the negative regulatory element ( NRE ) of human immunodeficiency virus type 1 ( HIV-1 ) were detected in the nuclear extract of a virus-infected human T cell line .

Two different proteins which independently bound to neighboring sequences within the <dna>negative regulatory element</dna> ( <dna>NRE</dna> ) of human immunodeficiency virus type 1 ( HIV-1 ) were detected in the nuclear extract of a <cell_line>virus-infected human T cell line</cell_line> .


One of the factors bound to a novel dyad symmetrical sequence .

One of the factors bound to a <dna>novel dyad symmetrical sequence</dna> .


This sequence is well conserved in various HIV-1 isolates and partial homology was found with the promoter region of the human retinoblastoma gene .

This sequence is well conserved in various HIV-1 isolates and partial homology was found with the <dna>promoter region</dna> of the <dna>human retinoblastoma gene</dna> .


Similar DNA binding activity was detected in a variety of virus-uninfected human T cell lines and HeLa cells by means of a gel mobility shift assay .

Similar DNA binding activity was detected in a variety of <cell_line>virus-uninfected human T cell lines</cell_line> and <cell_line>HeLa cells</cell_line> by means of a gel mobility shift assay .


The other factor bound to a putative AP-1 recognition sequence predicted for the HIV-1 NRE .

The other factor bound to a <dna>putative AP-1 recognition sequence</dna> predicted for the HIV-1 <dna>NRE</dna> .


However , this factor did not bind to a typical AP-1 site .

However , this factor did not bind to a typical <dna>AP-1 site</dna> .


The insertion of multiple copies of the binding site for the former or latter factor into a heterologous promoter reduced the promoter activity to one-tenth or one-third , respectively .

The insertion of multiple copies of the <dna>binding site</dna> for the former or latter factor into a <dna>heterologous promoter</dna> reduced the promoter activity to one-tenth or one-third , respectively .


Thus , each factor may function as a novel negative regulator of transcription .

Thus , each factor may function as a <protein>novel negative regulator</protein> of transcription .


Protein kinase C activation and protooncogene expression in differentiation/retrodifferentiation of human U-937 leukemia cells .

<protein>Protein kinase C</protein> activation and <dna>protooncogene</dna> expression in differentiation/retrodifferentiation of <cell_line>human U-937 leukemia cells</cell_line> .


Human U-937 leukemia cells differentiate along the monocytic lineage following 3-day exposures to 12-O-tetradecanoylphorbol-13-acetate ( TPA ) .

<cell_line>Human U-937 leukemia cells</cell_line> differentiate along the <cell_type>monocytic lineage</cell_type> following 3-day exposures to 12-O-tetradecanoylphorbol-13-acetate ( TPA ) .


This induction of differentiation is accompanied by adherence and loss of proliferation , as well as expression/repression of differentiation-associated genes .

This induction of differentiation is accompanied by adherence and loss of proliferation , as well as expression/repression of <dna>differentiation-associated genes</dna> .


Long term culture of TPA-differentiated U-937 cells in the absence of phorbol ester for 32-36 days resulted in a process of retrodifferentiation .

Long term culture of <cell_type>TPA-differentiated U-937 cells</cell_type> in the absence of phorbol ester for 32-36 days resulted in a process of retrodifferentiation .


The retrodifferentiated cells detached from the substrate and reinitiated proliferation .


Other cellular parameters , such as glycosidase activities , cytokine release , and filament expression , returned to levels similar to that observed in uninduced cells .

Other cellular parameters , such as glycosidase activities , <protein>cytokine</protein> release , and filament expression , returned to levels similar to that observed in <cell_type>uninduced cells</cell_type> .


Treatment of U-937 cells with TPA resulted in a rapid translocation of protein kinase C ( PKC ) from the cytosol to cell membrane fractions within 2-8 min .

Treatment of <cell_line>U-937 cells</cell_line> with TPA resulted in a rapid translocation of <protein>protein kinase C</protein> ( <protein>PKC</protein> ) from the cytosol to cell membrane fractions within 2-8 min .


Increased levels of membrane-associated PKC activity persisted until 17-29 days .

Increased levels of membrane-associated <protein>PKC</protein> activity persisted until 17-29 days .


However , longer periods of incubation were associated with a return to the distribution of PKC in control cells .

However , longer periods of incubation were associated with a return to the distribution of <protein>PKC</protein> in control cells .


Activation of PKC has been implicated in the regulation of certain immediate early response genes , and in the present studies , TPA rapidly induced c-fos and c-jun gene expression .

Activation of <protein>PKC</protein> has been implicated in the regulation of certain <dna>immediate early response genes</dna> , and in the present studies , TPA rapidly induced <dna>c-fos</dna> and <dna>c-jun gene expression</dna> .


Levels of c-fos and c-jun transcripts remained elevated during periods of PKC activation and also returned to levels observed in control cells by 30-36 days , when the cells entered retrodifferentiation .

Levels of <rna>c-fos and c-jun transcripts</rna> remained elevated during periods of <protein>PKC</protein> activation and also returned to levels observed in control cells by 30-36 days , when the cells entered retrodifferentiation .


Staurosporine , a nonspecific inhibitor of PKC , partially blocked TPA-induced adherence and growth inhibition and concomitantly prevented TPA-induced c-fos and c-jun gene expression .

Staurosporine , a nonspecific inhibitor of <protein>PKC</protein> , partially blocked TPA-induced adherence and growth inhibition and concomitantly prevented TPA-induced c-fos and c-jun gene expression .


( ABSTRACT TRUNCATED AT 250 WORDS )


Kappa B-specific DNA binding proteins are differentially inhibited by enhancer mutations and biological oxidation .

<protein>Kappa B-specific DNA binding proteins</protein> are differentially inhibited by enhancer mutations and biological oxidation .


Kappa B ( kappa B ) enhancer binding proteins isolated from the nuclei of activated human T cells produce two distinct nucleoprotein complexes when incubated with the kappa B element from the interleukin-2 receptor-alpha ( IL-2R alpha ) gene .

<protein>Kappa B ( kappa B ) enhancer binding proteins</protein> isolated from the nuclei of activated <cell_type>human T cells</cell_type> produce two distinct <protein>nucleoprotein complexes</protein> when incubated with the <dna>kappa B element</dna> from the <dna>interleukin-2 receptor-alpha ( IL-2R alpha ) gene</dna> .


These two DNA-protein complexes are composed of at least four host proteins ( p50 , p55 , p75 , p85 ) , each of which shares structural similarity with the v-rel oncogene product .

These two <protein>DNA-protein complexes</protein> are composed of at least four host proteins ( <protein>p50</protein> , <protein>p55</protein> , <protein>p75</protein> , <protein>p85</protein> ) , each of which shares structural similarity with the <protein>v-rel oncogene product</protein> .


Nuclear expression of these proteins is induced with distinctly biphasic kinetics following phorbol ester activation of T cells ( p55/p75 early and p50/p85 late ) .

Nuclear expression of these proteins is induced with distinctly biphasic kinetics following phorbol ester activation of <cell_type>T cells</cell_type> ( <protein>p55/p75 early</protein> and <protein>p50/p85 late</protein> ) .


DNA-protein crosslinking studies have revealed that the more rapidly migrating B2 complex contains both p50 and p55 while the more slowly migrating B1 complex is composed of p50 , p55 , p75 , and p85 .

DNA-protein crosslinking studies have revealed that the more rapidly migrating <protein>B2 complex</protein> contains both <protein>p50</protein> and <protein>p55</protein> while the more slowly migrating <protein>B1 complex</protein> is composed of <protein>p50</protein> , <protein>p55</protein> , <protein>p75</protein> , and <protein>p85</protein> .


Site-directed mutagenesis of the wild-type IL-2R alpha kappa B enhancer ( GGGGAATCTCCC ) has revealed that the binding of p50 and p55 ( B2 complex ) is particularly sensitive to alteration of the 5 ' triplet of deoxyguanosine residues .

Site-directed mutagenesis of the <dna>wild-type IL-2R alpha kappa B enhancer</dna> ( GGGGAATCTCCC ) has revealed that the binding of p50 and <protein>p55</protein> ( <protein>B2 complex</protein> ) is particularly sensitive to alteration of the <dna>5 ' triplet</dna> of deoxyguanosine residues .


In contrast , formation of the B1 complex , reflecting the binding of p75 and p85 , critically depends upon the more 3 ' sequences of this enhancer element .

In contrast , formation of the <protein>B1 complex</protein> , reflecting the binding of <protein>p75</protein> and <protein>p85</protein> , critically depends upon the more 3 ' sequences of this <dna>enhancer element</dna> .


DNA binding by all four of these Rel-related factors is blocked by selective chemical modification of lysine and arginine residues , suggesting that both of these basic amino acids are required for binding to the kappa B element .

DNA binding by all four of these <protein>Rel-related factors</protein> is blocked by selective chemical modification of lysine and arginine residues , suggesting that both of these basic amino acids are required for binding to the <dna>kappa B element</dna> .


Similarly , covalent modification of free sulfhydryl groups with diamide ( reversible ) or N-ethylmaleimide ( irreversible ) results in a complete loss of DNA binding activity .


In contrast , mild oxidation with glucose oxidase selectively inhibits p75 and p85 binding while not blocking p50 and p55 interactions .

In contrast , mild oxidation with <protein>glucose oxidase</protein> selectively inhibits <protein>p75</protein> and <protein>p85</protein> binding while not blocking <protein>p50</protein> and <protein>p55</protein> interactions .


These findings suggest that reduced cysteine thiols play an important role in the DNA binding activity of this family of Rel-related transcription factors .

These findings suggest that reduced cysteine thiols play an important role in the DNA binding activity of this family of <protein>Rel-related transcription factors</protein> .


[ Changes in leucocytic estrogen receptor levels in patients with climacteric syndrome and therapeutic effect of liuwei dihuang pills ]

[ Changes in leucocytic <protein>estrogen receptor</protein> levels in patients with climacteric syndrome and therapeutic effect of liuwei dihuang pills ]


The numbers of estrogen receptor ( ER ) in human peripheral leucocytes in 22 women with climacteric syndrome were measured by radioligand method .

The numbers of <protein>estrogen receptor</protein> ( <protein>ER</protein> ) in <cell_type>human peripheral leucocytes</cell_type> in 22 women with climacteric syndrome were measured by radioligand method .


The results were compared with those of 12 normal child-bearing-age women .


It wat found that the contents of leucocytic ER in climacteric syndrome patients were significantly lower than normal child-bearing-age women .

It wat found that the contents of <protein>leucocytic ER</protein> in climacteric syndrome patients were significantly lower than normal child-bearing-age women .


The authors used a Chinese prescription -- Liuwei Dihuang Pills ( LDP ) to treat the patients for 2 months .


The numbers of leucocytic ER were significantly increased after treatment .

The numbers of <protein>leucocytic ER</protein> were significantly increased after treatment .


The data indicate that decrease of ER levels in cell may involve in the pathogenesis of climacteric syndrome .

The data indicate that decrease of <protein>ER</protein> levels in cell may involve in the pathogenesis of climacteric syndrome .


LDP not only increases plasma estradiol levels , but also increases the leucocytic ER levels .

LDP not only increases plasma estradiol levels , but also increases the leucocytic <protein>ER</protein> levels .


This may be the basis of the therapeutic effect on the disease .


Evaluation of the role of ligand and thermal activation of specific DNA binding by in vitro synthesized human glucocorticoid receptor .

Evaluation of the role of ligand and thermal activation of specific DNA binding by <protein>in vitro synthesized human glucocorticoid receptor</protein> .


We have used a DNA-binding/immunoprecipitation assay to analyze the capacity of human glucocorticoid receptor ( hGR ) , generated in rabbit reticulocyte lysates , to bind DNA .

We have used a DNA-binding/immunoprecipitation assay to analyze the capacity of <protein>human glucocorticoid receptor</protein> ( <protein>hGR</protein> ) , generated in rabbit reticulocyte lysates , to bind DNA .


In vitro translated hGR was indistinguishable from native hGR , as determined by migration on sodium dodecyl sulfate-polyacrylamide gels , sedimentation on sucrose density gradients , and reactivity with antipeptide antibodies generated against hGR .

<protein>In vitro translated hGR</protein> was indistinguishable from <protein>native hGR</protein> , as determined by migration on sodium dodecyl sulfate-polyacrylamide gels , sedimentation on sucrose density gradients , and reactivity with <protein>antipeptide antibodies</protein> generated against <protein>hGR</protein> .


In addition , cell-free synthesized hGR was capable of specific binding to glucocorticoid response element ( GRE ) -containing DNA fragments .

In addition , <protein>cell-free synthesized hGR</protein> was capable of specific binding to <dna>glucocorticoid response element ( GRE ) -containing DNA fragments</dna> .


Using this assay system , we have evaluated the contributions of ligand binding and heat activation to DNA binding by these glucocorticoid receptors .

Using this assay system , we have evaluated the contributions of ligand binding and heat activation to DNA binding by these <protein>glucocorticoid receptors</protein> .


In vitro translated hGR was capable of selective DNA binding even in the absence of glucocorticoid .

<protein>In vitro translated hGR</protein> was capable of selective DNA binding even in the absence of glucocorticoid .


Treatment with dexamethasone or the antiglucocorticoid RU486 had no additional effect on the DNA-binding capacity when receptor preparations were maintained at 0 C ( no activation ) .


In contrast , addition of either ligand or antagonist in combination with a heat activation step promoted DNA binding by approximately 3-fold over that of heat-activated unliganded receptors .

In contrast , addition of either ligand or antagonist in combination with a heat activation step promoted DNA binding by approximately 3-fold over that of heat-activated <protein>unliganded receptors</protein> .


Agonist ( dexamethasone ) was slightly more effective in supporting specific DNA binding than antagonist ( RU486 ) .


DNA binding by in vitro synthesized GR was blocked by the addition of sodium molybdate to the receptor preparations before steroid addition and thermal activation .

DNA binding by <protein>in vitro synthesized GR</protein> was blocked by the addition of sodium molybdate to the receptor preparations before steroid addition and thermal activation .


Addition of KCl resulted in less DNA binding either due to blockage of DNA- receptor complex formation or disruption of the complexes .

Addition of KCl resulted in less DNA binding either due to blockage of DNA- <protein>receptor complex</protein> formation or disruption of the complexes .


The specificity of DNA binding by cell-free synthesized hGR was analyzed further by examining the abilities of various DNAs to compete for binding to a naturally occurring GRE found in the mouse mammary tumor virus-long terminal repeat .

The specificity of DNA binding by <protein>cell-free synthesized hGR</protein> was analyzed further by examining the abilities of <dna>various DNAs</dna> to compete for binding to a naturally occurring <dna>GRE</dna> found in the <dna>mouse mammary tumor virus-long terminal repeat</dna> .


Oligonucleotides containing the consensus GRE were the most efficient competitors , and fragments containing regulatory sequences from glucocorticoid-repressible genes were somewhat competitive , whereas single stranded oligonucleotides were unable to compete for mouse mammary tumor virus-long terminal repeat DNA binding , except when competitor was present at extremely high concentrations .

Oligonucleotides containing the <dna>consensus GRE</dna> were the most efficient competitors , and fragments containing <dna>regulatory sequences</dna> from <dna>glucocorticoid-repressible genes</dna> were somewhat competitive , whereas single stranded oligonucleotides were unable to compete for <dna>mouse mammary tumor virus-long terminal repeat</dna> DNA binding , except when competitor was present at extremely high concentrations .


Together these studies indicate that hGR synthesized in rabbit reticulocyte lysates displays many of the same properties , including GRE -specific DNA binding , observed for glucocorticoid receptor present in cytosolic extracts of mammalian cells and tissues .

Together these studies indicate that <protein>hGR</protein> synthesized in rabbit reticulocyte lysates displays many of the same properties , including <dna>GRE</dna> -specific DNA binding , observed for <protein>glucocorticoid receptor</protein> present in cytosolic extracts of <cell_type>mammalian cells</cell_type> and tissues .


Similarities between the effects of dexamethasone and RU486 suggest that the antiglucocorticoid properties of RU486 do not occur at the level of specific DNA binding .


Expression of 1 , 25 ( OH ) 2D3 receptors on alveolar lymphocytes from patients with pulmonary granulomatous diseases .

Expression of <protein>1 , 25 ( OH ) 2D3 receptors</protein> on <cell_type>alveolar lymphocytes</cell_type> from patients with pulmonary granulomatous diseases .


1 , 25 ( OH ) 2D3 is known to be produced at sites of granulomatous reactions .


In order to characterize the cell types that are targets for this immunoregulatory hormone , we have evaluated the expression of 1 , 25 ( OH ) 2D3 receptors on peripheral blood T-lymphocytes and those recovered from the lung by bronchoalveolar lavage from patients with pulmonary granulomatous diseases ( tuberculosis and sarcoidosis ) and from normal control subjects using combined autoradiographic and immunohistochemical techniques .

In order to characterize the cell types that are targets for this immunoregulatory hormone , we have evaluated the expression of <protein>1 , 25 ( OH ) 2D3 receptors</protein> on <cell_type>peripheral blood T-lymphocytes</cell_type> and those recovered from the lung by bronchoalveolar lavage from patients with pulmonary granulomatous diseases ( tuberculosis and sarcoidosis ) and from normal control subjects using combined autoradiographic and immunohistochemical techniques .


Lavage T-lymphocytes from patients with tuberculosis or with sarcoidosis , but not those from normal control subjects , expressed 1 , 25 ( OH ) 2D3 receptors as demonstrated by binding of [ 3H ] 1 , 25 ( OH ) 2D3 , which was inhibited by the presence of excess unlabeled 1 , 25 ( OH ) 2D3 , but not by the presence of unlabeled 25 ( OH ) D3 ( receptor-positive lymphocytes : sarcoidosis , 20 +/- 12 % ; tuberculosis , 31 +/- 17 % ) .

Lavage T-lymphocytes from patients with tuberculosis or with sarcoidosis , but not those from normal control subjects , expressed <protein>1 , 25 ( OH ) 2D3 receptors</protein> as demonstrated by binding of [ 3H ] 1 , 25 ( OH ) 2D3 , which was inhibited by the presence of excess unlabeled 1 , 25 ( OH ) 2D3 , but not by the presence of unlabeled 25 ( OH ) D3 ( <cell_type>receptor-positive lymphocytes</cell_type> : sarcoidosis , 20 +/- 12 % ; tuberculosis , 31 +/- 17 % ) .


In contrast , blood lymphocytes from patients with granulomatous diseases did not express detectable 1 , 25 ( OH ) 2D3 receptors .

In contrast , <cell_type>blood lymphocytes</cell_type> from patients with granulomatous diseases did not express detectable <protein>1 , 25 ( OH ) 2D3 receptors</protein> .


The percentage of lavage T-lymphocytes expressing 1 , 25 ( OH ) 2D3 receptors was significantly greater for patients with tuberculosis presenting with isolated hilar adenopathy than for patients with pulmonary infiltrates and/or cavities .

The percentage of <cell_type>lavage T-lymphocytes</cell_type> expressing <protein>1 , 25 ( OH ) 2D3 receptors</protein> was significantly greater for patients with tuberculosis presenting with isolated hilar adenopathy than for patients with pulmonary infiltrates and/or cavities .


1 , 25 ( OH ) 2D3 receptors were expressed to a greater extent on CD8+ T-lymphocytes than on CD4+ T-lymphocytes in sarcoidosis , whereas a greater proportion of CD4+ than of CD8+ T-lymphocytes from patients with tuberculosis were receptor-positive .

<protein>1 , 25 ( OH ) 2D3 receptors</protein> were expressed to a greater extent on <cell_type>CD8+ T-lymphocytes</cell_type> than on <cell_type>CD4+ T-lymphocytes</cell_type> in sarcoidosis , whereas a greater proportion of <cell_type>CD4+</cell_type> than of <cell_type>CD8+ T-lymphocytes</cell_type> from patients with tuberculosis were receptor-positive .


These findings support the conclusion that the interaction of 1 , 25 ( OH ) 2D3 with its receptor on T-lymphocytes may play an important role in the regulation of granulomatous reactions , but because these receptors are expressed on different lymphocyte populations , the net effect of this potent immunoregulatory molecule is likely different in sarcoidosis and tuberculosis .

These findings support the conclusion that the interaction of 1 , 25 ( OH ) 2D3 with its receptor on <cell_type>T-lymphocytes</cell_type> may play an important role in the regulation of granulomatous reactions , but because these receptors are expressed on different <cell_type>lymphocyte populations</cell_type> , the net effect of this potent <protein>immunoregulatory molecule</protein> is likely different in sarcoidosis and tuberculosis .


Role for the Epstein-Barr virus nuclear antigen 2 in viral promoter switching during initial stages of infection .

Role for the <protein>Epstein-Barr virus nuclear antigen 2</protein> in <dna>viral promoter</dna> switching during initial stages of infection .


During latent Epstein-Barr virus ( EBV ) infection of human B lymphocytes , six viral nuclear antigen ( EBNAs ) are expressed from long primary transcripts by means of alternative splicing and alternative polyadenylylation sites .

During latent Epstein-Barr virus ( EBV ) infection of <cell_type>human B lymphocytes</cell_type> , <protein>six viral nuclear antigen</protein> ( <protein>EBNAs</protein> ) are expressed from <rna>long primary transcripts</rna> by means of <rna>alternative splicing</rna> and <rna>alternative polyadenylylation sites</rna> .


These transcripts initiate from one of two promoters , Cp or Wp , that function in a mutually exclusive fashion .

These transcripts initiate from one of two <dna>promoters</dna> , <dna>Cp</dna> or Wp , that function in a mutually exclusive fashion .


Wp is exclusively utilized during the initial stages of infection of primary B lymphocytes , followed by a switch to Cp usage .

Wp is exclusively utilized during the initial stages of infection of <cell_type>primary B lymphocytes</cell_type> , followed by a switch to <dna>Cp</dna> usage .


These studies have been extended to show that ( i ) a mutant EBV strain lacking the gene encoding EBNA 2 fails to switch from Wp to Cp usage in primary B lymphocytes , although the virus contains a functional Cp ; ( ii ) a region from -429 to -245 base pairs upstream of Cp is essential for Cp activity in B lymphocytes , but only in the context of upstream and downstream sequences ; ( iii ) this region contains an EBNA 2-dependent enhancer ; and ( iv ) DNase I protection employing nuclear extracts from B and T lymphocytes revealed a B-cell-specific footprint in the region of the EBNA 2-dependent enhancer .

These studies have been extended to show that ( i ) a mutant EBV strain lacking the gene encoding <protein>EBNA 2</protein> fails to switch from Wp to <dna>Cp</dna> usage in <cell_type>primary B lymphocytes</cell_type> , although the virus contains a functional <dna>Cp</dna> ; ( ii ) a region from <dna>-429 to -245 base pairs</dna> upstream of <dna>Cp</dna> is essential for <dna>Cp</dna> activity in <cell_type>B lymphocytes</cell_type> , but only in the context of <dna>upstream and downstream sequences</dna> ; ( iii ) this region contains an <dna>EBNA 2-dependent enhancer</dna> ; and ( iv ) <protein>DNase I</protein> protection employing nuclear extracts from <cell_type>B and T lymphocytes</cell_type> revealed a <dna>B-cell-specific footprint</dna> in the region of the <dna>EBNA 2-dependent enhancer</dna> .


These results support a model for viral promoter switching during the initial stages of infection in which Wp activity leads to the expression of EBNA 2 , followed by activation of Cp through the EBNA 2-dependent enhancer .

These results support a model for <dna>viral promoter</dna> switching during the initial stages of infection in which Wp activity leads to the expression of <protein>EBNA 2</protein> , followed by activation of <dna>Cp</dna> through the <dna>EBNA 2-dependent enhancer</dna> .


Immune response of peripheral blood mononuclear cells to HBx-antigen of hepatitis B virus .

Immune response of <cell_type>peripheral blood mononuclear cells</cell_type> to <protein>HBx-antigen</protein> of hepatitis B virus .


The hepatitis B virus genome encodes a transcriptional transactivator protein designated HBxAg .

The <dna>hepatitis B virus genome</dna> encodes a <protein>transcriptional transactivator protein</protein> designated <protein>HBxAg</protein> .


We have investigated whether this antigen is a target structure for human T-lymphocytes .

We have investigated whether this antigen is a target structure for <cell_type>human T-lymphocytes</cell_type> .


Using recombinant HBxAg protein , we found HBxAg -specific stimulation of peripheral blood mononuclear cells in patients with acute hepatitis B virus infection ( 6 of 6 ) and chronic hepatitis B virus infection ( 6 of 17 ) but not in healthy individuals .

Using <protein>recombinant HBxAg protein</protein> , we found <protein>HBxAg</protein> -specific stimulation of <cell_type>peripheral blood mononuclear cells</cell_type> in patients with acute hepatitis B virus infection ( 6 of 6 ) and chronic hepatitis B virus infection ( 6 of 17 ) but not in healthy individuals .


With HBxAg -specific synthetic polypeptides , several T-cell epitopes were identified .

With <protein>HBxAg</protein> -specific synthetic polypeptides , several T-cell epitopes were identified .


Most were located in the carboxyterminal half of the HBxAg protein .

Most were located in the <protein>carboxyterminal half</protein> of the <protein>HBxAg protein</protein> .


Five T-cell clones specific for a T-cell epitope located at the carboxyterminal region of HBxAg were established and found to belong to the CD2/CD4-positive , CD8-negative subtype .

Five <cell_line>T-cell clones</cell_line> specific for a <protein>T-cell epitope</protein> located at the <protein>carboxyterminal region</protein> of <protein>HBxAg</protein> were established and found to belong to the <cell_line>CD2/CD4-positive , CD8-negative subtype</cell_line> .


These data establish for the first time HBxAg as an antigen in the cellular immune response .

These data establish for the first time <protein>HBxAg</protein> as an antigen in the cellular immune response .


[ Changes in leucocytic estrogen receptor levels in patients with gynecomastia ]

[ Changes in <protein>leucocytic estrogen receptor</protein> levels in patients with gynecomastia ]


The number of estrogen receptor ( ER ) in human peripheral leucocytes in 13 men with gynecomastia were measured by radioligand binding method. The results were compared with those of 13 sex-and age-matched healthy subjects .

The number of <protein>estrogen receptor</protein> ( <protein>ER</protein> ) in <cell_type>human peripheral leucocytes</cell_type> in 13 men with gynecomastia were measured by radioligand binding method. The results were compared with those of 13 sex-and age-matched healthy subjects .


It was found that the number of ER in leucocytes was significantly increased in gynecomastia ( Rs of leucocytes were 1054 +/- 254 sites/cell ) .

It was found that the number of <protein>ER</protein> in <cell_type>leucocytes</cell_type> was significantly increased in gynecomastia ( Rs of <cell_type>leucocytes</cell_type> were 1054 +/- 254 sites/cell ) .


It suggested that increase of ER levels play an important role in the pathogenesis of gynecomastia .


The NF kappa B independent cis-acting sequences in HIV-1 LTR responsive to T-cell activation .

The <dna>NF kappa B independent cis-acting sequences</dna> in <dna>HIV-1 LTR</dna> responsive to T-cell activation .


The rate of transcription initiation directed by the long terminal repeat ( LTR ) of HIV-1 increases in response to mitogenic stimuli of T cells .

The rate of transcription initiation directed by the <dna>long terminal repeat</dna> ( LTR ) of HIV-1 increases in response to mitogenic stimuli of <cell_type>T cells</cell_type> .


Here we show that the response of the HIV-1 LTR may be governed by two independent sequences located 5 ' to the site of transcription initiation sequences that bind either NFAT-1 or NF kappa B .

Here we show that the response of the <dna>HIV-1 LTR</dna> may be governed by two independent sequences located 5 ' to the site of transcription initiation sequences that bind either <protein>NFAT-1</protein> or <protein>NF kappa B</protein> .


The rate of LTR -directed gene expression increased in response to treatment with either a phorbol ester or tumor necrosis factor alpha if either the NFAT-1 or NF kappa B binding sites were deleted , but failed to respond to these mitogenic stimuli if both sequences were absent .

The rate of <dna>LTR</dna> -directed gene expression increased in response to treatment with either a phorbol ester or <protein>tumor necrosis factor alpha</protein> if either the <protein>NFAT-1</protein> or <dna>NF kappa B binding sites</dna> were deleted , but failed to respond to these mitogenic stimuli if both sequences were absent .


The HIV-1 mutant virus containing both NF kappa B and NFAT-1 deletion was able to replicate although at a much decreased growth rate , while the deletion of NFAT-1 alone increased the viral growth rate in Jurkat cells .

The HIV-1 mutant virus containing both <dna>NF kappa B and NFAT-1 deletion</dna> was able to replicate although at a much decreased growth rate , while the deletion of <protein>NFAT-1</protein> alone increased the viral growth rate in <cell_line>Jurkat cells</cell_line> .


Neither deletion of NF kappa B nor deletion of NFAT-1 decreased activation of viral replication by phorbol ester .

Neither deletion of <protein>NF kappa B</protein> nor deletion of <protein>NFAT-1</protein> decreased activation of viral replication by phorbol ester .


cAMP-dependent regulation of proenkephalin by JunD and JunB : positive and negative effects of AP-1 proteins .

cAMP-dependent regulation of proenkephalin by <protein>JunD</protein> and <protein>JunB</protein> : positive and negative effects of <protein>AP-1 proteins</protein> .


We demonstrate that JunD , a component of the AP-1 transcription factor complex , activates transcription of the human proenkephalin gene in a fashion that is completely dependent upon the cAMP-dependent protein kinase , protein kinase A .

We demonstrate that <protein>JunD</protein> , a component of the <protein>AP-1 transcription factor complex</protein> , activates transcription of the <dna>human proenkephalin gene</dna> in a fashion that is completely dependent upon the <protein>cAMP-dependent protein kinase</protein> , <protein>protein kinase A</protein> .


Activation of proenkephalin transcription by JunD is dependent upon a previously characterized cAMP- , phorbol ester- , and Ca ( 2+ ) -inducible enhancer , and JunD is shown to bind the enhancer as a homodimer .

Activation of proenkephalin transcription by <protein>JunD</protein> is dependent upon a previously characterized <dna>cAMP- , phorbol ester- , and Ca ( 2+ ) -inducible enhancer</dna> , and <protein>JunD</protein> is shown to bind the <dna>enhancer</dna> as a <protein>homodimer</protein> .


Another component of the AP-1 transcription complex , JunB , is shown to inhibit activation mediated by JunD .

Another component of the <protein>AP-1 transcription complex</protein> , <protein>JunB</protein> , is shown to inhibit activation mediated by <protein>JunD</protein> .


As a homodimer JunB is unable to bind the enhancer ; however in the presence of c-Fos , high-affinity binding is observed .

As a homodimer <protein>JunB</protein> is unable to bind the enhancer ; however in the presence of <protein>c-Fos</protein> , high-affinity binding is observed .


Furthermore , JunD is shown to activate transcription of genes linked to both cAMP and phorbol ester response elements in a protein kinase A -dependent fashion , further blurring the distinction between these response elements .

Furthermore , <protein>JunD</protein> is shown to activate transcription of genes linked to both cAMP and phorbol ester response elements in a <protein>protein kinase A</protein> -dependent fashion , further blurring the distinction between these <dna>response elements</dna> .


These results demonstrate that the transcriptional activity of an AP-1-related protein is regulated by the cAMP-dependent second-messenger pathway and suggest that JunD and other AP-1-related proteins may play an important role in the regulation of gene expression by cAMP-dependent intracellular signaling pathways .

These results demonstrate that the transcriptional activity of an <protein>AP-1-related protein</protein> is regulated by the cAMP-dependent second-messenger pathway and suggest that <protein>JunD</protein> and other <protein>AP-1-related proteins</protein> may play an important role in the regulation of gene expression by cAMP-dependent intracellular signaling pathways .


[ Plasma cortisol concentration and blood leukocyte content of glucocorticoid receptors in patients with deficiency-cold vs deficiency-heat syndromes ]

[ Plasma cortisol concentration and blood leukocyte content of <protein>glucocorticoid receptors</protein> in patients with deficiency-cold vs deficiency-heat syndromes ]


Plasma cortisol concentration and blood leukocyte content of glucocorticoid receptors ( GCR ) were assayed in 20 patients with deficiency syndromes , 10 cold in property ( deficiency-cold ) , the other 10 hot in property ( deficiency-heat ) , and also in 10 healthy individuals as normal control for the purpose of investigating the nature of cold and heat syndromes .

Plasma cortisol concentration and blood leukocyte content of <protein>glucocorticoid receptors</protein> ( <protein>GCR</protein> ) were assayed in 20 patients with deficiency syndromes , 10 cold in property ( deficiency-cold ) , the other 10 hot in property ( deficiency-heat ) , and also in 10 healthy individuals as normal control for the purpose of investigating the nature of cold and heat syndromes .


As a result , the cases of deficiency-cold syndrome ( DCS ) had a normal concentration of plasma cortisol but a lowered content of GCR in leukocytes when compared with the normal control ( P less than 0.05 ) ; the cases of deficiency-heat syndrome ( DHS ) had a higher concentration of plasma cortisol than the normal control ( P less than 0.05 ) and a slightly higher content of GCR in leukocytes .

As a result , the cases of deficiency-cold syndrome ( DCS ) had a normal concentration of plasma cortisol but a lowered content of <protein>GCR</protein> in <cell_type>leukocytes</cell_type> when compared with the normal control ( P less than 0.05 ) ; the cases of deficiency-heat syndrome ( DHS ) had a higher concentration of plasma cortisol than the normal control ( P less than 0.05 ) and a slightly higher content of <protein>GCR</protein> in <cell_type>leukocytes</cell_type> .


It was concluded that the DCS is characterized by diminished biological effects of adrenocortical activity , while the DHS , by augmented biological effects of adrenocortical activity .


The role of jun and fos gene family members in 12-O-tetradecanoylphorbol-13-acetate induced hemopoietic differentiation .

The role of <dna>jun and fos gene family members</dna> in 12-O-tetradecanoylphorbol-13-acetate induced hemopoietic differentiation .


Terminal differentiation of the leukemic cell lines U-937 and HL-60 by 12-O-tetradecanoylphorbol-13-acetate is accompanied by marked changes in gene expression .

Terminal differentiation of the <cell_line>leukemic cell lines</cell_line> <cell_line>U-937</cell_line> and <cell_line>HL-60</cell_line> by 12-O-tetradecanoylphorbol-13-acetate is accompanied by marked changes in gene expression .


In this study , we demonstrate that the expression of jun and fos gene family members is induced with variable kinetics during 12-O-tetradecanoylphorbol-13-acetate induced differentiation , with c-jun expression best paralleling differentiation .

In this study , we demonstrate that the expression of <dna>jun and fos gene family members</dna> is induced with variable kinetics during 12-O-tetradecanoylphorbol-13-acetate induced differentiation , with <dna>c-jun</dna> expression best paralleling differentiation .


The generation of AP-1 complexes , as measured by DNA binding activity , closely parallels morphological differentiation .

The generation of <protein>AP-1 complexes</protein> , as measured by DNA binding activity , closely parallels morphological differentiation .


Furthermore , the ability of these complexes to regulate gene expression is demonstrated by increased transcription from an AP-1 driven reporter construct and marked increases in the expression of endogenous AP-1 regulated genes .

Furthermore , the ability of these complexes to regulate gene expression is demonstrated by increased transcription from an <dna>AP-1 driven reporter construct</dna> and marked increases in the expression of <dna>endogenous AP-1 regulated genes</dna> .


Differentiation assays using water soluble phorbol esters reveal that differentiation becomes irreversible soon after AP-1 appears .

Differentiation assays using water soluble phorbol esters reveal that differentiation becomes irreversible soon after <protein>AP-1</protein> appears .


This tight correlation between c-jun expression , the generation of AP-1 activity , and differentiation suggests a critical role for this gene and transcriptional complex during this process .

This tight correlation between <dna>c-jun</dna> expression , the generation of <protein>AP-1</protein> activity , and differentiation suggests a critical role for this gene and <protein>transcriptional complex</protein> during this process .


Nuclear association of a T-cell transcription factor blocked by FK-506 and cyclosporin A [ see comments ]

Nuclear association of a <protein>T-cell transcription factor</protein> blocked by FK-506 and cyclosporin A [ see comments ]


Cyclosporin A and FK506 inhibit T- and B-cell activation and other processes essential to an effective immune response .


In T lymphocytes these drugs disrupt an unknown step in the transmission of signals from the T-cell antigen receptor to cytokine genes that coordinate the immune response .

In <cell_type>T lymphocytes</cell_type> these drugs disrupt an unknown step in the transmission of signals from the <protein>T-cell antigen receptor</protein> to <dna>cytokine genes</dna> that coordinate the immune response .


The putative intracellular receptors for FK506 and cyclosporin are cis-trans prolyl isomerases .

The <protein>putative intracellular receptors</protein> for FK506 and cyclosporin are cis-trans prolyl isomerases .


Binding of the drug inhibits isomerase activity , but studies with other prolyl isomerase inhibitors and analysis of cyclosporin-resistant mutants in yeast suggest that the effects of the drug result from the formation of an inhibitory complex between the drug and isomerase , and not from inhibition of isomerase activity .

Binding of the drug inhibits <protein>isomerase</protein> activity , but studies with other prolyl <protein>isomerase</protein> inhibitors and analysis of <cell_line>cyclosporin-resistant mutants</cell_line> in yeast suggest that the effects of the drug result from the formation of an <protein>inhibitory complex</protein> between the drug and <protein>isomerase</protein> , and not from inhibition of <protein>isomerase</protein> activity .


A transcription factor , NF-AT , which is essential for early T-cell gene activation , seems to be a specific target of cyclosporin A and FK506 action because transcription directed by this protein is blocked in T cells treated with these drugs , with little or no effect on other transcription factors such as AP-1 and NF-kappa B .

A <protein>transcription factor</protein> , <protein>NF-AT</protein> , which is essential for early T-cell gene activation , seems to be a specific target of cyclosporin A and FK506 action because transcription directed by this protein is blocked in <cell_type>T cells</cell_type> treated with these drugs , with little or no effect on other <protein>transcription factors</protein> such as <protein>AP-1</protein> and <protein>NF-kappa B</protein> .


Here we demonstrate that NF-AT is formed when a signal from the antigen receptor induces a pre-existing cytoplasmic subunit to translocate to the nucleus and combine with a newly synthesized nuclear subunit of NF-AT .

Here we demonstrate that <protein>NF-AT</protein> is formed when a signal from the <protein>antigen receptor</protein> induces a pre-existing cytoplasmic subunit to translocate to the nucleus and combine with a newly synthesized nuclear subunit of <protein>NF-AT</protein> .


FK506 and cyclosporin A block translocation of the cytoplasmic component without affecting synthesis of the nuclear subunit .

FK506 and cyclosporin A block translocation of the <protein>cytoplasmic component</protein> without affecting synthesis of the <protein>nuclear subunit</protein> .


Glucocorticoid receptors in lymphocytes in anorexia nervosa .

<protein>Glucocorticoid receptors</protein> in <cell_type>lymphocytes</cell_type> in anorexia nervosa .


OBJECTIVE : The aim was to explore the down-regulation of the glucocorticoid receptors during hypercortisolaemia in anorexia nervosa .

OBJECTIVE : The aim was to explore the down-regulation of the <protein>glucocorticoid receptors</protein> during hypercortisolaemia in anorexia nervosa .


DESIGN : Urine and plasma samples were obtained for cortisol determination and blood lymphocytes were isolated for receptor binding studies .

DESIGN : Urine and plasma samples were obtained for cortisol determination and <cell_type>blood lymphocytes</cell_type> were isolated for receptor binding studies .


PATIENTS : Sixteen anorexic patients , aged 16-27 years , with a mean +/- SEM body mass index of 14.2 +/- 2.0 ( ranging from 11.1 to 17.4 ) , and 15 normal women were studied .


Six patients were reinvestigated after a significant weight gain .


MEASUREMENTS : The binding capacity and affinity of the glucocorticoid receptors were measured with dexamethasone as ligand on lymphocytes .

MEASUREMENTS : The binding capacity and affinity of the <protein>glucocorticoid receptors</protein> were measured with dexamethasone as ligand on <cell_type>lymphocytes</cell_type> .


RESULTS : In patients , both total and free plasma cortisol concentrations were higher than in the normal women , as was their urinary free cortisol ; the number of glucocorticoid receptors per cell ( Ro ) and the binding affinity ( Kd ) for dexamethasone were , however , not significantly different ( Ro : 7687 +/- 1750 vs 7347 +/- 1285 sites/cell ; Kd : 7.7 +/- 2.4 vs 7.4 +/- 1.7 nM at 24 degrees C ) .

RESULTS : In patients , both total and free plasma cortisol concentrations were higher than in the normal women , as was their urinary free cortisol ; the number of <protein>glucocorticoid receptors</protein> per cell ( Ro ) and the binding affinity ( Kd ) for dexamethasone were , however , not significantly different ( Ro : 7687 +/- 1750 vs 7347 +/- 1285 sites/cell ; Kd : 7.7 +/- 2.4 vs 7.4 +/- 1.7 nM at 24 degrees C ) .


After weight gain ( 14 +/- 2 to 16 +/- 2 kg/m2 ) , receptor numbers were 8421 +/- 2126 ( pre ) and 9011 +/- 500 ( post ) sites/cell , which are not significantly different ( P greater than 0.2 ) ; the Kd was unchanged ( 9.3 +/- 2.6 vs 9.2 +/- 2.4 nM ) .


CONCLUSIONS Hypercortisolaemia does not down-regulate the lymphocyte glucocorticoid receptors in anorexia nervosa and a post-receptor defect might be involved in peripheral tissue resistance to the effects of glucocorticoid hormones in undernutrition .

CONCLUSIONS Hypercortisolaemia does not down-regulate the lymphocyte <protein>glucocorticoid receptors</protein> in anorexia nervosa and a post-receptor defect might be involved in peripheral tissue resistance to the effects of glucocorticoid hormones in undernutrition .


Inhibition of protein phosphatases by okadaic acid induces AP1 in human T cells .

Inhibition of <protein>protein phosphatases</protein> by okadaic acid induces <protein>AP1</protein> in <cell_type>human T cells</cell_type> .


To examine the role of protein phosphatases in T cell activation , Jurkat cells were treated with okadaic acid , an inhibitor of type 1 and 2A phosphatases , and nuclear extracts were examined for the presence of AP1 as a measure of early T cell activation .

To examine the role of <protein>protein phosphatases</protein> in T cell activation , <cell_line>Jurkat cells</cell_line> were treated with okadaic acid , an inhibitor of <protein>type 1 and 2A phosphatases</protein> , and nuclear extracts were examined for the presence of <protein>AP1</protein> as a measure of early T cell activation .


Okadaic acid was found to be a potent inducer of AP1 .

Okadaic acid was found to be a potent inducer of <protein>AP1</protein> .


In contrast to phorbol esters such as phorbol myristate acetate ( PMA ) , the induction of AP1 by okadaic acid occurs predominantly by transcriptional activation of the jun and fos family of proto-oncogenes .

In contrast to phorbol esters such as phorbol myristate acetate ( PMA ) , the induction of <protein>AP1</protein> by okadaic acid occurs predominantly by transcriptional activation of the <dna>jun and fos family</dna> of <dna>proto-oncogenes</dna> .


Surprisingly , while the addition of phytohemagglutinin further enhanced the induction of AP1 , the addition of PMA inhibited it .

Surprisingly , while the addition of <protein>phytohemagglutinin</protein> further enhanced the induction of <protein>AP1</protein> , the addition of PMA inhibited it .


Okadaic acid treatment was found to dramatically increase mRNA transcripts of the jun family of proto-oncogenes including c-jun , junD , and junB and to a lesser extent the fos family including c-fos and fra-1 .

Okadaic acid treatment was found to dramatically increase <rna>mRNA transcripts</rna> of the <dna>jun family of proto-oncogenes</dna> including <dna>c-jun</dna> , <dna>junD</dna> , and <dna>junB</dna> and to a lesser extent the <dna>fos family</dna> including <dna>c-fos</dna> and <dna>fra-1</dna> .


By comparison , PMA is a very inefficient inducer of the jun gene family in Jurkat cells .

By comparison , PMA is a very inefficient inducer of the <dna>jun gene family</dna> in <cell_line>Jurkat cells</cell_line> .


Similar to its effect on the induction of AP1 by okadaic acid , PMA inhibits the induction of c-jun mRNA by okadaic acid .

Similar to its effect on the induction of <protein>AP1</protein> by okadaic acid , PMA inhibits the induction of <rna>c-jun mRNA</rna> by okadaic acid .


Transfection of c-jun promoter constructs confirmed the marked difference between PMA and okadaic acid in inducing c-jun transcription .

Transfection of <dna>c-jun promoter constructs</dna> confirmed the marked difference between PMA and okadaic acid in inducing <dna>c-jun</dna> transcription .


The induction of AP1 by okadaic acid suggests that protein phosphatases 1 and 2A ( PP1 and PP2A ) may be involved in T cell activation as important negative regulators of the transcription factor AP1 .

The induction of <protein>AP1</protein> by okadaic acid suggests that <protein>protein phosphatases 1 and 2A</protein> ( <protein>PP1</protein> and <protein>PP2A</protein> ) may be involved in T cell activation as important negative regulators of the <protein>transcription factor</protein> <protein>AP1</protein> .


Cloning of murine TCF-1 , a T cell-specific transcription factor interacting with functional motifs in the CD3-epsilon and T cell receptor alpha enhancers .

Cloning of <protein>murine TCF-1</protein> , a T cell-specific <protein>transcription factor</protein> interacting with <dna>functional motifs</dna> in the <dna>CD3-epsilon and T cell receptor alpha enhancers</dna> .


CD3 -epsilon gene expression is confined to the T cell lineage .

<protein>CD3</protein> -epsilon gene expression is confined to the <cell_line>T cell lineage</cell_line> .


We have recently identified and cloned a human transcription factor , TCF-1 , that binds to a functional element in the T lymphocyte-specific enhancer of CD3-epsilon .

We have recently identified and cloned a <protein>human transcription factor</protein> , <protein>TCF-1</protein> , that binds to a functional element in the T lymphocyte-specific enhancer of CD3-epsilon .


In a panel of human cell lines , TCF-1 expression was restricted to T lineage cells .

In a panel of human cell lines , <protein>TCF-1</protein> expression was restricted to <cell_type>T lineage cells</cell_type> .


TCF-1 belonged to a novel family of genes that contain the so-called high mobility group 1 ( HMG ) box .

<protein>TCF-1</protein> belonged to a novel family of genes that contain the so-called high <dna>mobility group 1 ( HMG ) box</dna> .


Here we report the cloning of murine TCF-1 .

Here we report the cloning of <protein>murine TCF-1</protein> .


Two splice alternatives were identified that were not previously observed in human TCF-1 .

Two splice alternatives were identified that were not previously observed in <protein>human TCF-1</protein> .


Murine and human TCF-1 displayed a 95.5 % overall amino acid homology .

<protein>Murine and human TCF-1</protein> displayed a 95.5 % overall amino acid homology .


Recombinant murine and human TCF-1 recognized the same sequence motif in the CD3-epsilon enhancer as judged by gel retardation and methylation interference assays .

<protein>Recombinant murine and human TCF-1</protein> recognized the same sequence motif in the <dna>CD3-epsilon enhancer</dna> as judged by gel retardation and methylation interference assays .


With the murine cDNA clones several aspects of TCF-1 were analyzed .

With the <dna>murine cDNA clones</dna> several aspects of <protein>TCF-1</protein> were analyzed .


First , deletion analysis revealed that a region of TCF-1 containing the HMG box was sufficient for sequence-specific binding .

First , deletion analysis revealed that a region of <protein>TCF-1</protein> containing the <dna>HMG box</dna> was sufficient for sequence-specific binding .


Second , by high stringency Northern blotting and in situ hybridization , TCF-1 expression was shown to be confined to the thymus and to the T cell areas of the spleen .

Second , by high stringency Northern blotting and in situ hybridization , <protein>TCF-1</protein> expression was shown to be confined to the thymus and to the T cell areas of the spleen .


Third , TCF-1 bound specifically to a functional T cell-specific element in the T cell receptor alpha ( TCR-alpha ) enhancer .

Third , <protein>TCF-1</protein> bound specifically to a functional <dna>T cell-specific element</dna> in the <dna>T cell receptor alpha ( TCR-alpha ) enhancer</dna> .


The T lineage-specific expression and the affinity for functional motifs in the TCR-alpha and CD3-epsilon enhancers imply an important role for TCF-1 in the establishment of the mature T cell phenotype .

The T lineage-specific expression and the affinity for functional motifs in the <dna>TCR-alpha and CD3-epsilon enhancers</dna> imply an important role for <protein>TCF-1</protein> in the establishment of the <cell_type>mature T cell phenotype</cell_type> .


Cloning of a human homeobox gene that resembles a diverged Drosophila homeobox gene and is expressed in activated lymphocytes .

Cloning of a <dna>human homeobox gene</dna> that resembles a <dna>diverged Drosophila homeobox gene</dna> and is expressed in activated <cell_type>lymphocytes</cell_type> .


A new homeobox gene , HB24 , has been isolated from a human B-lymphocyte cDNA library .

A new <dna>homeobox gene</dna> , <dna>HB24</dna> , has been isolated from a human B-lymphocyte cDNA library .


Northern blot analysis of polyadenylated RNA purified from activated human B cells revealed a single mRNA transcript of approximately 2.3 kb .

Northern blot analysis of <rna>polyadenylated RNA</rna> purified from <cell_type>activated human B cells</cell_type> revealed a <rna>single mRNA transcript</rna> of approximately 2.3 kb .


Two cDNA clones were sequenced and provided 2 , 250 nucleotides ( nt ) of DNA sequence information .

Two <dna>cDNA clones</dna> were sequenced and provided 2 , 250 nucleotides ( nt ) of <dna>DNA sequence</dna> information .


There is a single methionine codon-initiated open reading frame of 1 , 458 nt in frame with a homeobox and a CAX repeat , and the open reading frame is predicted to encode a protein of 51 , 659 daltons .

There is a single <dna>methionine codon-initiated open reading frame</dna> of 1 , 458 nt in frame with a <dna>homeobox</dna> and a <dna>CAX repeat</dna> , and the <dna>open reading frame</dna> is predicted to encode a protein of 51 , 659 daltons .


When the homeodomain from HB24 was compared to known mammalian and Drosophila homeodomains it was found to be only moderately conserved , but when it was compared to a highly diverged Drosophila homeodomain , H2.0 , it was found to be 80 % identical .

When the <dna>homeodomain</dna> from <dna>HB24</dna> was compared to known <dna>mammalian and Drosophila homeodomains</dna> it was found to be only moderately conserved , but when it was compared to a highly diverged <dna>Drosophila homeodomain</dna> , H2.0 , it was found to be 80 % identical .


The HB24 mRNA was absent or present at low levels in normal B and T lymphocytes ; however , with the appropriate activation signal HB24 mRNA was induced within several hours even in the presence of cycloheximide .

The <rna>HB24 mRNA</rna> was absent or present at low levels in normal B and <cell_type>T lymphocytes</cell_type> ; however , with the appropriate activation signal <rna>HB24 mRNA</rna> was induced within several hours even in the presence of cycloheximide .


Characterization of HB24 expression in lymphoid and select developing tissues was performed by in situ hybridization .

Characterization of <dna>HB24</dna> expression in lymphoid and select developing tissues was performed by in situ hybridization .


Positive hybridization was found in thymus , tonsil , bone marrow , developing vessels , and in fetal brain .


HB24 is likely to have an important role in lymphocytes as well as in certain developing tissues .

<dna>HB24</dna> is likely to have an important role in <cell_type>lymphocytes</cell_type> as well as in certain developing tissues .


Platelet-activating factor induces phospholipid turnover , calcium flux , arachidonic acid liberation , eicosanoid generation , and oncogene expression in a human B cell line .

<protein>Platelet-activating factor</protein> induces phospholipid turnover , calcium flux , arachidonic acid liberation , eicosanoid generation , and <dna>oncogene</dna> expression in a <cell_line>human B cell line</cell_line> .


Platelet-activating factor is a potent mediator of the inflammatory response .

<protein>Platelet-activating factor</protein> is a potent mediator of the inflammatory response .


Studies of the actions of platelet-activating factor have centered mainly around neutrophils , monocytes , and platelets .

Studies of the actions of <protein>platelet-activating factor</protein> have centered mainly around <cell_type>neutrophils</cell_type> , <cell_type>monocytes</cell_type> , and <cell_type>platelets</cell_type> .


In this report we begin to uncover the influence of platelet-activating factor on B lymphocytes .

In this report we begin to uncover the influence of <protein>platelet-activating factor</protein> on <cell_type>B lymphocytes</cell_type> .


Employing the EBV-transformed human B cell line SKW6.4 , we demonstrate that platelet-activating factor significantly alters membrane phospholipid metabolism indicated by the incorporation of 32P into phosphatidylcholine , phosphatidylinositol , and phosphatidic acid but not significantly into phosphatidylethanolamine at concentrations ranging from 10 ( -9 ) to 10 ( -6 ) M .

Employing the <cell_line>EBV-transformed human B cell line</cell_line> <cell_line>SKW6.4</cell_line> , we demonstrate that <protein>platelet-activating factor</protein> significantly alters membrane phospholipid metabolism indicated by the incorporation of 32P into phosphatidylcholine , phosphatidylinositol , and phosphatidic acid but not significantly into phosphatidylethanolamine at concentrations ranging from 10 ( -9 ) to 10 ( -6 ) M .


The inactive precursor , lyso-platelet-activating factor , at a concentration as high as 10 ( -7 ) M had no effect on any of the membrane phospholipids .

The inactive precursor , <protein>lyso-platelet-activating factor</protein> , at a concentration as high as 10 ( -7 ) M had no effect on any of the membrane phospholipids .


We also show that platelet-activating factor from 10 ( -12 ) to 10 ( -6 ) M induced rapid and significant elevation in intracellular calcium levels , whereas lyso- platelet-activating factor was again ineffective .

We also show that <protein>platelet-activating factor</protein> from 10 ( -12 ) to 10 ( -6 ) M induced rapid and significant elevation in intracellular calcium levels , whereas lyso- <protein>platelet-activating factor</protein> was again ineffective .


We further demonstrate the impact of platelet-activating factor binding to B cells by measuring platelet-activating factor induced arachidonic acid release and 5-hydroxyeicosatetraenoic acid production .

We further demonstrate the impact of <protein>platelet-activating factor</protein> binding to <cell_type>B cells</cell_type> by measuring <protein>platelet-activating factor</protein> induced arachidonic acid release and 5-hydroxyeicosatetraenoic acid production .


Moreover , platelet-activating factor was capable of inducing transcription of the nuclear proto-oncogenes c-fos and c-jun .

Moreover , <protein>platelet-activating factor</protein> was capable of inducing transcription of the <dna>nuclear proto-oncogenes</dna> <dna>c-fos</dna> and <dna>c-jun</dna> .


Finally we explored the possible role of 5-hydroxyeicosatetraenoic acid as a regulator of arachidonic acid liberation demonstrating that endogenous 5-lipoxygenase activity modulates platelet-activating factor induced arachidonic acid release perhaps acting at the level of phospholipase A2 .

Finally we explored the possible role of 5-hydroxyeicosatetraenoic acid as a regulator of arachidonic acid liberation demonstrating that endogenous <protein>5-lipoxygenase</protein> activity modulates <protein>platelet-activating factor</protein> induced arachidonic acid release perhaps acting at the level of <protein>phospholipase A2</protein> .


In summary , platelet-activating factor is shown here to have a direct and profound effect on a pure B cell line .

In summary , <protein>platelet-activating factor</protein> is shown here to have a direct and profound effect on a <cell_line>pure B cell line</cell_line> .


Positive and negative regulation of immunoglobulin gene expression by a novel B-cell-specific enhancer element .

Positive and negative regulation of <dna>immunoglobulin gene</dna> expression by a novel <dna>B-cell-specific enhancer element</dna> .


A new B-cell-specific enhancer element has been identified 3 ' of E4 and the octamerlike motifs in the human immunoglobulin heavy-chain gene enhancer .

A new <dna>B-cell-specific enhancer element</dna> has been identified 3 ' of <dna>E4 and the octamerlike motifs</dna> in the <dna>human immunoglobulin heavy-chain gene enhancer</dna> .


Tandem copies of this 67-bp MnlI-AluI fragment , when fused to the chloramphenicol acetyltransferase gene driven by the conalbumin promoter , stimulated transcription in B cells but not in Jurkat T cells or HeLa cells .

Tandem copies of this <dna>67-bp MnlI-AluI fragment</dna> , when fused to the <dna>chloramphenicol acetyltransferase gene</dna> driven by the <dna>conalbumin promoter</dna> , stimulated transcription in <cell_type>B cells</cell_type> but not in <cell_line>Jurkat T cells</cell_line> or <cell_line>HeLa cells</cell_line> .


Footprinting analysis revealed that the identical sequence CCGAAACTGAAAAGG , designated E6 , was protected by nuclear extracts from B cells , T cells , or HeLa cells .

Footprinting analysis revealed that the identical sequence CCGAAACTGAAAAGG , designated <dna>E6</dna> , was protected by nuclear extracts from <cell_type>B cells</cell_type> , <cell_type>T cells</cell_type> , or HeLa cells .


Gel mobility shift assays using a synthetic E6 motif detected a B-cell-specific complex in addition to a ubiquitous band found also in T cells and HeLa cells .

Gel mobility shift assays using a <dna>synthetic E6 motif</dna> detected a <protein>B-cell-specific complex</protein> in addition to a ubiquitous band found also in <cell_type>T cells</cell_type> and <cell_line>HeLa cells</cell_line> .


In agreement with the results of gel retardation assays , tandem copies of the E6 motif stimulated transcription in ARH77 and Raji cells but not in Jurkat or HeLa cells .

In agreement with the results of gel retardation assays , tandem copies of the <dna>E6 motif</dna> stimulated transcription in <cell_line>ARH77</cell_line> and <cell_line>Raji cells</cell_line> but not in <cell_line>Jurkat</cell_line> or <cell_line>HeLa cells</cell_line> .


Furthermore , a mutant E6 motif lost both in vitro binding activity and in vivo enhancer activity .

Furthermore , a <dna>mutant E6 motif</dna> lost both in vitro binding activity and in vivo enhancer activity .


In striking contrast to the mouse Ig heavy-chain enhancer , in which the octamer motif acts as a B-cell-specific enhancer element , the human enhancer contains an octamerlike sequence with one base substitution which bound octamer-binding proteins with only very low affinity and showed no enhancer activity of its own .

In striking contrast to the <dna>mouse Ig heavy-chain enhancer</dna> , in which the <dna>octamer motif</dna> acts as a <dna>B-cell-specific enhancer element</dna> , the <dna>human enhancer</dna> contains an <dna>octamerlike sequence</dna> with one base substitution which bound <protein>octamer-binding proteins</protein> with only very low affinity and showed no enhancer activity of its own .


Interestingly , the MnlI-AluI fragment could suppress the basal-level activity of the conalbumin promoter in both Jurkat and HeLa cells .

Interestingly , the <dna>MnlI-AluI fragment</dna> could suppress the basal-level activity of the <dna>conalbumin promoter</dna> in both <cell_line>Jurkat</cell_line> and <cell_line>HeLa cells</cell_line> .


Moreover , simian virus 40 enhancer activity was blocked by the MnlI-AluI fragment in HeLa cells but not in B cells .

Moreover , simian virus 40 enhancer activity was blocked by the <dna>MnlI-AluI fragment</dna> in <cell_line>HeLa cells</cell_line> but not in <cell_type>B cells</cell_type> .


Thus , the novel enhancer element identified in this study is probably a target site for both positive and negative factors .

Thus , the novel enhancer element identified in this study is probably a target site for both <protein>positive and negative factors</protein> .


Charybdotoxin-sensitive , Ca ( 2+ ) -dependent membrane potential changes are not involved in human T or B cell activation and proliferation .

Charybdotoxin-sensitive , Ca ( 2+ ) -dependent membrane potential changes are not involved in human <cell_type>T or B cell</cell_type> activation and proliferation .


The involvement of ion channels in B and T lymphocyte activation is supported by many reports of changes in ion fluxes and membrane potential after mitogen binding .

The involvement of ion channels in B and T lymphocyte activation is supported by many reports of changes in ion fluxes and membrane potential after <protein>mitogen</protein> binding .


Human T and B lymphocytes demonstrate an early and transient hyperpolarization after ligand binding .

<cell_type>Human T and B lymphocytes</cell_type> demonstrate an early and transient hyperpolarization after ligand binding .


Inasmuch as the change in membrane potential is dependent on elevation of free cytosolic calcium , the hyperpolarization is presumably through opening of Ca ( 2+ ) -stimulated K+ channels .


We have used charybdotoxin , a known inhibitor of Ca ( 2+ ) -dependent K+ channels , to study the role of these channels in lymphocyte activation and mitogenesis .

We have used charybdotoxin , a known inhibitor of <protein>Ca ( 2+ ) -dependent K+ channels</protein> , to study the role of these channels in lymphocyte activation and mitogenesis .


We demonstrate that charybdotoxin inhibits the ligand-induced transient membrane hyperpolarization in B and T cells in a dose-dependent fashion , without affecting changes in cytosolic Ca2+ .

We demonstrate that charybdotoxin inhibits the ligand-induced transient membrane hyperpolarization in <cell_type>B and T cells</cell_type> in a dose-dependent fashion , without affecting changes in cytosolic Ca2+ .


However , blockade of the Ca ( 2+ ) -activated K+ channel is not associated with changes in cell-cycle gene activation , IL-2 production , IL-2R expression or B and T cell mitogenesis .

However , blockade of the <protein>Ca ( 2+ ) -activated K+ channel</protein> is not associated with changes in cell-cycle gene activation , <protein>IL-2</protein> production , <protein>IL-2R</protein> expression or B and T cell mitogenesis .


These results imply that membrane potential changes secondary to the ligand-dependent opening of Ca ( 2+ ) -activated K+ channels are not involved in B and T lymphocyte activation and mitogenesis .

These results imply that membrane potential changes secondary to the ligand-dependent opening of <protein>Ca ( 2+ ) -activated K+ channels</protein> are not involved in <cell_type>B and T lymphocyte</cell_type> activation and mitogenesis .


Activity of the kappa B enhancer of the interleukin-2 receptor alpha chain in somatic cell hybrids is accompanied by the nuclear localization of NF-kappa B .

Activity of the <dna>kappa B enhancer</dna> of the <protein>interleukin-2 receptor alpha chain</protein> in <cell_line>somatic cell hybrids</cell_line> is accompanied by the nuclear localization of <protein>NF-kappa B</protein> .


The two nuclear proteins NF-kappa B ( consisting of subunits p50 an dp65 ) and the DNA-binding subunit of NF-kappa B ( p50 ) by itself , also called KBF1 , are constitutively expressed and localized in the nucleus of the human T-cell line IARC 301.5 .

The <protein>two nuclear proteins</protein> <protein>NF-kappa B</protein> ( consisting of subunits <protein>p50</protein> an <protein>dp65</protein> ) and the <protein>DNA-binding subunit</protein> of <protein>NF-kappa B</protein> ( <protein>p50</protein> ) by itself , also called <protein>KBF1</protein> , are constitutively expressed and localized in the nucleus of the <cell_line>human T-cell line</cell_line> <cell_line>IARC 301.5</cell_line> .


In order to define the roles of these two factors , which bind to the same kappa B enhancers , in transcription activation we have prepared somatic cell hybrids between IARC 301.5 and a murine myeloma .

In order to define the roles of these two <protein>factors</protein> , which bind to the same <dna>kappa B enhancers</dna> , in transcription activation we have prepared somatic cell hybrids between <cell_line>IARC 301.5</cell_line> and a <cell_line>murine myeloma</cell_line> .


Most hybrids express both KBF1 and NF-kappa B in their nuclei , but one hybrid expresses only KBF1 .

Most hybrids express both <protein>KBF1</protein> and <protein>NF-kappa B</protein> in their nuclei , but one hybrid expresses only <protein>KBF1</protein> .


The kappa B enhancer of the gene encoding the interleukin-2 ( IL-2 ) receptor alpha chain ( IL-2R alpha ) is functional only in the hybrids expressing nuclear NF-kappa B .

The <dna>kappa B enhancer</dna> of the gene encoding the <protein>interleukin-2 ( IL-2 ) receptor alpha chain</protein> ( <protein>IL-2R alpha</protein> ) is functional only in the <cell_line>hybrids</cell_line> expressing <protein>nuclear NF-kappa B</protein> .


These findings show that nuclear NF-kappa B is necessary to activate the kappa B enhancer , while KBF1 by itself is not sufficient .

These findings show that <protein>nuclear NF-kappa B</protein> is necessary to activate the <dna>kappa B enhancer</dna> , while <protein>KBF1</protein> by itself is not sufficient .


We propose that KBF1 is a competitive inhibitor of NF-kappa B and discuss how these factors may be involved in the transient expression of IL-2 and IL-2 alpha genes during the immune response .

We propose that <protein>KBF1</protein> is a competitive inhibitor of <protein>NF-kappa B</protein> and discuss how these factors may be involved in the transient expression of <protein>IL-2</protein> and <protein>IL-2 alpha</protein> genes during the immune response .


T-helper-cell determinants in protein antigens are preferentially located in cysteine-rich antigen segments resistant to proteolytic cleavage by cathepsin B , L , and D .

<protein>T-helper-cell determinants</protein> in <protein>protein antigens</protein> are preferentially located in <protein>cysteine-rich antigen segments</protein> resistant to proteolytic cleavage by <protein>cathepsin B , L , and D</protein> .


We report on a computer algorithm capable of predicting the location of T-helper-cell epitopes in protein antigen ( Ag ) by analysing the Ag amino acid sequence .

We report on a computer algorithm capable of predicting the location of <protein>T-helper-cell epitopes</protein> in <protein>protein antigen</protein> ( <protein>Ag</protein> ) by analysing the <protein>Ag</protein> <protein>amino acid sequence</protein> .


The algorithm was constructed with the aim of identifying segments in Ag which are resistant to proteolytic degradation by the enzymes cathepsin B , L , and D .

The algorithm was constructed with the aim of identifying segments in <protein>Ag</protein> which are resistant to proteolytic degradation by the enzymes <protein>cathepsin B , L , and D</protein> .


These are prominent enzymes in the endocytic pathway through which soluble protein Ag enter APC , and resistant segments in Ag may , therefore , be expected to contain more T-cell determinants than susceptible segments .

These are prominent <protein>enzymes</protein> in the endocytic pathway through which <protein>soluble protein Ag</protein> enter <protein>APC</protein> , and <protein>resistant segments</protein> in <protein>Ag</protein> may , therefore , be expected to contain more <protein>T-cell determinants</protein> than <protein>susceptible segments</protein> .


From information available in the literature on the substrate specificity of the three enzymes , it is clear that a cysteine is not accepted in any of the S2 , S1 , S1 ' , and S2 ' subsites of cathepsin B and L , and not in the S1 and S1 ' subsites of cathepsin D .

From information available in the literature on the substrate specificity of the three <protein>enzymes</protein> , it is clear that a cysteine is not accepted in any of the <protein>S2 , S1 , S1 ' , and S2 ' subsites</protein> of <protein>cathepsin B and L</protein> , and not in the <protein>S1</protein> and <protein>S1 '</protein> subsites of <protein>cathepsin D</protein> .


Moreover , we have noticed that cysteine-containing T-cell determinants in a number of protein Ag are particularly rich in the amino acids alanine , glycine , lysine , leucine , serine , threonine , and valine .

Moreover , we have noticed that <protein>cysteine-containing T-cell determinants</protein> in a number of <protein>protein Ag</protein> are particularly rich in the amino acids alanine , glycine , lysine , leucine , serine , threonine , and valine .