In Northern blot analysis , mRNA species of approximately 1.8 kilobases that hybridized with human FKBP cDNA were detected in poly ( A ) + RNAs from brain , lung , liver , and placental cells and leukocytes .

In Northern blot analysis , <rna>mRNA species</rna> of approximately 1.8 kilobases that hybridized with <dna>human FKBP cDNA</dna> were detected in <rna>poly ( A ) + RNAs</rna> from brain , lung , liver , and <cell_type>placental cells</cell_type> and <cell_type>leukocytes</cell_type> .


Induction of Jurkat leukemic T cells with phorbol 12-myristate 13-acetate and ionomycin did not affect the level of FKBP mRNA .

Induction of <cell_line>Jurkat leukemic T cells</cell_line> with phorbol 12-myristate 13-acetate and ionomycin did not affect the level of <rna>FKBP mRNA</rna> .


Southern blot analysis of human genomic DNA digested with different restriction enzymes suggests the existence of only a few copies of the DNA sequence encoding FKBP .

Southern blot analysis of <dna>human genomic DNA</dna> digested with different <protein>restriction enzymes</protein> suggests the existence of only a few copies of the DNA sequence encoding <protein>FKBP</protein> .


This is in contrast to the result that as many as 20 copies of the cyclophilin gene and possible pseudogenes may be present in the mammalian genome .

This is in contrast to the result that as many as 20 copies of the <dna>cyclophilin gene</dna> and possible pseudogenes may be present in the <dna>mammalian genome</dna> .


Involvement of a second lymphoid-specific enhancer element in the regulation of immunoglobulin heavy-chain gene expression .

Involvement of a second <dna>lymphoid-specific enhancer element</dna> in the regulation of <dna>immunoglobulin heavy-chain gene</dna> expression .


To determine whether enhancer elements in addition to the highly conserved octamer ( OCTA ) -nucleotide motif are important for lymphoid-specific expression of the immunoglobulin heavy-chain ( IgH ) gene , we have investigated the effect of mutating the binding site for a putative additional lymphoid-specific transcription factor , designated NF-microB , in the murine IgH enhancer .

To determine whether <dna>enhancer elements</dna> in addition to the highly conserved <dna>octamer ( OCTA ) -nucleotide motif</dna> are important for lymphoid-specific expression of the <dna>immunoglobulin heavy-chain ( IgH ) gene</dna> , we have investigated the effect of mutating the <dna>binding site</dna> for a <protein>putative additional lymphoid-specific transcription factor</protein> , designated <protein>NF-microB</protein> , in the <dna>murine IgH enhancer</dna> .


We demonstrate that the NF-microB-binding site plays a critical role in the IgH enhancer , because mutation of the microB DNA motif decreased transcriptional activity of the IgH enhancer in cells of the B-cell lineage but not in nonlymphoid cells .

We demonstrate that the <dna>NF-microB-binding site</dna> plays a critical role in the <dna>IgH enhancer</dna> , because mutation of the microB DNA motif decreased transcriptional activity of the <dna>IgH enhancer</dna> in cells of the <cell_type>B-cell lineage</cell_type> but not in <cell_type>nonlymphoid cells</cell_type> .


This effect was comparable to or even stronger than the effect of a mutation in the OCTA site .

This effect was comparable to or even stronger than the effect of a mutation in the <dna>OCTA site</dna> .


Moreover , combined mutation of both microB and OCTA sites further reduced enhancer activity in lymphoid cells .

Moreover , combined mutation of both <dna>microB</dna> and <dna>OCTA sites</dna> further reduced enhancer activity in <cell_type>lymphoid cells</cell_type> .


Interestingly , alteration of either the microB or E3 site in a 70-base-pair fragment of the IgH enhancer that lacks the binding site for OCTA abolished enhancer activity in lymphoid cells completely .

Interestingly , alteration of either the <dna>microB</dna> or <dna>E3 site</dna> in a <dna>70-base-pair fragment</dna> of the <dna>IgH enhancer</dna> that lacks the binding site for OCTA abolished enhancer activity in <cell_type>lymphoid cells</cell_type> completely .


Nevertheless , a multimer of the microB motif alone showed no enhancer activity .

Nevertheless , a multimer of the <dna>microB motif</dna> alone showed no enhancer activity .


DNase footprinting analysis corroborated the functional data showing that a lymphoid-specific protein binds to the microB DNA motif .

DNase footprinting analysis corroborated the functional data showing that a <protein>lymphoid-specific protein</protein> binds to the <dna>microB DNA motif</dna> .


Our results suggest that the microB element is a new crucial element important for lymphoid-specific expression of the IgH gene but that interaction with another enhancer element is essential for its activity .

Our results suggest that the <dna>microB element</dna> is a new crucial element important for lymphoid-specific expression of the IgH gene but that interaction with another <dna>enhancer element</dna> is essential for its activity .


Stimulation of the human immunodeficiency virus type 2 ( HIV-2 ) gene expression by the cytomegalovirus and HIV-2 transactivator gene .

Stimulation of the human immunodeficiency virus type 2 ( HIV-2 ) gene expression by the cytomegalovirus and <dna>HIV-2 transactivator gene</dna> .


Human immunodeficiency virus ( HIV ) often causes latent infection .


Transactivation by some DNA viruses has been implicated in inducing HIV-1 replication and pathogenesis .


The transactivator ( IE-2 ) gene of the human cytomegalovirus ( CMV ) can enhance HIV-2 as well as HIV-1 gene expression in vitro .

The <dna>transactivator ( IE-2 ) gene</dna> of the human cytomegalovirus ( CMV ) can enhance HIV-2 as well as HIV-1 gene expression in vitro .


This inducer can act in concert with the HIV-2 tat gene and T-cell activation in enhancing gene expression in human CD4+ lymphocytes .

This inducer can act in concert with the <dna>HIV-2 tat gene</dna> and T-cell activation in enhancing gene expression in <cell_type>human CD4+ lymphocytes</cell_type> .


While the HIV-2 and HIV-1 tat genes and T-cell activators apparently employ independent modes of action , the CMV transactivator in combination with the HIV-2 tat or T-cell activators may employ a gene activation pathway with some common and some distinct components .

While the HIV-2 and <dna>HIV-1 tat genes</dna> and <protein>T-cell activators</protein> apparently employ independent modes of action , the <dna>CMV transactivator</dna> in combination with the <dna>HIV-2 tat</dna> or <protein>T-cell activators</protein> may employ a gene activation pathway with some common and some distinct components .


Both HIV-2 and CMV transactivators enhance HIV-2 gene expression by transcriptional activation involving transcript initiation as well as elongation , with CMV transactivator affecting elongation more than the initiation .

Both HIV-2 and <dna>CMV transactivators</dna> enhance HIV-2 gene expression by transcriptional activation involving transcript initiation as well as elongation , with <dna>CMV transactivator</dna> affecting elongation more than the initiation .


A significant proportion of transcripts appear to terminate prematurely in the absence of transactivators .

A significant proportion of <rna>transcripts</rna> appear to terminate prematurely in the absence of <protein>transactivators</protein> .


Deletion mutation analysis of the HIV-2 long terminal repeat ( LTR ) suggests that the element that responds to CMV transactivation in human CD4+ lymphocytes is either a diffuse one or located downstream of the HIV-2 enhancer element .

Deletion mutation analysis of the <dna>HIV-2 long terminal repeat</dna> ( <dna>LTR</dna> ) suggests that the element that responds to CMV transactivation in <cell_type>human CD4+ lymphocytes</cell_type> is either a diffuse one or located downstream of the <dna>HIV-2 enhancer element</dna> .


Quantitative immunohistochemical analysis of mononuclear infiltrates in breast carcinomas -- correlation with tumour differentiation .

Quantitative immunohistochemical analysis of <cell_type>mononuclear infiltrates</cell_type> in breast carcinomas -- correlation with tumour differentiation .


Inflammatory infiltrates were analysed in tissue sections of 76 breast carcinomas by counting the percentage of macrophages , IgA+ and IgG+ plasma cells , T cells with their subpopulations , and natural killer cells , and by measuring postcapillary venules ( PCVs , found in 12 cases ) within the infiltrates .

<cell_type>Inflammatory infiltrates</cell_type> were analysed in tissue sections of 76 breast carcinomas by counting the percentage of <cell_type>macrophages</cell_type> , <cell_type>IgA+ and IgG+ plasma cells</cell_type> , <cell_type>T cells</cell_type> with their subpopulations , and <cell_type>natural killer cells</cell_type> , and by measuring postcapillary venules ( PCVs , found in 12 cases ) within the infiltrates .


These parameters were correlated with nuclear grade and biochemically determined hormone receptor status , known markers of tumour differentiation .


A direct correlation was found between the extent of inflammation and nuclear grade ( P less than 0.0001 ) , and an inverse correlation between inflammation and oestrogen receptor ( OR ) positivity ( P less than 0.05 ) as well as inflammation and progesterone receptor ( PR ) positivity ( P less than 0.05 ) .

A direct correlation was found between the extent of inflammation and nuclear grade ( P less than 0.0001 ) , and an inverse correlation between inflammation and <protein>oestrogen receptor</protein> ( <protein>OR</protein> ) positivity ( P less than 0.05 ) as well as inflammation and <protein>progesterone receptor</protein> ( <protein>PR</protein> ) positivity ( P less than 0.05 ) .


The percentage of the OKT8+ suppressor/cytotoxic T cells increased when the inflammation expanded from scanty to moderate ( P less than 0.02 ) .

The percentage of the <cell_line>OKT8+ suppressor/cytotoxic T cells</cell_line> increased when the inflammation expanded from scanty to moderate ( P less than 0.02 ) .


The diameter of the PCVs also increased with increasing inflammatory infiltrate ( P less than 0.02 ) .


In addition , a direct correlation exists between the diameter of the PCVs and both the percentage of the OKT8+ T cells ( P less than 0.04 ) and the Leu-7+ natural killer cells ( P less than 0.03 ) .

In addition , a direct correlation exists between the diameter of the PCVs and both the percentage of the <cell_line>OKT8+ T cells</cell_line> ( P less than 0.04 ) and the Leu-7+ <cell_type>natural killer cells</cell_type> ( P less than 0.03 ) .


Reactivity of lymphocytes to a progesterone receptor-specific monoclonal antibody .

Reactivity of <cell_line>lymphocytes</cell_line> to a <protein>progesterone receptor-specific monoclonal antibody</protein> .


In this study we present evidence for reactivity of pregnancy lymphocytes , but not nonpregnancy lymphocytes , with the progesterone receptor-specific monoclonal antibody mPRI .

In this study we present evidence for reactivity of <cell_type>pregnancy lymphocytes</cell_type> , but not <cell_type>nonpregnancy lymphocytes</cell_type> , with the <protein>progesterone receptor-specific monoclonal antibody</protein> <protein>mPRI</protein> .


Using an avidin -biotin peroxidase detection system , we found a nuclear staining in 14.6 +/- 3.7 % ( mean +/- SEM , N = 27 ) of pregnancy lymphocytes , while only 0.47 +/- 0.33 % ( mean +/- SEM , N = 15 ) of nonpregnancy lymphocytes reacted with the antibody .

Using an <protein>avidin</protein> <protein>-biotin peroxidase</protein> detection system , we found a nuclear staining in 14.6 +/- 3.7 % ( mean +/- SEM , N = 27 ) of <cell_type>pregnancy lymphocytes</cell_type> , while only 0.47 +/- 0.33 % ( mean +/- SEM , N = 15 ) of <cell_type>nonpregnancy lymphocytes</cell_type> reacted with the antibody .


To characterize the receptor-bearing subset , CD8+ and CD4+ cells were depleted by complement-dependent lysis .

To characterize the receptor-bearing subset , <cell_line>CD8+ and CD4+ cells</cell_line> were depleted by complement-dependent lysis .


Depletion of CD8+ cells was accompanied by 62 +/- 18 % loss of progesterone receptor-bearing cells , while depletion of CD4+ cells resulted in a twofold increase in the number of positively staining lymphocytes .

Depletion of <cell_line>CD8+ cells</cell_line> was accompanied by 62 +/- 18 % loss of <cell_line>progesterone receptor-bearing cells</cell_line> , while depletion of <cell_line>CD4+ cells</cell_line> resulted in a twofold increase in the number of positively staining <cell_line>lymphocytes</cell_line> .


In nonpregnancy lymphocytes a 3-day PHA treatment , as well as allogeneic stimulation , resulted in a significant increase in the number of receptor-containing cells .

In <cell_line>nonpregnancy lymphocytes</cell_line> a 3-day <protein>PHA</protein> treatment , as well as allogeneic stimulation , resulted in a significant increase in the number of <cell_type>receptor-containing cells</cell_type> .


These results suggest that pregnancy , but not nonpregnancy , lymphocytes contain progesterone binding structures , and that these are inducible by mitogenic or alloantigenic stimuli .

These results suggest that pregnancy , but not nonpregnancy , <cell_line>lymphocytes</cell_line> contain <protein>progesterone binding structures</protein> , and that these are inducible by mitogenic or alloantigenic stimuli .


Activation of human CD4 T lymphocytes .

Activation of <cell_line>human CD4 T lymphocytes</cell_line> .


Interaction of fibronectin with VLA-5 receptor on CD4 cells induces the AP-1 transcription factor .

Interaction of <protein>fibronectin</protein> with <protein>VLA-5 receptor</protein> on <cell_line>CD4 cells</cell_line> induces the <protein>AP-1 transcription factor</protein> .


Fibronectin synergized with anti-CD3 antibody to promote CD4 cell proliferation in a serum-free culture system whereas no proliferation was observed when CD4 cells were cultured with anti-CD3 alone or fibronectin alone .

<protein>Fibronectin</protein> synergized with <protein>anti-CD3 antibody</protein> to promote <protein>CD4</protein> cell proliferation in a serum-free culture system whereas no proliferation was observed when <cell_line>CD4 cells</cell_line> were cultured with <protein>anti-CD3</protein> alone or <protein>fibronectin</protein> alone .


In addition , anti-CD29 ( integrin beta 1 ) as well as anti-VLA-5 ( human fibronectin receptor ) antibodies blocked this CD4 cell activation in this system .

In addition , <protein>anti-CD29</protein> ( <protein>integrin beta 1</protein> ) as well as <protein>anti-VLA-5</protein> ( <protein>human fibronectin receptor</protein> ) antibodies blocked this <cell_line>CD4 cell</cell_line> activation in this system .


Although anti-CD3 alone or fibronectin alone can not induce IL-2 message by CD4 cells , the combination of anti-CD3 plus fibronectin induced IL-2 message by CD4 cells .

Although <protein>anti-CD3</protein> alone or <protein>fibronectin</protein> alone can not induce <protein>IL-2</protein> message by <cell_line>CD4 cells</cell_line> , the combination of <protein>anti-CD3</protein> plus <protein>fibronectin</protein> induced <protein>IL-2</protein> message by <cell_line>CD4 cells</cell_line> .


In an analysis of the molecular mechanism by which IL-2 message was generated , we showed that a fibronectin -VLA-5 fibronectin receptor interaction may contribute an independent signal distinct from the CD3 pathway of activation by the induction of an AP-1 transcriptional factor .

In an analysis of the molecular mechanism by which <protein>IL-2</protein> message was generated , we showed that a <protein>fibronectin</protein> -VLA-5 <protein>fibronectin receptor</protein> interaction may contribute an independent signal distinct from the <protein>CD3</protein> pathway of activation by the induction of an <protein>AP-1 transcriptional factor</protein> .


Thus the VLA-5 fibronectin receptor on CD4 cells can play a complementary role in CD3 - TCR -mediated signal transduction through its interaction with fibronectin .

Thus the <protein>VLA-5 fibronectin receptor</protein> on <cell_line>CD4 cells</cell_line> can play a complementary role in <protein>CD3</protein> - <protein>TCR</protein> -mediated signal transduction through its interaction with <protein>fibronectin</protein> .


Glucocorticoid receptors on mononuclear leukocytes in Alzheimer 's disease .

<protein>Glucocorticoid receptors</protein> on <cell_type>mononuclear leukocytes</cell_type> in Alzheimer 's disease .


Several lines of evidence suggest disturbances of the hypothalamic-pituitary-adrenal ( HPA ) system in Alzheimer 's disease ( AD ) .


In an exploration of the potential role of the glucocorticoid receptor ( GR ) in AD , GR density and affinity were assessed on mononuclear leukocytes of 12 AD patients and 12 healthy controls .

In an exploration of the potential role of the glucocorticoid receptor ( GR ) in AD , GR density and affinity were assessed on <cell_type>mononuclear leukocytes</cell_type> of 12 AD patients and 12 healthy controls .


GR binding characteristics did not differ between patients and controls or between patients subdivided according to diagnosis or associated clinical features .


These data suggest that the abnormalities of the HPA system in AD are not related to a GR deficiency .

These data suggest that the abnormalities of the HPA system in AD are not related to a <protein>GR</protein> deficiency .


Oncogene amplification correlates with dense lymphocyte infiltration in human breast cancers : a role for hematopoietic growth factor release by tumor cells ?

Oncogene amplification correlates with dense lymphocyte infiltration in human breast cancers : a role for <protein>hematopoietic growth factor</protein> release by <cell_type>tumor cells</cell_type> ?


One hundred six primary breast cancer samples were analysed for c-erbB2 , int-2 , and c-myc gene amplification .


Surgically confirmed nodal involvement was observed in 42 % .


Level of gene amplification was studied by Southern and/or slot blot techniques .


Amplified c-erbB2 gene sequences were present in 21.5 % of all samples .

Amplified <dna>c-erbB2 gene sequences</dna> were present in 21.5 % of all samples .


Int-2 was amplified in 13.1 % and c-myc was amplified in 10.3 % .

<dna>Int-2</dna> was amplified in 13.1 % and <dna>c-myc</dna> was amplified in 10.3 % .


In a non-parametric test ( Kruskal-Wallis ) a strong negative association was found between high levels of c-erbB2 amplification and absence of estrogen receptor ( ER ) ( P = .0009 ) or progesterone receptor ( PR ) ( P = .011 ) expression .

In a non-parametric test ( Kruskal-Wallis ) a strong negative association was found between high levels of <dna>c-erbB2</dna> amplification and absence of estrogen receptor ( ER ) ( P = .0009 ) or <protein>progesterone receptor</protein> ( <protein>PR</protein> ) ( P = .011 ) expression .


No correlations were found between all or high levels of amplification of each oncogene separately or combined with T , N , grade , multifocality of tumor , or associated carcinoma in situ .


There was a trend approaching statistical significance for patients with c-erbB2 amplifications to have positive lymph nodes at surgery ( P = 0.09 ) .

There was a trend approaching statistical significance for patients with <dna>c-erbB2</dna> amplifications to have positive lymph nodes at surgery ( P = 0.09 ) .


A somewhat surprising finding however was a very strong association between oncogene amplification and dense lymphocyte infiltration of the tumor ( P = .05 ) . This correlation is even stronger when only high levels of amplification are considered , either for each oncogene separately ( P = .0048 ) or in combination ( P = .0007 ) .

A somewhat surprising finding however was a very strong association between <dna>oncogene</dna> amplification and dense lymphocyte infiltration of the tumor ( P = .05 ) . This correlation is even stronger when only high levels of amplification are considered , either for each oncogene separately ( P = .0048 ) or in combination ( P = .0007 ) .


We propose that malignant cell cytokine production may help explain this observation .

We propose that malignant cell <protein>cytokine</protein> production may help explain this observation .


Suppression of signals required for activation of transcription factor NF-kappa B in cells constitutively expressing the HTLV-I Tax protein .

Suppression of signals required for activation of <protein>transcription factor NF-kappa B</protein> in cells constitutively expressing the <protein>HTLV-I Tax protein</protein> .


Transient short-term expression of the Tax protein of human T-cell leukemia virus type-I ( HTLV-I ) leads to activation of the pleiotropic transcription factor NF-kappa B .

Transient short-term expression of the <protein>Tax protein</protein> of human T-cell leukemia virus type-I ( HTLV-I ) leads to activation of the pleiotropic <protein>transcription factor NF-kappa B</protein> .


Consistent with findings obtained with transient expression assays , we observed marked accumulation of the transcription factor NF-kappa B in the nucleus of Namalwa B lymphoid cells , which constitutively express Tax .

Consistent with findings obtained with transient expression assays , we observed marked accumulation of the <protein>transcription factor NF-kappa B</protein> in the nucleus of <cell_line>Namalwa B lymphoid cells</cell_line> , which constitutively express <protein>Tax</protein> .


In contrast , NF-kappa B activity was not detected in the nucleus following long-term expression of Tax in Jurkat T lymphocytes .

In contrast , <protein>NF-kappa B</protein> activity was not detected in the nucleus following long-term expression of <protein>Tax</protein> in <cell_line>Jurkat T lymphocytes</cell_line> .


The ability of both mitogens and cytokines to activate NF-kappa B was also blocked in Jurkat cells constitutively expressing Tax .

The ability of both mitogens and <protein>cytokines</protein> to activate <protein>NF-kappa B</protein> was also blocked in <cell_line>Jurkat cells</cell_line> constitutively expressing <protein>Tax</protein> .


However , the activation of other mitogen-inducible transcription factors , such as Fos and Jun , was unaffected .

However , the activation of other <protein>mitogen-inducible transcription factors</protein> , such as <protein>Fos</protein> and <protein>Jun</protein> , was unaffected .


Thus , depending on the cellular environment , the short- and long-term effects of Tax expression can be quite different .

Thus , depending on the cellular environment , the short- and long-term effects of <protein>Tax</protein> expression can be quite different .


Consequently , one function of Tax in cells infected with HTLV-I might involve cell-type-specific suppression , as opposed to activation , of distinct signal pathways .

Consequently , one function of <protein>Tax</protein> in cells infected with HTLV-I might involve cell-type-specific suppression , as opposed to activation , of distinct signal pathways .


The cells lines described here should be useful for the delineation of signaling pathways utilized in the selective regulation of gene expression .


Interferon-gamma and the sexual dimorphism of autoimmunity .

<protein>Interferon-gamma</protein> and the sexual dimorphism of autoimmunity .


The sexual difference in the incidence of autoimmune diseases has remained an enigma for many years .


In the examination of the induction of autoimmunity in transgenic mice , evidence has been obtained further implicating the lymphokine interferon-gamma in the etiology of autoimmunity .

In the examination of the induction of autoimmunity in transgenic mice , evidence has been obtained further implicating the <protein>lymphokine</protein> <protein>interferon-gamma</protein> in the etiology of autoimmunity .


Sex steroid regulation of the production of this molecule , as well as other cytokines , may help explain the gender-specific differences in the immune system , including autoimmunity .

Sex steroid regulation of the production of this molecule , as well as other <protein>cytokines</protein> , may help explain the gender-specific differences in the immune system , including autoimmunity .


Cloning of a transcriptionally active human TATA binding factor .

Cloning of a <protein>transcriptionally active human TATA binding factor</protein> .


Transcription factor IID ( TFIID ) binds to the TATA box promoter element and regulates the expression of most eukaryotic genes transcribed by RNA polymerase II .

<protein>Transcription factor IID</protein> ( <protein>TFIID</protein> ) binds to the <dna>TATA box promoter element</dna> and regulates the expression of most <dna>eukaryotic genes</dna> transcribed by <protein>RNA polymerase II</protein> .


Complementary DNA ( cDNA ) encoding a human TFIID protein has been cloned .

<dna>Complementary DNA</dna> ( <dna>cDNA</dna> ) encoding a <protein>human TFIID protein</protein> has been cloned .


The human TFIID polypeptide has 339 amino acids and a molecular size of 37 , 745 daltons .

The <protein>human TFIID polypeptide</protein> has 339 amino acids and a molecular size of 37 , 745 daltons .


The carboxyl-terminal 181 amino acids of the human TFIID protein shares 80 % identity with the TFIID protein from Saccharomyces cerevisiae .

The <protein>carboxyl-terminal 181 amino acids</protein> of the <protein>human TFIID protein</protein> shares 80 % identity with the <protein>TFIID</protein> protein from Saccharomyces cerevisiae .


The amino terminus contains an unusual repeat of 38 consecutive glutamine residues and an X-Thr-Pro repeat .

The <protein>amino terminus</protein> contains an unusual repeat of 38 consecutive glutamine residues and an <protein>X-Thr-Pro repeat</protein> .


Expression of DNA in reticulocyte lysates or in Escherichia coli yielded a protein that was competent for both DNA binding and transcription activation .


A novel T-cell trans-activator that recognizes a phorbol ester-inducible element of the interleukin-2 promoter .

A novel <protein>T-cell trans-activator</protein> that recognizes a <dna>phorbol ester-inducible element</dna> of the <dna>interleukin-2 promoter</dna> .


The interleukin 2 ( IL-2 ) gene promoter is recognized by several cell-type-specific and ubiquitous transcriptional regulators that integrate information transmitted by various signaling systems leading to IL-2 production and T-cell activation .

The <dna>interleukin 2 ( IL-2 ) gene promoter</dna> is recognized by several <protein>cell-type-specific and ubiquitous transcriptional regulators</protein> that integrate information transmitted by various signaling systems leading to <protein>IL-2</protein> production and <cell_type>T-cell</cell_type> activation .


Using a combination of transfection , protein-DNA binding , and in vitro transcription methods , we have discovered the novel T-cell-specific transcriptional activator TCF-1 ( for T-Cell Factor-1 ) , which recognizes a T-cell-specific response element ( TCE ) located within the IL-2 promoter .

Using a combination of transfection , protein-DNA binding , and in vitro transcription methods , we have discovered the <protein>novel T-cell-specific transcriptional activator</protein> <protein>TCF-1</protein> ( for <protein>T-Cell Factor-1</protein> ) , which recognizes a <dna>T-cell-specific response element</dna> ( <dna>TCE</dna> ) located within the <dna>IL-2 promoter</dna> .


Although the TCE is similar in sequence to a consensus NF kappa B site , several criteria indicate that TCF-1 is distinct from NF kappa B .

Although the <dna>TCE</dna> is similar in sequence to a <dna>consensus NF kappa B site</dna> , several criteria indicate that <protein>TCF-1</protein> is distinct from <protein>NF kappa B</protein> .


However , like NF kappa B , TCF-1 activity is induced by phorbol esters and other T-cell activators .

However , like <protein>NF kappa B</protein> , <protein>TCF-1</protein> activity is induced by phorbol esters and other T-cell activators .


Risk factors for breast recurrence in premenopausal and postmenopausal patients with ductal cancers treated by conservation therapy .


Risk factors for local failure were evaluated for 496 clinical Stage I-II patients with infiltrating ductal carcinomas ( median follow-up , 71 months ) treated by conservative surgery and radiotherapy .


Monofactorial analysis identified the following factors to be correlated with increased risk : moderate/marked mononuclear cell reaction ( MCR ) , high histologic grade ( G ) , extensive intraductal component ( EIC ) , tumor necrosis , macroscopic multiplicity , estrogen receptor negativity , anatomic tumor size , age younger than 40 years , and vascular invasion .

Monofactorial analysis identified the following factors to be correlated with increased risk : moderate/marked mononuclear cell reaction ( MCR ) , high histologic grade ( G ) , extensive intraductal component ( EIC ) , tumor necrosis , macroscopic multiplicity , <protein>estrogen receptor</protein> negativity , anatomic tumor size , age younger than 40 years , and vascular invasion .


Only MCR , G , and EIC proved significant in Cox multivariate analysis .


These risk factors were highly age dependent , with EIC markedly more prevalent in women younger than 50 , MCR and G in women younger than 40 .


Separate Cox analysis for premenopausal patients showed that MCR/EIC determined risk independent of resection margins : tumors with MCR had a 28 % , and with EIC a 22 % probability of recurring locally by 5 years .


Premenopausal patients with neither risk factor had a very low failure rate ( 2.6 % at 5 years ) , regardless of age .


For postmenopausal patients risk of breast recurrence was determined both by adequacy of resection margins and grade , with a high local failure rate for patients having G3 tumors with positive or indeterminate margins ( 31 % at 5 years ) .


The authors conclude that the microscopic examination is the only useful tool for assessing the risk of local failure , which is quite low for the majority of patients treated with breast conservation .


High-risk patients can be recognized morphologically .


The age dependence of morphologic risk factors appears to explain the high local failure rate seen in patients younger than 40 .


Tax -independent binding of multiple cellular factors to Tax-response element DNA of HTLV-I .

<protein>Tax</protein> -independent binding of multiple <protein>cellular factors</protein> to <dna>Tax-response element DNA</dna> of HTLV-I .


The human T-cell leukemia virus type I ( HTLV-I ) promoter contains three copies of imperfect repeats of a 21-base pair sequence designated here as TRE ( Tax-response element ) that is responsive to the virally encoded transactivator protein Tax .

The <dna>human T-cell leukemia virus type I ( HTLV-I ) promoter</dna> contains three copies of imperfect repeats of a 21-base pair sequence designated here as <dna>TRE</dna> ( <dna>Tax-response element</dna> ) that is responsive to the <protein>virally encoded transactivator protein</protein> <protein>Tax</protein> .


We have identified and separated four nuclear proteins from C81-66-45 cells , an HTLV-I immortalized Tax-expressing human T-lymphocyte line ( Salahuddin et al. , 1983 ) , that interact with the TRE-DNA , none of which are identical with the Tax-protein .

We have identified and separated four <protein>nuclear proteins</protein> from C81-66-45 cells , an <cell_line>HTLV-I immortalized Tax-expressing human T-lymphocyte line</cell_line> ( Salahuddin et al. , 1983 ) , that interact with the <dna>TRE-DNA</dna> , none of which are identical with the <protein>Tax-protein</protein> .


The proteins identified have molecular weights of about 32 , 36 to 42 , 50 and 110 kD .


Four different methods were used to identify the proteins .


First , from different cell lines three or all four of the nuclear proteins were specifically cross-linked by UV irradiation to the radioactively labeled TRE-DNA fragment .

First , from different cell lines three or all four of the <protein>nuclear proteins</protein> were specifically cross-linked by UV irradiation to the radioactively labeled <dna>TRE-DNA fragment</dna> .


Second , TRE-DNA binding proteins sedimented through a glycerol density gradient at rates corresponding to proteins of native molecular weights of 35 to 50 kD and 110 kD .

Second , <protein>TRE-DNA binding proteins</protein> sedimented through a glycerol density gradient at rates corresponding to proteins of native molecular weights of 35 to 50 kD and 110 kD .


Third , only the 50 kD protein was retained on a biotinylated DNA-streptavidin matrix when the DNA fragment contained the TRE-DNA .

Third , only the <protein>50 kD protein</protein> was retained on a biotinylated DNA-streptavidin matrix when the DNA fragment contained the <dna>TRE-DNA</dna> .


Fourth , extensive purification by several cycles of TRE -DNA affinity chromatography resulted in the 32 , 36 to 42 and 110 kD proteins and to less extent the 50 kD factor .

Fourth , extensive purification by several cycles of <dna>TRE</dna> -DNA affinity chromatography resulted in the <protein>32 , 36 to 42 and 110 kD proteins</protein> and to less extent the <protein>50 kD factor</protein> .


Two abundant proteins of 75 and 80 kD were competed out by poly [ d ( I-C ) ] in all reactions .


The cAMP-response element CRE , TGACGTCA , present in the 21 base-pair sequence , appears to be essential for specific protein- TRE -DNA interactions because mutation of the two G 's destroys this complex .

The <dna>cAMP-response element</dna> <dna>CRE</dna> , TGACGTCA , present in the <dna>21 base-pair sequence</dna> , appears to be essential for specific protein- <dna>TRE</dna> -DNA interactions because mutation of the two G 's destroys this complex .


This result suggests that the cAMP response element binding protein , CREB , is involved in the protein-TRE-DNA complex and in mediating the Tax response .

This result suggests that the <protein>cAMP response element binding protein</protein> , <protein>CREB</protein> , is involved in the <protein>protein-TRE-DNA complex</protein> and in mediating the <protein>Tax</protein> response .


Two distinct transcription factors that bind the immunoglobulin enhancer microE5/kappa 2 motif .

Two distinct <protein>transcription factors</protein> that bind the <dna>immunoglobulin enhancer</dna> <dna>microE5/kappa 2 motif</dna> .


Activity of the immunoglobulin heavy and kappa light chain gene enhancers depends on a complex interplay of ubiquitous and developmentally regulated proteins .

Activity of the <dna>immunoglobulin heavy and kappa light chain gene enhancers</dna> depends on a complex interplay of <protein>ubiquitous and developmentally regulated proteins</protein> .


Two complementary DNAs were isolated that encode proteins , denoted ITF-1 and ITF-2 , that are expressed in a variety of cell types and bind the microE5/kappa 2 motif found in both heavy and kappa light chain enhancers .

Two <dna>complementary DNAs</dna> were isolated that encode proteins , denoted <protein>ITF-1</protein> and <protein>ITF-2</protein> , that are expressed in a variety of cell types and bind the <dna>microE5/kappa 2 motif</dna> found in both <dna>heavy and kappa light chain enhancers</dna> .


The complementary DNAs are the products of distinct genes , yet both ITF-1 and ITF-2 are structurally and functionally similar .

The <dna>complementary DNAs</dna> are the products of distinct genes , yet both <protein>ITF-1</protein> and <protein>ITF-2</protein> are structurally and functionally similar .


The two proteins interact with one another through their putative helix-loop-helix motifs and each possesses a distinct domain that dictates transcription activation .

The two proteins interact with one another through their putative <protein>helix-loop-helix motifs</protein> and each possesses a distinct domain that dictates transcription activation .


Elevated glucocorticoid receptor concentrations before and after glucocorticoid therapy in peripheral mononuclear leukocytes of patients with atopic dermatitis .

Elevated <protein>glucocorticoid receptor</protein> concentrations before and after glucocorticoid therapy in <cell_type>peripheral mononuclear leukocytes</cell_type> of patients with atopic dermatitis .


The number and affinity of glucocorticoid binding sites in peripheral mononuclear leukocytes of patients with atopic dermatitis ( AD ) and healthy controls were determined under baseline conditions and after a defined oral glucocorticoid treatment .

The number and affinity of glucocorticoid binding sites in <cell_type>peripheral mononuclear leukocytes</cell_type> of patients with atopic dermatitis ( AD ) and healthy controls were determined under baseline conditions and after a defined oral glucocorticoid treatment .


Patients with AD ( n = 15 ) exhibited significantly more glucocorticoid receptors ( GR ) per cell than the control group ( n = 22 ) , while the GR affinity did not differ .

Patients with AD ( n = 15 ) exhibited significantly more <protein>glucocorticoid receptors</protein> ( <protein>GR</protein> ) per cell than the control group ( n = 22 ) , while the <protein>GR</protein> affinity did not differ .


Methylprednisolone treatment resulted in a significant reduction of the GR sites per cell in the steroid-treated control group ( n = 10 ) in contrast to the patients .

Methylprednisolone treatment resulted in a significant reduction of the <protein>GR</protein> sites per cell in the steroid-treated control group ( n = 10 ) in contrast to the patients .


The dissociation constant was not affected by methylprednisolone treatment in either group .


In view of the therapeutic efficiency of glucocorticoids in AD and findings of abnormal cAMP and cAMP-phosphodiesterase activity , the elevated GR concentrations in AD lend support to the hypothesis of a compensatory GR upregulation due to an insufficient action of endogenous cortisol or to altered cAMP-induced GR expression .

In view of the therapeutic efficiency of glucocorticoids in AD and findings of abnormal cAMP and cAMP-phosphodiesterase activity , the elevated <protein>GR</protein> concentrations in AD lend support to the hypothesis of a compensatory <protein>GR</protein> upregulation due to an insufficient action of endogenous cortisol or to altered cAMP-induced <protein>GR</protein> expression .


The actions of cyclosporin A and FK506 suggest a novel step in the activation of T lymphocytes .

The actions of cyclosporin A and FK506 suggest a novel step in the activation of <cell_type>T lymphocytes</cell_type> .


Cyclosporin A and FK506 are immunosuppressive compounds that have similar inhibitory effects on the expression of several lymphokines produced by T lymphocytes .

Cyclosporin A and FK506 are immunosuppressive compounds that have similar inhibitory effects on the expression of several <protein>lymphokines</protein> produced by <cell_type>T lymphocytes</cell_type> .


Despite their similar effects the drugs bind to two different cytosolic protein , cyclophilin and FKBP respectively , which raises the possibility that they have different modes of action .

Despite their similar effects the drugs bind to two different <protein>cytosolic protein</protein> , <protein>cyclophilin</protein> and <protein>FKBP</protein> respectively , which raises the possibility that they have different modes of action .


Using constructs in which mRNA production controlled by a specific transcription factor could be readily measured we found that both cyclosporin A and FK506 completely inhibited transcription activated by NF-AT , NFIL2 A , NFIL2 B and partially inhibited transcription activated by NF kappa B .

Using constructs in which <rna>mRNA</rna> production controlled by a specific <protein>transcription factor</protein> could be readily measured we found that both cyclosporin A and FK506 completely inhibited transcription activated by <protein>NF-AT</protein> , <protein>NFIL2 A</protein> , <protein>NFIL2 B</protein> and partially inhibited transcription activated by <protein>NF kappa B</protein> .


Cyclosporin A and FK506 inhibited only transcriptional activation that was dependent on Ca2+ mobilization .


However , cyclosporin A and FK506 did not inhibit Ca2+ mobilization dependent expression of c-fos mRNA indicating that only a subset of signalling pathways regulated by Ca2+ is sensitive to these drugs .

However , cyclosporin A and FK506 did not inhibit Ca2+ mobilization dependent expression of <rna>c-fos mRNA</rna> indicating that only a subset of signalling pathways regulated by Ca2+ is sensitive to these drugs .


Furthermore , we did not observe any qualitative differences between the effect of cyclosporin A and FK506 on six different transcription factors which suggests that these drugs may interfere with the activity of a novel Ca2+ dependent step that regulates several transcription factors .

Furthermore , we did not observe any qualitative differences between the effect of cyclosporin A and FK506 on six different <protein>transcription factors</protein> which suggests that these drugs may interfere with the activity of a novel Ca2+ dependent step that regulates several <protein>transcription factors</protein> .


The internal methionine codons of human T-cell leukemia virus type II rex gene are not required for p24rex production or virus replication and transformation .

The internal methionine codons of <dna>human T-cell leukemia virus type II rex gene</dna> are not required for <protein>p24rex</protein> production or virus replication and transformation .


Human T-cell leukemia virus types I ( HTLV-I ) and II ( HTLV-II ) have two nonstructural trans-acting regulatory genes , tax and rex , located in the 3 ' region of the viral genome .

Human T-cell leukemia virus types I ( HTLV-I ) and II ( HTLV-II ) have two <dna>nonstructural trans-acting regulatory genes</dna> , <dna>tax</dna> and <dna>rex</dna> , located in the <dna>3 ' region</dna> of the <dna>viral genome</dna> .


The tax gene product ( HTLV-I p40tax and HTLV-II p37tax ) is the transcriptional activator of the viral long terminal repeat .

The <protein>tax gene product</protein> ( <protein>HTLV-I p40tax</protein> and <protein>HTLV-II p37tax</protein> ) is the transcriptional activator of the <dna>viral long terminal repeat</dna> .


The rex gene encodes two protein products , p27rex/p21rex and p26rex/p24rex in HTLV-I and HTLV-II , respectively .

The <dna>rex gene</dna> encodes two protein products , <protein>p27rex/p21rex</protein> and <protein>p26rex/p24rex</protein> in HTLV-I and HTLV-II , respectively .


Rex acts posttranscriptionally to facilitate accumulation of full-length gag/pol and singly spliced env mRNA in the cytoplasm of HTLV-infected cells .

<protein>Rex</protein> acts posttranscriptionally to facilitate accumulation of full-length <protein>gag/pol</protein> and singly spliced <rna>env mRNA</rna> in the cytoplasm of <cell_type>HTLV-infected cells</cell_type> .


Previous studies showed that the first ATG of the rex gene is critical for Rex production and function .

Previous studies showed that the first ATG of the <dna>rex gene</dna> is critical for <protein>Rex</protein> production and function .


The importance of the internal ATGs to Rex function is not known .

The importance of the internal ATGs to <protein>Rex</protein> function is not known .


However , in vitro mutagenesis of the HTLV-I rex gene has provided indirect evidence which suggests that p21rex , and by analogy HTLV-II p24rex , results from initiation at an internal AUG of the tax/rex mRNA .

However , in vitro mutagenesis of the HTLV-I <dna>rex gene</dna> has provided indirect evidence which suggests that <protein>p21rex</protein> , and by analogy HTLV-II <protein>p24rex</protein> , results from initiation at an internal AUG of the <rna>tax/rex mRNA</rna> .


By using an infectious molecular clone of HTLV-II , we investigated the importance of the internal ATGs of the rex gene on Rex protein production and function .

By using an infectious molecular clone of HTLV-II , we investigated the importance of the internal ATGs of the <dna>rex gene</dna> on <protein>Rex</protein> protein production and function .


Our results indicate that p24rex of HTLV-II is not initiated at an internal AUG and that the internal methionine codons are not crucial to the function of the rex gene and , ultimately , the transforming properties of the virus .

Our results indicate that <protein>p24rex</protein> of HTLV-II is not initiated at an internal AUG and that the internal methionine codons are not crucial to the function of the <dna>rex gene</dna> and , ultimately , the transforming properties of the virus .


Astrocytes and glioblastoma cells express novel octamer-DNA binding proteins distinct from the ubiquitous Oct-1 and B cell type Oct-2 proteins .

<cell_type>Astrocytes</cell_type> and <cell_type>glioblastoma cells</cell_type> express novel <protein>octamer-DNA binding proteins</protein> distinct from the <protein>ubiquitous Oct-1 and B cell type Oct-2 proteins</protein> .


The 'octamer ' sequence , ATGCAAAT or its complement ATTTGCAT , is a key element for the transcriptional regulation of immunoglobulin genes in B-lymphocytes as well as a number of housekeeping genes in all cell types .

The <dna>'octamer ' sequence</dna> , ATGCAAAT or its complement ATTTGCAT , is a key element for the transcriptional regulation of <dna>immunoglobulin genes</dna> in <cell_type>B-lymphocytes</cell_type> as well as a number of <dna>housekeeping genes</dna> in all cell types .


In lymphocytes , the octamer-binding protein Oct-2A and variants thereof are thought to contribute to the B-cell specific gene expression , while the ubiquitous protein Oct-1 seems to control general octamer site -dependent transcription .

In <cell_type>lymphocytes</cell_type> , the <protein>octamer-binding protein</protein> <protein>Oct-2A</protein> and variants thereof are thought to contribute to the <dna>B-cell specific gene</dna> expression , while the ubiquitous protein Oct-1 seems to control general <dna>octamer site</dna> -dependent transcription .


Various other genes , for example interleukin-1 and MHC class II genes , contain an octamer sequence in the promoter and are expressed in cells of both the immune and nervous systems .

Various other genes , for example <dna>interleukin-1 and MHC class II genes</dna> , contain an <dna>octamer sequence</dna> in the <dna>promoter</dna> and are expressed in cells of both the immune and nervous systems .


This prompted us to analyze the octamer-binding proteins in the latter cells .

This prompted us to analyze the <protein>octamer-binding proteins</protein> in the latter cells .


Using the electrophoretic mobility shift assay , at least six novel octamer binding proteins were detected in nuclear extracts of cultured mouse astrocytes .

Using the electrophoretic mobility shift assay , at least six novel <protein>octamer binding proteins</protein> were detected in nuclear extracts of <cell_type>cultured mouse astrocytes</cell_type> .


These proteins are differentially expressed in human glioblastoma and neuroblastoma cell lines .

These proteins are differentially expressed in <cell_line>human glioblastoma and neuroblastoma cell lines</cell_line> .


The nervous system-derived ( N-Oct ) proteins bound to the octamer DNA sequence in a manner which is indistinguishable from the Oct-1 and Oct-2A proteins .

The <protein>nervous system-derived ( N-Oct ) proteins</protein> bound to the <dna>octamer DNA sequence</dna> in a manner which is indistinguishable from the <protein>Oct-1</protein> and <protein>Oct-2A proteins</protein> .


The relationship of the N-Oct proteins to Oct-1 and Oct-2A was analyzed by proteolytic clipping bandshift assays and by their reactivity towards antisera raised against recombinant Oct-1 and Oct-2A proteins .

The relationship of the <protein>N-Oct proteins</protein> to <protein>Oct-1</protein> and <protein>Oct-2A</protein> was analyzed by proteolytic clipping bandshift assays and by their reactivity towards antisera raised against recombinant <protein>Oct-1</protein> and <protein>Oct-2A</protein> proteins .


On the basis of these assays , all N-Oct-factors were found to be distinct from the ubiquitous Oct-1 and the lymphoid-specific Oct-2A proteins .

On the basis of these assays , all <protein>N-Oct-factors</protein> were found to be distinct from the <protein>ubiquitous Oct-1</protein> and the <protein>lymphoid-specific Oct-2A</protein> proteins .


In melanoma cells that contain the N-Oct-3 factor , a transfected lymphocyte-specific promoter was neither activated nor was it repressed upon contransfection with an Oct-2A expression vector .

In <cell_type>melanoma cells</cell_type> that contain the <protein>N-Oct-3 factor</protein> , a transfected lymphocyte-specific promoter was neither activated nor was it repressed upon contransfection with an <dna>Oct-2A expression vector</dna> .


We therefore speculate that N-Oct-3 and other N-Oct factors have a specific role in gene expression in cells of the nervous system .

We therefore speculate that <protein>N-Oct-3</protein> and other <protein>N-Oct factors</protein> have a specific role in gene expression in cells of the nervous system .


Detection in non-erythroid cells of a factor with the binding characteristics of the erythroid cell transcription factor EF1 .

Detection in <cell_type>non-erythroid cells</cell_type> of a factor with the binding characteristics of the <protein>erythroid cell transcription factor</protein> <protein>EF1</protein> .


The erythroid transcription factor erythroid factor-1 ( EF1 ) plays a critical role in the transcription of erythroid-specific genes .

The <protein>erythroid transcription factor</protein> <protein>erythroid factor-1</protein> ( <protein>EF1</protein> ) plays a critical role in the transcription of <dna>erythroid-specific genes</dna> .


Here we report the presence of a factor with the mobility and sequence-specific DNA-binding characteristics of EF1 at low abundance in a wide variety of non-erythroid cell types .

Here we report the presence of a factor with the mobility and sequence-specific DNA-binding characteristics of <protein>EF1</protein> at low abundance in a wide variety of <cell_type>non-erythroid cell types</cell_type> .


This is the first report of an EF1 -like activity in non-erythroid cells and indicates that this factor may play a role in the regulation of genes expressed in such cells .

This is the first report of an <protein>EF1</protein> -like activity in <cell_type>non-erythroid cells</cell_type> and indicates that this factor may play a role in the regulation of <dna>genes</dna> expressed in such cells .


Protein kinase inhibitor H-7 blocks accumulation of unspliced mRNA of human T-cell leukemia virus type I ( HTLV-I ) .

Protein kinase inhibitor H-7 blocks accumulation of <rna>unspliced mRNA</rna> of human T-cell leukemia virus type I ( HTLV-I ) .


Rex , the post-transcriptional regulator of human T-cell leukemia virus type I ( HTLV-I ) , is known to induce accumulation of the unspliced viral gag-pol mRNA .

<protein>Rex</protein> , the <protein>post-transcriptional regulator</protein> of human T-cell leukemia virus type I ( HTLV-I ) , is known to induce accumulation of the <rna>unspliced viral gag-pol mRNA</rna> .


Rex is a phosphoprotein found in the cell nucleolus , whose function may be regulated by its localization and phosphorylation .

<protein>Rex</protein> is a <protein>phosphoprotein</protein> found in the cell nucleolus , whose function may be regulated by its localization and phosphorylation .


We have examined the role of phosphorylation on Rex function by using a protein kinase inhibitor , H-7 [ 1- ( 5-isoquinolinyl-sulfonyl ) -2-methylpiperazine ] .

We have examined the role of phosphorylation on <protein>Rex</protein> function by using a protein kinase inhibitor , H-7 [ 1- ( 5-isoquinolinyl-sulfonyl ) -2-methylpiperazine ] .


Treatment of an HTLV-I infected human T-cell line with H-7 blocked specifically accumulation of the unspliced gag-pol mRNA , resulting in the decreased Gag protein synthesis that corresponds with the decreased in vivo phosphorylation of Rex .

Treatment of an <cell_line>HTLV-I infected human T-cell line</cell_line> with H-7 blocked specifically accumulation of the <rna>unspliced gag-pol mRNA</rna> , resulting in the decreased <protein>Gag protein</protein> synthesis that corresponds with the decreased in vivo phosphorylation of <protein>Rex</protein> .


In contrast , other viral and cellular products have not been influenced by the level of H-7 used .


Therefore , the phosphorylation of Rex is required for the viral RNA partition of HTLV-I .

Therefore , the phosphorylation of <protein>Rex</protein> is required for the viral RNA partition of HTLV-I .


Increased glucocorticoid responsiveness of CD4+ T-cell clonal lines grown in serum-free media .

Increased glucocorticoid responsiveness of <cell_line>CD4+ T-cell clonal lines</cell_line> grown in serum-free media .


CEM-C7 , a human leukemic CD4+ T-lymphocyte cell line and three of its subclones , CEM-4R4 , CEM-3R43 , and ICR-27 , previously cultured in a medium supplemented with 5 to 10 % fetal bovine serum , have been adapted to serum-free media .

<cell_line>CEM-C7</cell_line> , a <cell_line>human leukemic CD4+ T-lymphocyte cell line</cell_line> and three of its subclones , <cell_line>CEM-4R4</cell_line> , <cell_line>CEM-3R43</cell_line> , and <cell_line>ICR-27</cell_line> , previously cultured in a medium supplemented with 5 to 10 % fetal bovine serum , have been adapted to serum-free media .


The best medium of those tested was RPMI 1640 supplemented with 5 micrograms/ml each transferrin and insulin + 5 ng/ml sodium selenite +/- 0.1 % bovine serum albumin .

The best medium of those tested was RPMI 1640 supplemented with 5 micrograms/ml each <protein>transferrin</protein> and <protein>insulin</protein> + 5 ng/ml sodium selenite +/- 0.1 % <protein>bovine serum albumin</protein> .


While growing either with or without albumin , the several clonal lines of CEM cells displayed growth similar to serum-supplemented cultures .

While growing either with or without albumin , the several <cell_line>clonal lines</cell_line> of <cell_line>CEM</cell_line> cells displayed growth similar to serum-supplemented cultures .


Cell proliferation of CEM-C7 cells cultured in both serum-free media has been sustained for 3 mo .

Cell proliferation of <cell_line>CEM-C7</cell_line> cells cultured in both serum-free media has been sustained for 3 mo .


with culture doubling times of about 25 h for both serum-supplemented and serum-free cultures ( viability greater than or equal to 90 % ) .

with culture doubling times of about 25 h for both <cell_line>serum-supplemented and serum-free cultures</cell_line> ( viability greater than or equal to 90 % ) .


Cell morphology remained essentially the same in serum-free or serum containing media .


The expression of CD4 , a marker for T-derived lymphoid cells , was not significantly different in serum-free medium .

The expression of <protein>CD4</protein> , a marker for <cell_type>T-derived lymphoid cells</cell_type> , was not significantly different in serum-free medium .


When grown in serum-free medium , CEM-C7 cells exhibited increased steroid responsiveness as evidenced by increased glucocorticoid receptor binding sites , increased induction of glutamine synthetase , and cell lysis at lower concentrations of steroid .

When grown in serum-free medium , <cell_line>CEM-C7</cell_line> cells exhibited increased steroid responsiveness as evidenced by increased <protein>glucocorticoid receptor</protein> binding sites , increased induction of <protein>glutamine synthetase</protein> , and cell lysis at lower concentrations of steroid .


Receptor mutant subclones of CEM-C7 , which are proven to be completely unresponsive to micromolar concentrations of dexamethasone when grown in serum-supplemented medium , become partially sensitive to the hormone after growth in defined medium .

Receptor mutant subclones of <cell_line>CEM-C7</cell_line> , which are proven to be completely unresponsive to micromolar concentrations of dexamethasone when grown in serum-supplemented medium , become partially sensitive to the hormone after growth in defined medium .


The increased sensitivity of CEM-C7 cells and its subclones to dexamethasone in serum-free medium returned to previous levels when these cells were recultured in serum-containing medium .

The increased sensitivity of <cell_line>CEM-C7 cells</cell_line> and its subclones to dexamethasone in serum-free medium returned to previous levels when these cells were recultured in serum-containing medium .


Our results suggest that substances in serum influence steroid effects on these cells and that the molecular details of glucocorticoid hormone action may be pursued more precisely in a clearly defined culture medium .


[ Glucocorticoid receptors on human peripheral mononuclear and polymorphonuclear leucocytes : changes in patients with yang-deficiency ]

[ <protein>Glucocorticoid receptors</protein> on <cell_type>human peripheral mononuclear and polymorphonuclear leucocytes</cell_type> : changes in patients with yang-deficiency ]


It was found that , in former works , the glucocorticoid receptors ( GCR ) on peripheral mixed leucocytes in patients with Yang-deficiency were decreased .

It was found that , in former works , the <protein>glucocorticoid receptors</protein> ( <protein>GCR</protein> ) on <cell_type>peripheral mixed leucocytes</cell_type> in patients with Yang-deficiency were decreased .


In this work , the mixed leucocytes were further separated into mononuclear ( MNL ) and polymorphonuclear ( PML ) leucocytes , and GCR were determined in each part of leucocytes .

In this work , the <cell_type>mixed leucocytes</cell_type> were further separated into <cell_type>mononuclear ( MNL ) and polymorphonuclear ( PML ) leucocytes</cell_type> , and <protein>GCR</protein> were determined in each part of <cell_type>leucocytes</cell_type> .


GCR on MNL and PML in 6 Yang deficient patients were 3473 +/- 413 and 4433 +/- 651 sites/cell respectively , statistically significant from the normal control group ( 4462 +/- 962 and 5622 +/- 782 sites/cell respectively , P less than 0.05 ) .

<protein>GCR</protein> on <cell_type>MNL</cell_type> and <cell_type>PML</cell_type> in 6 Yang deficient patients were 3473 +/- 413 and 4433 +/- 651 sites/cell respectively , statistically significant from the normal control group ( 4462 +/- 962 and 5622 +/- 782 sites/cell respectively , P less than 0.05 ) .


GCR on MNL , PML and mixed leucocytes in 5 patients were determined simultaneously , and all lowered from the control group .

<protein>GCR</protein> on <cell_type>MNL</cell_type> , <cell_type>PML</cell_type> and <cell_type>mixed leucocytes</cell_type> in 5 patients were determined simultaneously , and all lowered from the control group .


The results were 3369 +/- 370 , 4986 +/- 419 and 4524 +/- 852 sites/cell respectively , with the lowest GCR on MNL and highest on PML .

The results were 3369 +/- 370 , 4986 +/- 419 and 4524 +/- 852 sites/cell respectively , with the lowest <protein>GCR</protein> on <cell_type>MNL</cell_type> and highest on <cell_type>PML</cell_type> .


The ubiquitous octamer-binding protein ( s ) is sufficient for transcription of immunoglobulin genes .

The <protein>ubiquitous octamer-binding protein</protein> ( s ) is sufficient for transcription of <dna>immunoglobulin genes</dna> .


All immunoglobulin genes contain a conserved octanucleotide promoter element , ATGCAAAT , which has been shown to be required for their normal B-cell-specific transcription .

All <dna>immunoglobulin genes</dna> contain a conserved <dna>octanucleotide promoter element</dna> , ATGCAAAT , which has been shown to be required for their normal B-cell-specific transcription .


Proteins that bind this octamer have been purified , and cDNAs encoding octamer-binding proteins have been cloned .

Proteins that bind this octamer have been purified , and <dna>cDNAs</dna> encoding <protein>octamer-binding proteins</protein> have been cloned .


Some of these proteins ( referred to as OTF-2 ) are lymphoid specific , whereas at least one other , and possibly more ( referred to as OTF-1 ) , is found ubiquitously in all cell types .

Some of these proteins ( referred to as <protein>OTF-2</protein> ) are lymphoid specific , whereas at least one other , and possibly more ( referred to as <protein>OTF-1</protein> ) , is found ubiquitously in all cell types .


The exact role of these different proteins in directing the tissue-specific expression of immunoglobulin genes is unclear .

The exact role of these different proteins in directing the tissue-specific expression of <dna>immunoglobulin genes</dna> is unclear .


We have identified two human pre-B-cell lines that contain extremely low levels of OTF-2 yet still express high levels of steady-state immunoglobulin heavy-chain mRNA in vivo and efficiently transcribe an immunoglobulin gene in vitro .

We have identified two <cell_line>human pre-B-cell lines</cell_line> that contain extremely low levels of <protein>OTF-2</protein> yet still express high levels of <rna>steady-state immunoglobulin heavy-chain mRNA</rna> in vivo and efficiently transcribe an <dna>immunoglobulin gene</dna> in vitro .


Addition of a highly enriched preparation of OTF-1 made from one of these pre-B cells or from HeLa cells specifically stimulated in vitro transcription of an immunoglobulin gene .

Addition of a highly enriched preparation of <protein>OTF-1</protein> made from one of these <cell_line>pre-B cells</cell_line> or from <cell_line>HeLa cells</cell_line> specifically stimulated in vitro transcription of an <dna>immunoglobulin gene</dna> .


Furthermore , OFT-1 appeared to have approximately the same transactivation ability as OTF-2 when normalized for binding activity .

Furthermore , OFT-1 appeared to have approximately the same transactivation ability as <protein>OTF-2</protein> when normalized for binding activity .


These results suggest that OTF-1 , without OTF-2 , is sufficient for transcription of immunoglobulin genes and that OTF-2 alone is not responsible for the B-cell-specific regulation of immunoglobulin gene expression .

These results suggest that <protein>OTF-1</protein> , without <protein>OTF-2</protein> , is sufficient for transcription of <dna>immunoglobulin genes</dna> and that <protein>OTF-2</protein> alone is not responsible for the B-cell-specific regulation of <dna>immunoglobulin gene</dna> expression .


Effects of aldosterone on intralymphocytic sodium and potassium in patients with essential hypertension .


In vitro binding of aldosterone to mineralocorticoid receptors on human mononuclear leukocytes ( HML ) and its effects on the intracellular sodium and potassium concentrations of HML have already been described .

In vitro binding of aldosterone to <protein>mineralocorticoid receptors</protein> on <cell_type>human mononuclear leukocytes</cell_type> ( <cell_type>HML</cell_type> ) and its effects on the intracellular sodium and potassium concentrations of <cell_type>HML</cell_type> have already been described .


In the present paper this easily accessible human cell model was investigated in 13 patients with essential hypertension .


In only four patients sodium in HML without incubation was elevated compared with the range for normal persons .

In only four patients sodium in <cell_type>HML</cell_type> without incubation was elevated compared with the range for normal persons .


A decrease of intracellular sodium or potassium occurred during incubation without aldosterone ( P less than 0.02 ) .


The addition of 1.4 nM aldosterone did not prevent this loss of electrolytes as observed in normal persons .


Plasma renin activity and aldosterone were not correlated with the electrolyte response and were within the normal limits .

<protein>Plasma renin</protein> activity and aldosterone were not correlated with the electrolyte response and were within the normal limits .


The number of mineralocorticoid receptors /cell were within or close to the normal range ( n = 9 ) .

The number of <protein>mineralocorticoid receptors</protein> /cell were within or close to the normal range ( n = 9 ) .


The independence of intracellular electrolytes from aldosterone despite a normal number of mineralocorticoid receptors may reflect an impairment of the mineralocorticoid effector mechanism in the HML of patients with essential hypertension .

The independence of intracellular electrolytes from aldosterone despite a normal number of <protein>mineralocorticoid receptors</protein> may reflect an impairment of the mineralocorticoid effector mechanism in the <cell_type>HML</cell_type> of patients with essential hypertension .


[ Differential diagnostic value of receptors of 1 , 25-dihydroxyvitamin D3 ( calcitriol ) determination in lymphocytes of children with rickets and rickets-like diseases ]

[ Differential diagnostic value of receptors of 1 , 25-dihydroxyvitamin D3 ( calcitriol ) determination in <cell_type>lymphocytes</cell_type> of children with rickets and rickets-like diseases ]


The authors provide the results of studying 1 , 25-dihydroxyvitamin D3 ( calcitriol ) in lymphocytes of children with rickets and rickets-like diseases .

The authors provide the results of studying 1 , 25-dihydroxyvitamin D3 ( calcitriol ) in <cell_type>lymphocytes</cell_type> of children with rickets and rickets-like diseases .


It is proposed that the character of their expression under the influence of vitamin D may be used with differential diagnostic purposes in view .


Regulation of gene expression with double-stranded phosphorothioate oligonucleotides .


Alteration of gene transcription by inhibition of specific transcriptional regulatory proteins is necessary for determining how these factors participate in cellular differentiation .

Alteration of gene transcription by inhibition of specific <protein>transcriptional regulatory proteins</protein> is necessary for determining how these factors participate in cellular differentiation .


The functions of these proteins can be antagonized by several methods , each with specific limitations .


Inhibition of sequence-specific DNA-binding proteins was achieved with double-stranded ( ds ) phosphorothioate oligonucleotides that contained octamer or kappa B consensus sequences .

Inhibition of <protein>sequence-specific DNA-binding proteins</protein> was achieved with double-stranded ( ds ) phosphorothioate oligonucleotides that contained <dna>octamer or kappa B consensus sequences</dna> .


The phosphorothioate oligonucleotides specifically bound either octamer transcription factor or nuclear factor ( NF ) -kappa B .

The phosphorothioate oligonucleotides specifically bound either <protein>octamer transcription factor</protein> or <protein>nuclear factor ( NF ) -kappa B</protein> .


The modified oligonucleotides accumulated in cells more effectively than standard ds oligonucleotides and modulated gene expression in a specific manner .


Octamer-dependent activation of a reporter plasmid or NF-kappa B -dependent activation of the human immunodeficiency virus ( HIV ) enhancer was inhibited when the appropriate phosphorothioate oligonucleotide was added to a transiently transfected B cell line .

Octamer-dependent activation of a <dna>reporter plasmid</dna> or <protein>NF-kappa B</protein> -dependent activation of the <dna>human immunodeficiency virus ( HIV ) enhancer</dna> was inhibited when the appropriate phosphorothioate oligonucleotide was added to a <cell_line>transiently transfected B cell line</cell_line> .


Addition of phosphorothioate oligonucleotides that contained the octamer consensus to Jurkat T leukemia cells inhibited interleukin-2 ( IL-2 ) secretion to a degree similar to that observed with a mutated octamer site in the IL-2 enhancer .

Addition of phosphorothioate oligonucleotides that contained the <dna>octamer consensus</dna> to <cell_line>Jurkat T leukemia cells</cell_line> inhibited <protein>interleukin-2</protein> ( <protein>IL-2</protein> ) secretion to a degree similar to that observed with a <dna>mutated octamer site</dna> in the <dna>IL-2 enhancer</dna> .


The ds phosphorothioate oligonucleotides probably compete for binding of specific transcription factors and may provide anti-viral , immunosuppressive , or other therapeutic effects .


[ Effect of the regimen of kidney-tonifying and qi-invigorating on aging changes of glucocorticoid receptor ]

[ Effect of the regimen of kidney-tonifying and qi-invigorating on aging changes of <protein>glucocorticoid receptor</protein> ]


The plasma cortisol concentration and the sites of glucocorticoid receptor ( GCR ) in the peripheral lymphocytes were measured in 32 healthy aged persons and 13 young adults .

The plasma cortisol concentration and the sites of <protein>glucocorticoid receptor</protein> ( <protein>GCR</protein> ) in the <cell_type>peripheral lymphocytes</cell_type> were measured in 32 healthy aged persons and 13 young adults .


In animal experiment , GCR of spleen lymphocytic cell was also measured in 18 aged rats and 9 young rats .

In animal experiment , <protein>GCR</protein> of <cell_type>spleen lymphocytic cell</cell_type> was also measured in 18 aged rats and 9 young rats .


The results showed that GCR was significantly lower in the aged persons or rats than that in the young while the plasma cortisol level did n't change with aging .

The results showed that <protein>GCR</protein> was significantly lower in the aged persons or rats than that in the young while the plasma cortisol level did n't change with aging .


So we think that GCR is more sensitive than the plasma cortisol level to reflect the aging change of the adrenal cortex function .

So we think that <protein>GCR</protein> is more sensitive than the plasma cortisol level to reflect the aging change of the adrenal cortex function .


After the treatment with the regimen of Kidney-tonifying and Qi-invigorating , the GCR of the aged persons and rats was enhanced , and in this way , the function of the aged adrenal cortex was improved .

After the treatment with the regimen of Kidney-tonifying and Qi-invigorating , the <protein>GCR</protein> of the aged persons and rats was enhanced , and in this way , the function of the aged adrenal cortex was improved .


Interferon affects nuclear proteins in cells of clinically sensitive chronic myelogenous leukemia patients .

Interferon affects <protein>nuclear proteins</protein> in cells of clinically sensitive chronic myelogenous leukemia patients .


Cytoplasmic protein extracts from chronic myelogenous leukemia ( CML ) cells contained an activity that altered the electrophoretic mobility of complexes formed between nuclear proteins and the transcriptional enhancers of interferon ( IFN ) -inducible genes .

Cytoplasmic protein extracts from <cell_type>chronic myelogenous leukemia ( CML ) cells</cell_type> contained an activity that altered the electrophoretic mobility of complexes formed between <protein>nuclear proteins</protein> and the transcriptional enhancers of interferon ( IFN ) -inducible genes .


Exposure of CML cells to IFN-alpha diminished the effect of the CML cytoplasmic proteins on these nuclear protein-DNA complexes .

Exposure of <cell_type>CML cells</cell_type> to <protein>IFN-alpha</protein> diminished the effect of the <protein>CML cytoplasmic proteins</protein> on these <protein>nuclear protein-DNA complexes</protein> .


The presence of clinical responsiveness to IFN-alpha correlated with the sensitivity to the IFN -induced change in the electrophoretic mobility of nuclear protein-DNA complexes .

The presence of clinical responsiveness to <protein>IFN-alpha</protein> correlated with the sensitivity to the <protein>IFN</protein> -induced change in the electrophoretic mobility of <protein>nuclear protein-DNA complexes</protein> .


These data suggest that the action of IFN-alpha in CML may be linked to a pathway that can result in posttranslational modification of nuclear proteins .

These data suggest that the action of <protein>IFN-alpha</protein> in CML may be linked to a pathway that can result in posttranslational modification of <protein>nuclear proteins</protein> .


Epstein-Barr virus nuclear antigen 2 transactivates latent membrane protein LMP1 .

<protein>Epstein-Barr virus nuclear antigen 2</protein> transactivates <protein>latent membrane protein</protein> <protein>LMP1</protein> .


Several lines of evidence are compatible with the hypothesis that Epstein-Barr virus ( EBV ) nuclear antigen 2 ( EBNA-2 ) or leader protein ( EBNA-LP ) affects expression of the EBV latent infection membrane protein LMP1 .

Several lines of evidence are compatible with the hypothesis that <protein>Epstein-Barr virus ( EBV ) nuclear antigen 2</protein> ( <protein>EBNA-2</protein> ) or <protein>leader protein</protein> ( <protein>EBNA-LP</protein> ) affects expression of the <protein>EBV latent infection membrane protein</protein> <protein>LMP1</protein> .


We now demonstrate the following .


( i ) Acute transfection and expression of EBNA-2 under control of simian virus 40 or Moloney murine leukemia virus promoters resulted in increased LMP1 expression in P3HR-1-infected Burkitt 's lymphoma cells and the P3HR-1 or Daudi cell line .

( i ) Acute transfection and expression of <protein>EBNA-2</protein> under control of <dna>simian virus 40 or Moloney murine leukemia virus promoters</dna> resulted in increased <protein>LMP1</protein> expression in <cell_line>P3HR-1-infected Burkitt 's lymphoma cells</cell_line> and the <cell_line>P3HR-1</cell_line> or <cell_line>Daudi cell line</cell_line> .


( ii ) Transfection and expression of EBNA-LP alone had no effect on LMP1 expression and did not act synergistically with EBNA-2 to affect LMP1 expression .

( ii ) Transfection and expression of <protein>EBNA-LP</protein> alone had no effect on <protein>LMP1</protein> expression and did not act synergistically with <protein>EBNA-2</protein> to affect <protein>LMP1</protein> expression .


( iii ) LMP1 expression in Daudi and P3HR-1-infected cells was controlled at the mRNA level , and EBNA-2 expression in Daudi cells increased LMP1 mRNA .

( iii ) <protein>LMP1</protein> expression in <cell_line>Daudi</cell_line> and <cell_line>P3HR-1-infected cells</cell_line> was controlled at the <rna>mRNA</rna> level , and <protein>EBNA-2</protein> expression in <cell_line>Daudi cells</cell_line> increased <rna>LMP1 mRNA</rna> .


( iv ) No other EBV genes were required for EBNA-2 transactivation of LMP1 since cotransfection of recombinant EBNA-2 expression vectors and genomic LMP1 DNA fragments enhanced LMP1 expression in the EBV-negative B-lymphoma cell lines BJAB , Louckes , and BL30 .

( iv ) No other <dna>EBV genes</dna> were required for <protein>EBNA-2</protein> transactivation of <protein>LMP1</protein> since cotransfection of <dna>recombinant EBNA-2 expression vectors</dna> and genomic <dna>LMP1 DNA fragments</dna> enhanced <protein>LMP1</protein> expression in the <cell_line>EBV-negative B-lymphoma cell lines</cell_line> <cell_line>BJAB</cell_line> , <cell_line>Louckes</cell_line> , and <cell_line>BL30</cell_line> .


( v ) An EBNA-2-responsive element was found within the -512 to +40 LMP1 DNA since this DNA linked to a chloramphenicol acetyltransferase reporter gene was transactivated by cotransfection with an EBNA-2 expression vector .

( v ) An <dna>EBNA-2-responsive element</dna> was found within the <dna>-512 to +40 LMP1 DNA</dna> since this DNA linked to a <dna>chloramphenicol acetyltransferase reporter gene</dna> was transactivated by cotransfection with an <dna>EBNA-2 expression vector</dna> .


( vi ) The EBV type 2 EBNA-2 transactivated LMP1 as well as the EBV type 1 EBNA-2 .

( vi ) The EBV type 2 <protein>EBNA-2</protein> transactivated <protein>LMP1</protein> as well as the <protein>EBV type 1 EBNA-2</protein> .


( vii ) Two deletions within the EBNA-2 gene which rendered EBV transformation incompetent did not transactivate LMP1 , whereas a transformation-competent EBNA-2 deletion mutant did transactivate LMP1 .

( vii ) Two deletions within the <protein>EBNA-2</protein> gene which rendered EBV transformation incompetent did not transactivate <protein>LMP1</protein> , whereas a <dna>transformation-competent EBNA-2 deletion mutant</dna> did transactivate <protein>LMP1</protein> .


LMP1 is a potent effector of B-lymphocyte activation and can act synergistically with EBNA-2 to induce cellular CD23 gene expression .

<protein>LMP1</protein> is a potent effector of B-lymphocyte activation and can act synergistically with <protein>EBNA-2</protein> to induce cellular CD23 gene expression .


Thus , EBNA-2 transactivation of LMP1 amplifies the biological impact of EBNA-2 and underscores its central role in EBV-induced growth transformation .

Thus , <protein>EBNA-2</protein> transactivation of <protein>LMP1</protein> amplifies the biological impact of <protein>EBNA-2</protein> and underscores its central role in EBV-induced growth transformation .


The expression of c-fos , c-jun , and c-myc genes is regulated by heat shock in human lymphoid cells .

The expression of <dna>c-fos</dna> , <dna>c-jun</dna> , and <dna>c-myc genes</dna> is regulated by heat shock in <cell_type>human lymphoid cells</cell_type> .


The effect of heat shock on the expression of the nuclear protooncogenes c-fos , c-jun , and c-myc was studied in human lymphoid cells .

The effect of heat shock on the expression of the <dna>nuclear protooncogenes</dna> <dna>c-fos</dna> , <dna>c-jun</dna> , and <dna>c-myc</dna> was studied in <cell_type>human lymphoid cells</cell_type> .


Heat shock caused an increase in c-fos and c-jun mRNA levels and a decrease in c-myc mRNA levels in pre-B ( Hyon ) and T ( DND-41 ) cell lines as well as in freshly isolated normal human thymocytes .

Heat shock caused an increase in c-fos and c-jun mRNA levels and a decrease in <rna>c-myc mRNA</rna> levels in <cell_line>pre-B ( Hyon ) and T ( DND-41 ) cell lines</cell_line> as well as in freshly isolated normal human thymocytes .


The changes in the mRNA levels of these protooncogenes in Hyon cells were most pronounced at 42 and 43 degrees C ; kinetic analysis demonstrated that the changes could be detected within 30 min of heat shock .

The changes in the mRNA levels of these <dna>protooncogenes</dna> in <cell_line>Hyon cells</cell_line> were most pronounced at 42 and 43 degrees C ; kinetic analysis demonstrated that the changes could be detected within 30 min of heat shock .


Altered transcription of c-fos and c-myc genes was the primary effect of heat shock .

Altered transcription of <dna>c-fos</dna> and <dna>c-myc genes</dna> was the primary effect of heat shock .


Secondarily , heat shock of Hyon cells stabilized the c-myc mRNA level by increasing its half-life from 24 to 45 min .

Secondarily , heat shock of <cell_line>Hyon cells</cell_line> stabilized the <rna>c-myc mRNA</rna> level by increasing its half-life from 24 to 45 min .


The overall effect of heat shock on c-myc mRNA level , however , was a marked inhibition of its transcription .

The overall effect of heat shock on <rna>c-myc mRNA</rna> level , however , was a marked inhibition of its transcription .


These results demonstrate that the transcription of nuclear protooncogenes is regulated by heat shock indicating a role for nuclear protooncogenes in the stress response of lymphoid cells .

These results demonstrate that the transcription of <dna>nuclear protooncogenes</dna> is regulated by heat shock indicating a role for <dna>nuclear protooncogenes</dna> in the stress response of <cell_type>lymphoid cells</cell_type> .


Mapping of B-cell epitopes of the human hepatitis B virus X protein .

Mapping of <protein>B-cell epitopes</protein> of the <protein>human hepatitis B virus X protein</protein> .


The immune response to the X protein of human hepatitis B virus ( HBV ) was studied by epitope mapping by using a set of MS2-HBx fusion proteins and synthetic peptides .

The immune response to the <protein>X protein</protein> of human hepatitis B virus ( HBV ) was studied by epitope mapping by using a set of <protein>MS2-HBx fusion proteins</protein> and synthetic peptides .


Antibodies in sera of patients with acute and chronic HBV infection showed a multispecific immune response .


Each serum contained antibodies to a different set of epitopes , which taken together cover most of the HBx sequence .

Each serum contained <protein>antibodies</protein> to a different set of <protein>epitopes</protein> , which taken together cover most of the <protein>HBx sequence</protein> .


Some of the epitopes were detectable only by immunoblotting with fusion proteins ; others were detectable only by an enzyme-linked immunosorbent assay ( ELISA ) with synthetic peptides .

Some of the epitopes were detectable only by immunoblotting with <protein>fusion proteins</protein> ; others were detectable only by an enzyme-linked immunosorbent assay ( ELISA ) with synthetic peptides .


The carboxy-terminal half of the HBx protein was preferentially recognized by antibodies from patients with chronic hepatitis and contained a short immunodominant antigenic region with at least two major nonoverlapping epitopes .

The <protein>carboxy-terminal half</protein> of the <protein>HBx protein</protein> was preferentially recognized by <protein>antibodies</protein> from patients with chronic hepatitis and contained a short <protein>immunodominant antigenic region</protein> with at least two major <protein>nonoverlapping epitopes</protein> .


Anti- HBx antibody titers as revealed by peptide ELISAs were highest and most frequent in patients with chronic hepatitis and usually low in acutely infected patients and asymptomatic carriers .

Anti- <protein>HBx</protein> antibody titers as revealed by peptide ELISAs were highest and most frequent in patients with chronic hepatitis and usually low in acutely infected patients and asymptomatic carriers .


The data demonstrate a remarkable qualitative and quantitative heterogeneity of the humoral HBx immune response which can be monitored by HBx -specific peptide ELISAs .

The data demonstrate a remarkable qualitative and quantitative heterogeneity of the humoral <protein>HBx</protein> immune response which can be monitored by <protein>HBx</protein> -specific peptide ELISAs .


Such tests may become useful diagnostic tools .


[ The inhibitory effect of hydrocortisone on the chemotactic migration of human leukocytes ]

[ The inhibitory effect of hydrocortisone on the chemotactic migration of <cell_type>human leukocytes</cell_type> ]


Random migration ( RM ) and chemotactic migration ( ChtM ) of human leukocytes to yeast activated serum were studied with the modified Boyden chamber method .

Random migration ( RM ) and chemotactic migration ( ChtM ) of <cell_type>human leukocytes</cell_type> to yeast activated serum were studied with the modified Boyden chamber method .


Both RM and ChtM showed circadian rhythm .


Leukocytes migrated most rapidly at night .

<cell_type>Leukocytes</cell_type> migrated most rapidly at night .


The difference between the peak ( 0 : 00 ) and trough values ( 8 : 00 ) of RM and ChtM was significant statistically ( P less than 0.01 ) .


ChtM was inhibited by hydrocortisone ( F ) of physiological concentration ( 10 ( -9 ) -10 ( -7 ) mol/L ) which was dose-dependent and completely antagonized by the competitive antagonist , RU38486 .


The inhibitory effect was much more evident with higher dose ( more than 10 ( -5 ) mol/L ) and it was also reversed by RU38486 , but only partially .


It is suggested that glucocorticoids ( GC ) may be a physiological regulator of the activity of leukocytes and its inhibitory action on ChtM may be involved in antiinflammatory mechanisms of GC of pharmacological doses .

It is suggested that glucocorticoids ( GC ) may be a physiological regulator of the activity of <cell_type>leukocytes</cell_type> and its inhibitory action on ChtM may be involved in antiinflammatory mechanisms of GC of pharmacological doses .


The action of physiological and pharmacological concentration of GC may be mediated by low affinity specific binding sites of glucocorticoid receptors .

The action of physiological and pharmacological concentration of GC may be mediated by <protein>low affinity specific binding sites</protein> of <protein>glucocorticoid receptors</protein> .


Heterogeneity of antigen molecules recognized by anti-tax1 monoclonal antibody Lt-4 in cell lines bearing human T cell leukemia virus type I and related retroviruses .

Heterogeneity of <protein>antigen molecules</protein> recognized by <protein>anti-tax1 monoclonal antibody</protein> <protein>Lt-4</protein> in cell lines bearing human T cell leukemia virus type I and related retroviruses .


Using a monoclonal antibody , Lt-4 , directed against human T cell leukemia virus type I ( HTLV-I ) trans-activator ( tax1 ) antigen , we examined the expression of tax1 and related antigens in a variety of T cell lines bearing HTLV-I and related retroviruses , simian T cell leukemia virus type I ( STLV-I ) and HTLV-II , by immunofluorescence and immunoblot assays .

Using a <protein>monoclonal antibody</protein> , <protein>Lt-4</protein> , directed against <protein>human T cell leukemia virus type I ( HTLV-I ) trans-activator ( tax1 ) antigen</protein> , we examined the expression of <protein>tax1</protein> and related <protein>antigens</protein> in a variety of <cell_line>T cell lines</cell_line> bearing HTLV-I and related retroviruses , simian T cell leukemia virus type I ( STLV-I ) and HTLV-II , by immunofluorescence and immunoblot assays .


Lt-4 reacted with all HTLV-I-bearing cell lines tested and five out of eight simian cell lines bearing STLV-I , but not with an HTLV-II-bearing cell line .

<protein>Lt-4</protein> reacted with all <cell_line>HTLV-I-bearing cell lines</cell_line> tested and five out of eight <cell_line>simian cell lines</cell_line> bearing STLV-I , but not with an <cell_line>HTLV-II-bearing cell line</cell_line> .


Lt-4 detected 40 kd tax1 antigen molecules in most HTLV-I-bearing cell lines except one cell line that expressed 39 kd tax1 antigen .

<protein>Lt-4</protein> detected 40 kd <protein>tax1 antigen molecules</protein> in most <cell_line>HTLV-I-bearing cell lines</cell_line> except one cell line that expressed <protein>39 kd tax1 antigen</protein> .


In the STLV-I-bearing T cell lines , tax1-related antigen molecules detected by Lt-4 were heterogeneous , having molecular weights in the range of 36-41 kd .

In the <cell_line>STLV-I-bearing T cell lines</cell_line> , <protein>tax1-related antigen molecules</protein> detected by <protein>Lt-4</protein> were heterogeneous , having molecular weights in the range of 36-41 kd .


Characterization of the human immunodeficiency virus type 1 enhancer-binding proteins from the human T-cell line Jurkat .

Characterization of the <protein>human immunodeficiency virus type 1 enhancer-binding proteins</protein> from the <cell_line>human T-cell line</cell_line> <cell_line>Jurkat</cell_line> .


The transcription of the human immunodeficiency virus type 1 ( HIV-1 ) is under the control of cellular proteins that bind to the viral long terminal repeat ( LTR ) .

The transcription of the human immunodeficiency virus type 1 ( HIV-1 ) is under the control of <protein>cellular proteins</protein> that bind to the <dna>viral long terminal repeat</dna> ( <dna>LTR</dna> ) .


Among the protein-binding regions of the HIV-1 LTR is the transcription-enhancer region .

Among the protein-binding regions of the <dna>HIV-1 LTR</dna> is the <dna>transcription-enhancer region</dna> .


We show that at least one inducible , C1 , and one constitutive , C2 , protein can bind to the HIV enhancer in Jurkat cells .

We show that at least one <protein>inducible</protein> , <protein>C1</protein> , and one <protein>constitutive , C2 , protein</protein> can bind to the <dna>HIV enhancer</dna> in <cell_line>Jurkat cells</cell_line> .


The two proteins differ in their surface charge , since they are separable by anion-exchange chromatography .


Bivalent cations such as Mg2+ and Zn2+ differentially affect their binding to oligonucleotides which contain the HIV-enhancer domain .

Bivalent cations such as Mg2+ and Zn2+ differentially affect their binding to oligonucleotides which contain the <dna>HIV-enhancer domain</dna> .


Both C1 and C2 proteins also bind to a similar sequence found in the interleukin-2-receptor alpha-subunit enhancer .

Both <protein>C1</protein> and <protein>C2 proteins</protein> also bind to a similar sequence found in the <dna>interleukin-2-receptor alpha-subunit enhancer</dna> .


The inducible C1 protein was partially purified by three chromatographic steps and characterized by u.v. cross-linking as a 47 kDa protein .

The <protein>inducible C1 protein</protein> was partially purified by three chromatographic steps and characterized by u.v. cross-linking as a <protein>47 kDa protein</protein> .


Differences in transcriptional enhancers of HIV-1 and HIV-2 .

Differences in <dna>transcriptional enhancers</dna> of HIV-1 and HIV-2 .


Response to T cell activation signals .

Response to <cell_type>T cell</cell_type> activation signals .


T cell activation results in high levels of HIV replication and is thought to be one mechanism leading to the conversion from latent to active viral infection .

<cell_type>T cell</cell_type> activation results in high levels of HIV replication and is thought to be one mechanism leading to the conversion from latent to active viral infection .


In HIV-1 , the sequences that respond to these signaling events are found in the long terminal repeat ( LTR ) and comprise the transcriptional enhancer , which contains two conserved binding sites for the nuclear factor kappa B ( NF kappa B ) .

In HIV-1 , the sequences that respond to these signaling events are found in the <dna>long terminal repeat</dna> ( <dna>LTR</dna> ) and comprise the <dna>transcriptional enhancer</dna> , which contains two <dna>conserved binding sites</dna> for the <protein>nuclear factor kappa B</protein> ( <protein>NF kappa B</protein> ) .


The corresponding region in the second AIDS retrovirus , HIV-2 , contains a conserved and a divergent NF kappa B binding site .

The corresponding region in the second AIDS retrovirus , HIV-2 , contains a conserved and a divergent <dna>NF kappa B binding site</dna> .


We demonstrate that the HIV-1 LTR responds better than the HIV-2 LTR to T cell activation signals .

We demonstrate that the <dna>HIV-1 LTR</dna> responds better than the <dna>HIV-2 LTR</dna> to T cell activation signals .


These qualitative differences in the response to T cell activation are reproduced not only when HIV-1 or HIV-2 enhancers are placed upstream of a heterologous promoter but also when these enhancers are switched between their respective LTR .

These qualitative differences in the response to <cell_type>T cell</cell_type> activation are reproduced not only when <dna>HIV-1 or HIV-2 enhancers</dna> are placed upstream of a <dna>heterologous promoter</dna> but also when these <dna>enhancers</dna> are switched between their respective <dna>LTR</dna> .


In electrophoretic mobility shift assays , NF kappa B binds to both conserved sites in the HIV-1 transcriptional enhancer and only to the single conserved site in the HIV-2 transcriptional enhancer .

In electrophoretic mobility shift assays , <protein>NF kappa B</protein> binds to both conserved sites in the <dna>HIV-1 transcriptional enhancer</dna> and only to the single conserved site in the <dna>HIV-2 transcriptional enhancer</dna> .


Instead of NF kappa B , the activator protein 3 binds to the divergent site in HIV-2 .

Instead of <protein>NF kappa B</protein> , the <protein>activator protein 3</protein> binds to the divergent site in HIV-2 .


In conclusion , HIV-1 and HIV-2 are differentially regulated by T cell activation signals , and this difference may account for the longer period of viral latency observed with HIV-2 than with HIV-1 infection .


NF-X2 that binds to the DRA X2-box is activator protein 1 .

<protein>NF-X2</protein> that binds to the <dna>DRA X2-box</dna> is <protein>activator protein 1</protein> .


Expression cloning of c-Jun .

Expression cloning of <protein>c-Jun</protein> .


Human class II MHC Ag are a family of cell surface glycoproteins .

<protein>Human class II MHC Ag</protein> are a family of <protein>cell surface glycoproteins</protein> .


Their constitutive expression is limited to B lymphocytes and thymic epithelial cells .

Their constitutive expression is limited to <cell_type>B lymphocytes</cell_type> and <cell_type>thymic epithelial cells</cell_type> .


In many other cells their expression can be induced by IFN-gamma .

In many other cells their expression can be induced by <protein>IFN-gamma</protein> .


Conserved upstream promoter sequences regulate this tissue-specific expression of class II genes .

Conserved upstream promoter sequences regulate this tissue-specific expression of <dna>class II genes</dna> .


In the DRA promoter , one of these cis-acting regulatory motifs is the X2-box to which nuclear factor X2 ( NF-X2 ) binds .

In the <dna>DRA promoter</dna> , one of these <dna>cis-acting regulatory motifs</dna> is the <dna>X2-box</dna> to which <protein>nuclear factor X2</protein> ( <protein>NF-X2</protein> ) binds .


Here , we present the isolation and characterization of the full-length cDNA clone encoding NF-X2 .

Here , we present the isolation and characterization of the <dna>full-length cDNA clone</dna> encoding <protein>NF-X2</protein> .


This cDNA clone was isolated by expression cDNA cloning , and encodes the human c-Jun protein , which together with c-Fos forms the heterodimeric activator protein-1 transcription complex .

This <dna>cDNA clone</dna> was isolated by expression <dna>cDNA</dna> cloning , and encodes the <protein>human c-Jun protein</protein> , which together with <protein>c-Fos</protein> forms the <protein>heterodimeric activator protein-1 transcription complex</protein> .


Whereas c-Fos/c-Jun heterodimers do not exist in B cells , they form and bind to the X2-box in class II nonexpressing cells .

Whereas <protein>c-Fos/c-Jun heterodimers</protein> do not exist in <cell_line>B cells</cell_line> , they form and bind to the <dna>X2-box</dna> in <cell_line>class II nonexpressing cells</cell_line> .


Thus , c-Fos/c-Jun heterodimers might contribute to the repression of DRA gene expression .

Thus , <protein>c-Fos/c-Jun heterodimers</protein> might contribute to the repression of <dna>DRA gene</dna> expression .


Synthesis of 4 , 19-disubstituted derivatives of DOC .


Radioreceptor assay of some corticosteroid derivatives in human mononuclear leukocytes .

Radioreceptor assay of some corticosteroid derivatives in <cell_type>human mononuclear leukocytes</cell_type> .


Several new 4 , 19-substituted steroids and previously synthesized corticosteroids were assayed for affinity to type 1 receptors in human mononuclear leukocytes .

Several new 4 , 19-substituted steroids and previously synthesized corticosteroids were assayed for affinity to <protein>type 1 receptors</protein> in <cell_type>human mononuclear leukocytes</cell_type> .


11 beta , 19-epoxy-4 , 21-dihydroxypregn-4-ene-3 , 20-dione ( 2 ) was hydrogenated with Pd-C to yield a mixture of all four dihydro derivatives 5 , accompanied by 4 , 21-diacetoxy-11 beta , 19-epoxy-3-hydroxypregnan-20-one ( 6 ) and 21-acetoxy-11 beta , 19-epoxy-4-hydroxypregnane-3 , 20-dione ( 7 ) .


With hot acetic + p-toluenesulfonic acid 5 underwent rearrangement to 21-acetoxy-11 beta , 19-epoxypregn-5-ene-4 , 20-dione ( 8 ) Pd-C hydrogenation of 3 , 21-diacetoxy-5 beta , 19-cyclopregna-2 , 9 ( 11 ) -diene-4 , 20-dione ( 10 ) gave 3 , 21-diacetoxy-5 beta , 19-cyclopregn-5-ene-4 , 20-dione ( 11 ) and the 9 , 11-dihydro derivative of the latter .


Treatment of 10 with warm HCl furnished 19-chloro-4 , 21-dihydroxypregna-4 , 9 ( 11 ) -diene-3 , 20-dione ( 13 ) .


Pd-C hydrogenation of its diacetate 14 afforded the 4 , 5-dihydro derivative 18 , 19-chloro-21-acetoxypregn-9 ( 11 ) -en-20-one ( 15 ) , its 4-acetoxy derivative 16 and the 3 , 4-diacetoxy derivative 17 .


When tested in a radioreceptor assay in human mononuclear leukocytes the synthesized compounds showed only low relative binding affinities ( RBA ) to type 1 receptor , the highest being 0.72 % for 13 ( aldosterone = 100 % ) .

When tested in a radioreceptor assay in <cell_type>human mononuclear leukocytes</cell_type> the synthesized compounds showed only low relative binding affinities ( RBA ) to <protein>type 1 receptor</protein> , the highest being 0.72 % for 13 ( aldosterone = 100 % ) .


For comparison , other RBA in this system were : 19-noraldosterone , 20 % ; 18-deoxyaldosterone , 5.8 % ; 18-deoxy-19-noraldosterone , 4.7 % ; 18 , 21-anhydroaldosterone , 0.37 % ; 17-isoaldosterone , 7.6 % and apoaldosterone , 4.3 %


Cell type specificity and activation requirements for NFAT-1 ( nuclear factor of activated T-cells ) transcriptional activity determined by a new method using transgenic mice to assay transcriptional activity of an individual nuclear factor .

Cell type specificity and activation requirements for <protein>NFAT-1</protein> ( <protein>nuclear factor</protein> of <cell_type>activated T-cells</cell_type> ) transcriptional activity determined by a new method using transgenic mice to assay transcriptional activity of an individual <protein>nuclear factor</protein> .


Nuclear factor of activated T-cells ( NFAT-1 ) is a transcription factor which is considered to be an important regulator in early T-cell activation .

<protein>Nuclear factor</protein> of <cell_type>activated T-cells</cell_type> ( <protein>NFAT-1</protein> ) is a <protein>transcription factor</protein> which is considered to be an important regulator in early T-cell activation .


We have developed a system to monitor the transcriptional activity of NFAT-1 at the single cell level in whole animals .

We have developed a system to monitor the transcriptional activity of <protein>NFAT-1</protein> at the single cell level in whole animals .


The system is based on the use of an oligomerized NFAT-1 binding motif that directs transcription of SV40 T-antigen in transgenic mice .

The system is based on the use of an oligomerized <protein>NFAT-1</protein> binding motif that directs <protein>transcription of SV40 T-antigen</protein> in transgenic mice .


This report represents the first demonstration that a multimerized short binding motif can function appropriately in transgenic mice .