Lymphocytes have been postulated to serve as a site of adenoviral persistence based upon the ability to isolate adenovirus from tonsils and to detect adenovirus DNA by Southern blot hybridization in peripheral blood mononuclear cells ( PBMC ) .

<cell_type>Lymphocytes</cell_type> have been postulated to serve as a site of adenoviral persistence based upon the ability to isolate adenovirus from tonsils and to detect <dna>adenovirus DNA</dna> by Southern blot hybridization in <cell_type>peripheral blood mononuclear cells</cell_type> ( <cell_type>PBMC</cell_type> ) .


To test this hypothesis , a more sensitive and specific polymerase chain reaction ( PCR ) assay was developed to detect adenovirus DNA .

To test this hypothesis , a more sensitive and specific polymerase chain reaction ( PCR ) assay was developed to detect <dna>adenovirus DNA</dna> .


Two sets of nested primers were designed to conserved sequences in the adenovirus E1A and hexon genes .

Two sets of <dna>nested primers</dna> were designed to conserved sequences in the <dna>adenovirus E1A and hexon genes</dna> .


The E1A and hexon primers amplified DNA from representative adenoviral serotypes in all six adenoviral groups ( A-F ) .

The <dna>E1A and hexon primers</dna> amplified DNA from representative adenoviral serotypes in all six adenoviral groups ( A-F ) .


Both primers detected a single copy of the adenovirus type 2 genome but were less sensitive for the group B type 35 .

Both primers detected a single copy of the <dna>adenovirus type 2 genome</dna> but were less sensitive for the group B type 35 .


of 33 PBMC specimens from healthy adults and only one of 40 pediatric samples was positive ( at a low level ) for adenovirus DNA by nested PCR assay .

of 33 <cell_type>PBMC</cell_type> specimens from healthy adults and only one of 40 pediatric samples was positive ( at a low level ) for <dna>adenovirus DNA</dna> by nested PCR assay .


In comparison , PBMC from two children with fatal adenoviral infection were both strongly positive for adenovirus DNA .

In comparison , <cell_type>PBMC</cell_type> from two children with fatal adenoviral infection were both strongly positive for <dna>adenovirus DNA</dna> .


It is concluded that , in contrast to a previous study , PBMC are not a common site of persistent group C adenoviral infection .

It is concluded that , in contrast to a previous study , <cell_type>PBMC</cell_type> are not a common site of persistent group C adenoviral infection .


In addition , assay of PBMC by the adenovirus-specific PCR may help detect early invasive disease and warrants further evaluation .

In addition , assay of <cell_type>PBMC</cell_type> by the adenovirus-specific PCR may help detect early invasive disease and warrants further evaluation .


Tumor necrosis factor receptor expression and signal transduction in HIV-1-infected cells .

<protein>Tumor necrosis factor receptor</protein> expression and signal transduction in <cell_type>HIV-1-infected cells</cell_type> .


OBJECTIVE : To examine the inter-relationship between HIV-1 infection and the cell surface receptors for tumor necrosis factor ( TNF ) -alpha , an immunoregulatory cytokine that can enhance HIV-1 replication .

OBJECTIVE : To examine the inter-relationship between HIV-1 infection and the cell surface receptors for <protein>tumor necrosis factor ( TNF ) -alpha</protein> , an immunoregulatory cytokine that can enhance HIV-1 replication .


DESIGN : Infected promyelocytic and promonocytic cells were examined because they normally express both types of TNF receptors .

DESIGN : Infected <cell_type>promyelocytic</cell_type> and <cell_type>promonocytic cells</cell_type> were examined because they normally express both types of <protein>TNF receptors</protein> .


METHODS : TNF receptor surface expression was determined by specific monoclonal antibody recognition and flow cytometry , and signal transduction was detected by gel shift analysis .

METHODS : <protein>TNF</protein> receptor surface expression was determined by specific <protein>monoclonal antibody</protein> recognition and flow cytometry , and signal transduction was detected by gel shift analysis .


HIV-1 activation and expression was quantitated by reverse transcriptase assay .

HIV-1 activation and expression was quantitated by <protein>reverse transcriptase</protein> assay .


RESULTS : In the OM-10.1 promyelocytic model of chronic infection , TNF-alpha-induced HIV-1 expression also resulted in a substantial increase in 75 kd TNF receptor ( TR75 ) expression although 55 kD TNF receptor ( TR55 ) levels were not dramatically altered .

RESULTS : In the OM-10.1 promyelocytic model of chronic infection , TNF-alpha-induced HIV-1 expression also resulted in a substantial increase in <protein>75 kd TNF receptor</protein> ( <protein>TR75</protein> ) expression although <protein>55 kD TNF receptor</protein> ( <protein>TR55</protein> ) levels were not dramatically altered .


A series of uninfected parental HL-60 subclones all reduced TR75 surface expression in response to TNF-alpha treatment .

A series of <cell_line>uninfected parental HL-60 subclones</cell_line> all reduced <protein>TR75</protein> surface expression in response to <protein>TNF-alpha</protein> treatment .


Enhanced TR75 expression on OM-10.1 cells followed the same TNF-alpha -dose dependency as that observed for HIV-1 production .

Enhanced <protein>TR75</protein> expression on OM-10.1 cells followed the same <protein>TNF-alpha</protein> -dose dependency as that observed for HIV-1 production .


An increase in TR75 expression was also evident during the peak of an acute HIV-1 infection of HL-60 promyelocytes .

An increase in <protein>TR75</protein> expression was also evident during the peak of an acute HIV-1 infection of <cell_line>HL-60 promyelocytes</cell_line> .


Although TR55 expression was unaltered during TNF-alpha -induced HIV activation , this receptor was still involved in the viral activation process .

Although <protein>TR55</protein> expression was unaltered during <protein>TNF-alpha</protein> -induced HIV activation , this receptor was still involved in the viral activation process .


Antibody cross-linking of TR55 , in the absence of exogenous TNF-alpha , induced maximal HIV-1 expression , an up-modulation of surface TR75 , and nuclear NF-kappa B activity in OM-10.1 cultures .

Antibody cross-linking of <protein>TR55</protein> , in the absence of <protein>exogenous TNF-alpha</protein> , induced maximal HIV-1 expression , an up-modulation of surface <protein>TR75</protein> , and nuclear <protein>NF-kappa B</protein> activity in OM-10.1 cultures .


Surprisingly , this was the case even when an antagonistic anti-TR55 antibody was used .

Surprisingly , this was the case even when an <protein>antagonistic anti-TR55 antibody</protein> was used .


Anti-TR55 antibody cross-linking in chronically infected U1 promonocytic cultures could only partially substitute for TNF-alpha-induced HIV-1 expression .

<protein>Anti-TR55 antibody</protein> cross-linking in <cell_line>chronically infected U1 promonocytic cultures</cell_line> could only partially substitute for TNF-alpha-induced HIV-1 expression .


CONCLUSIONS : Our results demonstrated that HIV-1 infection can selectively influence the surface expression of TNF receptors , potentially influencing its own expression and altering normal immunoregulatory signal transduction .

CONCLUSIONS : Our results demonstrated that HIV-1 infection can selectively influence the surface expression of <protein>TNF receptors</protein> , potentially influencing its own expression and altering normal <protein>immunoregulatory</protein> signal transduction .


Comparative mapping of SRY in the great apes .

Comparative mapping of <dna>SRY</dna> in the great apes .


Cytogenetic studies of the primate Y chromosomes have suggested that extensive rearrangements have occurred during evolution of the great apes .

Cytogenetic studies of the <dna>primate Y chromosomes</dna> have suggested that extensive rearrangements have occurred during evolution of the great apes .


We have used in situ hybridization to define these rearrangements at the molecular level .


pHU-14 , a probe including sequences from the sex determining gene SRY , hybridizes close to the early replicating pseudoautosomal segment in a telomeric or subtelomeric position of the Y chromosomes of all great apes .

<dna>pHU-14</dna> , a probe including sequences from the <dna>sex determining gene SRY</dna> , hybridizes close to the early replicating pseudoautosomal segment in a telomeric or subtelomeric position of the <dna>Y chromosomes</dna> of all great apes .


The low copy repeat detected by the probe Fr35-II is obviously included in Y chromosomal rearrangements during hominid evolution .

The <dna>low copy repeat</dna> detected by the probe <dna>Fr35-II</dna> is obviously included in Y chromosomal rearrangements during hominid evolution .


These results , combined with previous studies , suggest that the Y chromosome in great apes has a conserved region including the pseudoautosomal region and the testis-determining region .

These results , combined with previous studies , suggest that the Y chromosome in great apes has a conserved region including the <dna>pseudoautosomal region</dna> and the testis-determining region .


The rest of the Y chromosome has undergone several rearrangements in the different great apes .

The rest of the <dna>Y chromosome</dna> has undergone several rearrangements in the different great apes .


Calcium dependent activation of the NF-AT transcription factor by p59fyn .

Calcium dependent activation of the <protein>NF-AT transcription factor</protein> by <protein>p59fyn</protein> .


A reporter gene under the control of a T-cell antigen receptor element was activated in Jurkat cells by antigen receptor triggering or by a combination of phorbol myristate acetate , which activates protein kinase C , and a calcium ionophore .

A <dna>reporter gene</dna> under the control of a <dna>T-cell antigen receptor element</dna> was activated in <cell_line>Jurkat cells</cell_line> by antigen receptor triggering or by a combination of phorbol myristate acetate , which activates <protein>protein kinase C</protein> , and a calcium ionophore .


Both these signals were necessary for expression of the reporter gene .

Both these signals were necessary for expression of the <dna>reporter gene</dna> .


When co-transfected with a construct capable of overexpressing the tyrosine kinase p59fyn , the reporter gene was activated by PMA alone .

When co-transfected with a construct capable of overexpressing the <protein>tyrosine kinase</protein> <protein>p59fyn</protein> , the <dna>reporter gene</dna> was activated by <protein>PMA</protein> alone .


Thus p59fyn could replace the calcium ionophore but not activation of protein kinase C .

Thus <protein>p59fyn</protein> could replace the calcium ionophore but not activation of <protein>protein kinase C</protein> .


The activation by p59fyn plus PMA was blocked by EGTA and by the immunosuppressant drug cyclosporin A .

The activation by <protein>p59fyn</protein> plus <protein>PMA</protein> was blocked by EGTA and by the immunosuppressant drug cyclosporin A .


Dependence for the proliferative response to erythropoietin on an established erythroid differentiation program in a human hematopoietic cell line , UT-7 .

Dependence for the proliferative response to <protein>erythropoietin</protein> on an established erythroid differentiation program in a <cell_line>human hematopoietic cell line</cell_line> , <cell_line>UT-7</cell_line> .


Erythroid differentiation involves the activation of a number of erythroid-specific genes , most of which , including the globin genes and the erythropoietin receptor ( Epo-R ) gene , are , at least in part , regulated by the transcription factor GATA-1 .

Erythroid differentiation involves the activation of a number of erythroid-specific genes , most of which , including the <dna>globin genes</dna> and the <dna>erythropoietin receptor ( Epo-R ) gene</dna> , are , at least in part , regulated by the <protein>transcription factor</protein> <protein>GATA-1</protein> .


In order to understand the relationship , if any , between expression of GATA-1 , response to Epo and erythroid differentiation , we analyzed the expression of GATA-1 , Epo-R and globin genes in an Epo-dependent human cell line , UT-7 Epo .

In order to understand the relationship , if any , between expression of <protein>GATA-1</protein> , response to Epo and erythroid differentiation , we analyzed the expression of <protein>GATA-1</protein> , <protein>Epo-R</protein> and <dna>globin genes</dna> in an Epo-dependent human cell line , <cell_line>UT-7</cell_line> Epo .


The results were compared to those obtained with the parental granulocyte-macrophage colony-stimulating factor ( GM-CSF ) -dependent cell line , UT-7 , which has a predominantly megakaryoblastic phenotype and is unable to proliferate continuously in the presence of Epo .

The results were compared to those obtained with the <cell_line>parental granulocyte-macrophage colony-stimulating factor ( GM-CSF ) -dependent cell line</cell_line> , <cell_line>UT-7</cell_line> , which has a predominantly megakaryoblastic phenotype and is unable to proliferate continuously in the presence of <protein>Epo</protein> .


UT-7 Epo and UT-7 expressed similar levels of GATA-1 mRNA and binding activity .

<protein>UT-7 Epo</protein> and <cell_line>UT-7</cell_line> expressed similar levels of <rna>GATA-1 mRNA</rna> and binding activity .


The two lines also expressed comparable levels of Epo-R mRNA while the number of Epo -binding sites on UT-7 Epo cells was one-sixth the number of UT-7 cells ( 2400 +/- 3 vs. 13 , 800 +/- 300 ) .

The two lines also expressed comparable levels of <rna>Epo-R mRNA</rna> while the number of <protein>Epo</protein> -binding sites on <cell_line>UT-7 Epo cells</cell_line> was one-sixth the number of <cell_line>UT-7 cells</cell_line> ( 2400 +/- 3 vs. 13 , 800 +/- 300 ) .


This difference in the number of binding sites could be due to differences in cell surface ( UT-7 cells are 20 % smaller than the parental UT-7 cells ) or in receptor turnover .

This difference in the number of binding sites could be due to differences in cell surface ( <cell_line>UT-7 cells</cell_line> are 20 % smaller than the parental <cell_line>UT-7 cells</cell_line> ) or in receptor turnover .


By Northern analysis , UT-7 cells expressed detectable levels of beta- and gamma-globin but not alpha-globin .

By Northern analysis , <cell_line>UT-7 cells</cell_line> expressed detectable levels of <protein>beta- and gamma-globin</protein> but not <protein>alpha-globin</protein> .


In comparison , UT-7 Epo cells expressed alpha-globin and higher levels of gamma-globin ( 5-fold ) and beta-globin ( from barely to clearly detectable ) .

In comparison , <cell_line>UT-7 Epo cells</cell_line> expressed alpha-globin and higher levels of <protein>gamma-globin</protein> ( 5-fold ) and <protein>beta-globin</protein> ( from barely to clearly detectable ) .


Globin chains ( alpha , beta and gamma ) were clearly detectable by affinity chromatography in UT-7 Epo but not in UT-7 cells .

<protein>Globin chains</protein> ( <protein>alpha</protein> , <protein>beta</protein> and <protein>gamma</protein> ) were clearly detectable by affinity chromatography in <protein>UT-7 Epo</protein> but not in <cell_line>UT-7 cells</cell_line> .


The frequency of the cells which expressed beta- and gamma- globin genes in the two cell populations was measured by immunofluorescence with beta- and gamma-specific antibodies .

The frequency of the cells which expressed <dna>beta- and gamma- globin genes</dna> in the two cell populations was measured by immunofluorescence with <protein>beta- and gamma-specific antibodies</protein> .


The number of gamma-positive cells and their fluorescence intensity were higher in UT-7 Epo than in UT-7 cells ( 0 to 17 % barely positive cells and 23 to 40 % clearly positive cells , respectively ) , indicating that the increase in globin mRNA observed in UT-7 Epo is due to both an increase of gene expression per cell and an increase in numbers of cells containing gamma-globin .

The number of <cell_line>gamma-positive cells</cell_line> and their fluorescence intensity were higher in <protein>UT-7 Epo</protein> than in <cell_line>UT-7 cells</cell_line> ( 0 to 17 % barely positive cells and 23 to 40 % clearly positive cells , respectively ) , indicating that the increase in <rna>globin mRNA</rna> observed in <protein>UT-7 Epo</protein> is due to both an increase of gene expression per cell and an increase in numbers of cells containing <protein>gamma-globin</protein> .


The levels of GATA-1 , Epo-R and globin mRNA expressed were not affected by a 24-hour incubation of either cell line with Epo , GM-CSF or interleukin-3 ( IL-3 ) .

The levels of <protein>GATA-1</protein> , <protein>Epo-R</protein> and <rna>globin mRNA</rna> expressed were not affected by a 24-hour incubation of either cell line with <protein>Epo</protein> , <protein>GM-CSF</protein> or <protein>interleukin-3</protein> ( <protein>IL-3</protein> ) .


( ABSTRACT TRUNCATED AT 400 WORDS )


The Sp1 transcription factor binds the CD11b promoter specifically in myeloid cells in vivo and is essential for myeloid-specific promoter activity .

The <protein>Sp1 transcription factor</protein> binds the <dna>CD11b promoter</dna> specifically in myeloid cells in vivo and is essential for <dna>myeloid-specific promoter</dna> activity .


The myeloid integrin CD11b is expressed selectively on the surface of mature macrophages , monocytes , neutrophils , and natural killer cells .

The <protein>myeloid integrin CD11b</protein> is expressed selectively on the surface of <cell_type>mature macrophages</cell_type> , <cell_type>monocytes</cell_type> , <cell_type>neutrophils</cell_type> , and <cell_type>natural killer cells</cell_type> .


Lineage-specific expression is controlled at the level of mRNA transcription .


Recent isolation of the CD11b promoter shows that 92 base pairs ( bp ) of 5'-flanking DNA are sufficient to direct myeloid-specific expression of a reporter gene .

Recent isolation of the <dna>CD11b promoter</dna> shows that 92 base pairs ( bp ) of <dna>5'-flanking DNA</dna> are sufficient to direct myeloid-specific expression of a <dna>reporter gene</dna> .


To characterize regulatory sequences important for promoter activity , we performed linker scanning analysis of the 92-bp CD11b promoter and demonstrate that a sequence at bp -60 is essential for CD11b promoter activity .

To characterize regulatory sequences important for promoter activity , we performed linker scanning analysis of the <dna>92-bp CD11b promoter</dna> and demonstrate that a sequence at bp -60 is essential for <dna>CD11b promoter</dna> activity .


We show that this sequence binds the transcription factor Sp1 in vitro and in vivo .

We show that this sequence binds the <protein>transcription factor</protein> <protein>Sp1</protein> in vitro and in vivo .


In vivo the Sp1 site is bound only in myeloid ( U937 ) cells , not in cervical carcinoma ( HeLa ) cells .

In vivo the <dna>Sp1 site</dna> is bound only in <cell_line>myeloid ( U937 ) cells</cell_line> , not in <cell_line>cervical carcinoma ( HeLa ) cells</cell_line> .


In addition , the macrophage transcription factor PU.1 binds the CD11b promoter in vitro and in vivo close to the Sp1 site .

In addition , the macrophage <protein>transcription factor</protein> PU.1 binds the <dna>CD11b promoter</dna> in vitro and in vivo close to the <dna>Sp1 site</dna> .


We propose a model in which binding of a myeloid-specific factor ( PU.1 ) allows a general factor ( Sp1 ) to bind in a tissue-specific fashion thereby contributing to the myeloid-specific expression of CD11b .

We propose a model in which binding of a <protein>myeloid-specific factor</protein> ( <protein>PU.1</protein> ) allows a general factor ( <protein>Sp1</protein> ) to bind in a tissue-specific fashion thereby contributing to the myeloid-specific expression of <cell_line>CD11b</cell_line> .


Transcription factor jun-B is target of autoreactive T-cells in IDDM .

Transcription factor jun-B is target of <cell_type>autoreactive T-cells</cell_type> in IDDM .


Target antigens defined by autoantibodies in IDDM include insulin , a putative glycolipid that reacts with islet cell antibodies , and a 64 , 000-M ( r ) protein recently identified as glutamic acid decarboxylase .

Target antigens defined by <protein>autoantibodies</protein> in IDDM include insulin , a putative glycolipid that reacts with <protein>islet cell antibodies</protein> , and a <protein>64 , 000-M ( r ) protein</protein> recently identified as <protein>glutamic acid decarboxylase</protein> .


In addition , some IDDM sera that contain antibodies to glutamic acid decarboxylase also coprecipitate a 38 , 000-M ( r ) protein from islets .

In addition , some IDDM sera that contain <protein>antibodies</protein> to <protein>glutamic acid decarboxylase</protein> also coprecipitate a <protein>38 , 000-M ( r ) protein</protein> from islets .


This study used a high titer anti-38 , 000-M ( r ) serum to screen bacteriophage lambda cDNA expression libraries and identified human islet and placental clones encoding jun-B , the nuclear transcription protein , of predicted 38 , 000 M ( r ) .

This study used a high titer anti-38 , 000-M ( r ) serum to screen <dna>bacteriophage lambda cDNA</dna> expression libraries and identified <cell_type>human islet</cell_type> and <cell_line>placental clones</cell_line> encoding <protein>jun-B</protein> , the <protein>nuclear transcription protein</protein> , of predicted 38 , 000 M ( r ) .


Peripheral blood T-cells exhibited significant proliferation in response to a recombinant fragment of jun-B ( amino acids 1-180 ) in 12 of 17 ( 71 % ) recent-onset IDDM subjects , 8 of 16 ( 50 % ) ICA-positive first-degree relatives of IDDM subjects who were at risk , 3 of 12 ( 25 % ) other autoimmune disease subjects , and 0 of 10 healthy control subjects .

<cell_type>Peripheral blood T-cells</cell_type> exhibited significant proliferation in response to a recombinant fragment of <protein>jun-B</protein> ( amino acids 1-180 ) in 12 of 17 ( 71 % ) recent-onset IDDM subjects , 8 of 16 ( 50 % ) ICA-positive first-degree relatives of IDDM subjects who were at risk , 3 of 12 ( 25 % ) other autoimmune disease subjects , and 0 of 10 healthy control subjects .


Proliferation to tetanus toxoid did not differ significantly between the groups .


Responses to jun-B were not related to age , sex , or human leukocyte antigen status .

Responses to <protein>jun-B</protein> were not related to age , sex , or <protein>human leukocyte antigen</protein> status .


Thus , autoreactive T-cells identify a novel antigen , p38 jun-B , in IDDM and appear to indicate subjects at risk for the development of clinical disease .

Thus , <cell_type>autoreactive T-cells</cell_type> identify a <protein>novel antigen</protein> , <protein>p38 jun-B</protein> , in IDDM and appear to indicate subjects at risk for the development of clinical disease .


Stimulation of interleukin-1 alpha and interleukin-1 beta production in human monocytes by protein phosphatase 1 and 2A inhibitors .

Stimulation of <protein>interleukin-1 alpha</protein> and <protein>interleukin-1 beta</protein> production in <cell_type>human monocytes</cell_type> by protein phosphatase 1 and 2A inhibitors .


Protein phosphatases 1 and 2A are important in regulating cellular functions by controlling the phosphorylation state of their substrates .

<protein>Protein phosphatases 1 and 2A</protein> are important in regulating cellular functions by controlling the phosphorylation state of their substrates .


In human monocytes , the inhibitors of these phosphatases , okadaic acid and calyculin A , were found to increase the mRNA accumulation and cytokine production of interleukin-1 beta and interleukin-1 alpha .

In <cell_type>human monocytes</cell_type> , the inhibitors of these <protein>phosphatases</protein> , okadaic acid and calyculin A , were found to increase the mRNA accumulation and cytokine production of <protein>interleukin-1 beta</protein> and <protein>interleukin-1 alpha</protein> .


The increased mRNA accumulation was found to be primarily because of the increase in the transcription rate of the interleukin-1 genes .

The increased <rna>mRNA</rna> accumulation was found to be primarily because of the increase in the transcription rate of the <dna>interleukin-1 genes</dna> .


Stimulation of interleukin-1 gene transcription may be caused by the stimulation of transcription factor activities , including those of AP-1 , by these protein phosphatase inhibitors .

Stimulation of <dna>interleukin-1 gene</dna> transcription may be caused by the stimulation of <protein>transcription factor</protein> activities , including those of <protein>AP-1</protein> , by these <protein>protein phosphatase</protein> inhibitors .


Okadaic acid increased the synthesis of the interleukin-1 beta precursor and mature forms and their secretion .

Okadaic acid increased the synthesis of the <protein>interleukin-1 beta</protein> precursor and mature forms and their secretion .


This increased processing and secretion correlated with the stimulation of IL-1 beta convertase mRNA accumulation .

This increased processing and secretion correlated with the stimulation of <rna>IL-1 beta convertase mRNA</rna> accumulation .


The stimulation of interleukin-1 alpha production by okadaic acid was more modest than that of interleukin-1 beta .

The stimulation of <protein>interleukin-1 alpha</protein> production by okadaic acid was more modest than that of <protein>interleukin-1 beta</protein> .


However , the phosphorylation of the precursor interleukin-1 alpha cytokine was increased .

However , the phosphorylation of the <protein>precursor interleukin-1 alpha cytokine</protein> was increased .


These results show that protein phosphatase 1 and 2A inhibitors exert multiple effects on cytokine production in human monocytes and suggest that these two phosphatases play important roles in regulating interleukin-1 production .

These results show that protein phosphatase 1 and 2A inhibitors exert multiple effects on cytokine production in <cell_type>human monocytes</cell_type> and suggest that these two <protein>phosphatases</protein> play important roles in regulating <protein>interleukin-1</protein> production .


The interleukin 2 CD28-responsive complex contains at least three members of the NF kappa B family : c-Rel , p50 , and p65 .

The <protein>interleukin 2 CD28-responsive complex</protein> contains at least three members of the <protein>NF kappa B family</protein> : <protein>c-Rel</protein> , <protein>p50</protein> , and <protein>p65</protein> .


Optimal activation of T cells requires at least two signals .

Optimal activation of <cell_type>T cells</cell_type> requires at least two signals .


One signal can be delivered by the antigen-specific T-cell receptor , and the second signal is provided by the costimulatory molecule ( s ) delivered by the antigen-presenting cell .

One signal can be delivered by the <protein>antigen-specific T-cell receptor</protein> , and the second signal is provided by the costimulatory molecule ( s ) delivered by the <cell_type>antigen-presenting cell</cell_type> .


CD28 is a T-cell surface molecule and stimulation through this protein plays an important role in delivering the second activation signal .

<protein>CD28</protein> is a <protein>T-cell surface molecule</protein> and stimulation through this protein plays an important role in delivering the second activation signal .


In this report , we show that in human peripheral blood T cells , CD28 -mediated signal transduction involves the rel family proteins -- c-Rel , p50 , and p65 .

In this report , we show that in <cell_type>human peripheral blood T cells</cell_type> , <protein>CD28</protein> -mediated signal transduction involves the <protein>rel family proteins</protein> -- <protein>c-Rel</protein> , <protein>p50</protein> , and <protein>p65</protein> .


Treatment of peripheral blood T cells with phorbol 12-myristate 13-acetate ( PMA ) and anti-CD28 monoclonal antibody ( mAb ) results in augmentation of nuclear c-Rel , p50 , and p65 , and this augmentation can occur in the presence of the immunosuppressant cyclosporin A .

Treatment of <cell_type>peripheral blood T cells</cell_type> with phorbol 12-myristate 13-acetate ( PMA ) and <protein>anti-CD28 monoclonal antibody</protein> ( <protein>mAb</protein> ) results in augmentation of <protein>nuclear c-Rel</protein> , <protein>p50</protein> , and <protein>p65</protein> , and this augmentation can occur in the presence of the immunosuppressant cyclosporin A .


It is also shown in this report that , in response to PMA/anti-CD28 mAb or anti-CD3/anti-CD28 mAb , c-Rel , p50 , and p65 are associated with CD28-responsive element present in the promoter of the human interleukin 2 gene .

It is also shown in this report that , in response to <protein>PMA/anti-CD28 mAb</protein> or <protein>anti-CD3/anti-CD28 mAb</protein> , <protein>c-Rel</protein> , <protein>p50</protein> , and <protein>p65</protein> are associated with <dna>CD28-responsive element</dna> present in the <dna>promoter</dna> of the <dna>human interleukin 2 gene</dna> .


The functional significance of c-Rel involvement in the CD28-responsive complex is demonstrated by transient transfection analysis , where cotransfection of c-Rel augments the level of expression of a chloramphenicol acetyltransferase reporter gene linked to the CD28-responsive element .

The functional significance of <protein>c-Rel</protein> involvement in the <protein>CD28-responsive complex</protein> is demonstrated by transient transfection analysis , where cotransfection of <protein>c-Rel</protein> augments the level of expression of a <dna>chloramphenicol acetyltransferase reporter gene</dna> linked to the <dna>CD28-responsive element</dna> .


Expression of tal-1 and GATA-binding proteins during human hematopoiesis .

Expression of <protein>tal-1</protein> and <protein>GATA-binding proteins</protein> during human hematopoiesis .


Tal-1 rearrangements are associated with nearly 30 % of human T acute lymphoblastic leukemia .

<protein>Tal-1</protein> rearrangements are associated with nearly 30 % of human T acute lymphoblastic leukemia .


Tal-1 gene encodes a putative transcription factor with a basic helix-loop-helix domain and is known to be predominantly expressed in hematopoietic cells .

<dna>Tal-1 gene</dna> encodes a putative <protein>transcription factor</protein> with a <protein>basic helix-loop-helix domain</protein> and is known to be predominantly expressed in <cell_type>hematopoietic cells</cell_type> .


We investigated the pattern of tal-1 expression in purified human hematopoietic cells by in situ hybridization and reverse transcriptase polymerase chain reaction analysis .

We investigated the pattern of <protein>tal-1</protein> expression in <cell_type>purified human hematopoietic cells</cell_type> by in situ hybridization and <protein>reverse transcriptase polymerase</protein> chain reaction analysis .


Both methods demonstrated that the tal-1 gene is expressed in megakaryocytes and erythroblasts as well as in basophilic granulocytes .

Both methods demonstrated that the <protein>tal-1</protein> gene is expressed in megakaryocytes and erythroblasts as well as in <cell_type>basophilic granulocytes</cell_type> .


In addition , our results indicate that the tal-1 1A promoter , which contains two consensus GATA-binding sites , is active mainly in these lineages .

In addition , our results indicate that the <dna>tal-1 1A promoter</dna> , which contains two consensus <dna>GATA-binding sites</dna> , is active mainly in these lineages .


Because the GATA-1 gene is known to transactivate several genes specific for the erythroid , megakaryocytic , and mastocytic/basophilic lineages , we studied GATA-1 expression in these purified hematopoietic cells .

Because the <dna>GATA-1 gene</dna> is known to transactivate several genes specific for the <cell_type>erythroid , megakaryocytic , and mastocytic/basophilic lineages</cell_type> , we studied <protein>GATA-1</protein> expression in these purified <cell_type>hematopoietic cells</cell_type> .


We found that GATA-1 and tal-1 genes are coexpressed in these three lineages .

We found that <dna>GATA-1 and tal-1 genes</dna> are coexpressed in these three lineages .


Remarkably , the expression of both genes is downmodulated during erythroid and megakaryocytic terminal maturation .


In immature hematopoietic cells , tal-1 and GATA-1 genes are coexpressed in committed progenitors cells ( CD34+/CD38 ( 2+ ) ) , whereas they are not detectable in the most primitive cells ( CD34 ( 2+ ) /CD38- ) .

In <cell_type>immature hematopoietic cells</cell_type> , <dna>tal-1 and GATA-1 genes</dna> are coexpressed in <cell_type>committed progenitors cells</cell_type> ( <cell_line>CD34+/CD38 ( 2+ )</cell_line> ) , whereas they are not detectable in the most <cell_type>primitive cells</cell_type> ( <cell_line>CD34 ( 2+ ) /CD38-</cell_line> ) .


In contrast , GATA-2 is strongly expressed in both most primitive and committed progenitors cells , whereas GATA-3 is mostly detected in most primitive ones .

In contrast , <protein>GATA-2</protein> is strongly expressed in both <cell_type>most primitive and committed progenitors cells</cell_type> , whereas <protein>GATA-3</protein> is mostly detected in most primitive ones .


Altogether our results strongly suggest that GATA-1 modulates the transcription of tal-1 during the differentiation of the erythroid , megakaryocytic , and basosophilic lineages .

Altogether our results strongly suggest that <protein>GATA-1</protein> modulates the transcription of <protein>tal-1</protein> during the differentiation of the <cell_type>erythroid , megakaryocytic , and basosophilic lineages</cell_type> .


The lytic transition of Epstein-Barr virus is imitated by recombinant B-cells .

The lytic transition of Epstein-Barr virus is imitated by <cell_line>recombinant B-cells</cell_line> .


Lytic transition of Epstein-Barr virus ( EBV ) is initiated by distinct immediate early regulators of the viral cycle , in synchronization to temporary , permissive conditions during host cell differentiation .


We developed eukaryotic vectors suitable to imitate the processes involved in lytic transition in cell culture systems .


Two stable B cell lines were established : R59Z activator cells were used to induce lytic EBV expression in a constitutive manner by the production of the BZLF 1 trans-activator ( Zta ) .

Two stable <cell_line>B cell lines</cell_line> were established : <cell_line>R59Z activator cells</cell_line> were used to induce lytic EBV expression in a constitutive manner by the production of the <protein>BZLF 1 trans-activator</protein> ( <protein>Zta</protein> ) .


R7-57 reporter cells , on the other hand , signaled induced activity of the lytic origin of EBV replication ( ori Lyt ) .

<cell_line>R7-57 reporter cells</cell_line> , on the other hand , signaled induced activity of the <dna>lytic origin of EBV replication</dna> ( <dna>ori Lyt</dna> ) .


Different modes , like chemical induction , lytic superinfection with EBV and single gene trans-activation converted the recombinant ori Lyt element in R7-57 reporter cells .

Different modes , like chemical induction , lytic superinfection with EBV and single gene trans-activation converted the <dna>recombinant ori Lyt element</dna> in <cell_line>R7-57 reporter cells</cell_line> .


BZLF 1 , transiently expressed in R7-57 reporter cells , was the only EBV trans-activator found , sufficient in inducing the viral lytic cycle .

<protein>BZLF 1</protein> , transiently expressed in <cell_line>R7-57 reporter cells</cell_line> , was the only <protein>EBV trans-activator</protein> found , sufficient in inducing the viral lytic cycle .


Basing on these experiments , trans-cellular activation of EBV was tested by cocultivation of BZLF 1-expressing R59Z activator cells with the R7-57 reporter line .

Basing on these experiments , trans-cellular activation of EBV was tested by cocultivation of <cell_type>BZLF 1-expressing R59Z activator cells</cell_type> with the <cell_line>R7-57 reporter line</cell_line> .


No lytic effect on the reporter cells could be measured , neither by cocultivation of activator cells nor by coincubation of BZLF 1 -containing cell lysates .

No lytic effect on the reporter cells could be measured , neither by cocultivation of <cell_line>activator cells</cell_line> nor by coincubation of <protein>BZLF 1</protein> -containing cell lysates .


Latency breaking activity , however , was transferred from activator to reporter cells when active , exogenous virus was added .

Latency breaking activity , however , was transferred from <cell_line>activator</cell_line> to <cell_line>reporter cells</cell_line> when active , exogenous virus was added .


The cell system described in these experiments provides a tool for the detection of EBV reactivation and demonstrates the potential of the lytic regulatory gene BZLF 1

The cell system described in these experiments provides a tool for the detection of EBV reactivation and demonstrates the potential of the lytic <dna>regulatory gene BZLF 1</dna>


Costimulation of cAMP and protein kinase C pathways inhibits the CD3 -dependent T cell activation and leads to a persistent expression of the AP-1 transcription factor .

Costimulation of cAMP and <protein>protein kinase C</protein> pathways inhibits the <protein>CD3</protein> -dependent T cell activation and leads to a persistent expression of the <protein>AP-1 transcription factor</protein> .


The effects mediated by a combined stimulation of cAMP -and protein kinase C ( PKC ) -dependent pathways have been investigated in different cellular systems , and it has been shown that they may complement each other in activating cell proliferation and differentiation .

The effects mediated by a combined stimulation of cAMP -and <protein>protein kinase C</protein> ( <protein>PKC</protein> ) -dependent pathways have been investigated in different cellular systems , and it has been shown that they may complement each other in activating cell proliferation and differentiation .


In this report , we show that upon the stimulation of both pathways T lymphocytes became refractory to activation via the CD3/T cell receptor ( TcR ) complex .

In this report , we show that upon the stimulation of both pathways <cell_type>T lymphocytes</cell_type> became refractory to activation via the <protein>CD3/T cell receptor</protein> ( <protein>TcR</protein> ) complex .


T cells preincubated with phorbol 12-myristate 13-acetate ( PMA ) and dibutyryl cAMP ( Bt2cAMP ) displayed a deficient proliferative ability in response to anti-CD3 mAb stimulation , whereas lymphocytes treated individually with either Bt2cAMP or PMA responded comparably to untreated samples .

<cell_type>T cells</cell_type> preincubated with phorbol 12-myristate 13-acetate ( PMA ) and dibutyryl cAMP ( Bt2cAMP ) displayed a deficient proliferative ability in response to <protein>anti-CD3 mAb</protein> stimulation , whereas <cell_type>lymphocytes</cell_type> treated individually with either Bt2cAMP or PMA responded comparably to untreated samples .


We detected an association between the reduced mitogenic response and low expression of both interleukin-2 ( IL-2 ) and the alpha chain ( CD25 ) of the IL-2 receptor ( IL-2R ) .

We detected an association between the reduced mitogenic response and low expression of both <protein>interleukin-2</protein> ( <protein>IL-2</protein> ) and the <protein>alpha chain</protein> ( <protein>CD25</protein> ) of the <protein>IL-2 receptor</protein> ( <protein>IL-2R</protein> ) .


Analysis of intracellular Ca2+ mobilization suggested that the CD3 / TcR -dependent signal transduction was impaired in PMA/Bt2cAMP-treated cells .

Analysis of intracellular Ca2+ mobilization suggested that the <protein>CD3</protein> / <protein>TcR</protein> -dependent signal transduction was impaired in <cell_line>PMA/Bt2cAMP-treated cells</cell_line> .


Remarkably , we observed that these samples displayed a persistent expression of the c-fos protooncogene , associated to an increased AP-1 DNA-binding activity , whereas no variations of CREB or NF-kB were detected .

Remarkably , we observed that these samples displayed a persistent expression of the <dna>c-fos protooncogene</dna> , associated to an increased <protein>AP-1</protein> DNA-binding activity , whereas no variations of <protein>CREB</protein> or <protein>NF-kB</protein> were detected .


Neither Bt2cAMP nor PMA individually mediated these sustained effects , which therefore appear as a consequence of the interplay between both metabolic stimuli .


Altogether , the data provide the evidence that both pathways complement each other in regulating gene expression and , conversely , downregulate the TcR transduction mechanisms .

Altogether , the data provide the evidence that both pathways complement each other in regulating gene expression and , conversely , downregulate the <protein>TcR</protein> transduction mechanisms .


The lymphotoxin promoter is stimulated by HTLV-I tax activation of NF-kappa B in human T-cell lines .

The <dna>lymphotoxin promoter</dna> is stimulated by <protein>HTLV-I tax</protein> activation of <protein>NF-kappa B</protein> in <cell_line>human T-cell lines</cell_line> .


The HTLV-I transcriptional activator tax was used to gain insight into the mechanism of lymphotoxin ( LT ; TNF-beta ) gene induction .

The <protein>HTLV-I transcriptional activator tax</protein> was used to gain insight into the mechanism of <dna>lymphotoxin ( LT ; TNF-beta ) gene</dna> induction .


Tax-expressing cell lines produce LT biologic activity .

<cell_line>Tax-expressing cell lines</cell_line> produce <protein>LT</protein> biologic activity .


An LT promoter ( LT-293 ) CAT construct that contained an NF-kappa B site was active in the LT-producing C81-66-45 cell line , which contains defective HTLV-I but expresses tax .

An <dna>LT promoter ( LT-293 ) CAT construct</dna> that contained an <dna>NF-kappa B site</dna> was active in the <cell_line>LT-producing C81-66-45 cell line</cell_line> , which contains defective HTLV-I but expresses <protein>tax</protein> .


The observation that a mutated LT-kappa B construct ( M1-CAT ) was inactive in C81-66-45 , confirmed the importance of NF-kappa B in LT gene expression .

The observation that a <dna>mutated LT-kappa B construct</dna> ( <dna>M1-CAT</dna> ) was inactive in <cell_line>C81-66-45</cell_line> , confirmed the importance of <protein>NF-kappa B</protein> in <protein>LT</protein> gene expression .


Tax was transfected into HTLV-I-negative human T-cell lines .

<protein>Tax</protein> was transfected into <cell_line>HTLV-I-negative human T-cell lines</cell_line> .


Jurkat T cells stably expressing tax contained elevated levels of NF-kappa B that directly bound to the LT-kappa B site .

<cell_line>Jurkat T cells</cell_line> stably expressing <protein>tax</protein> contained elevated levels of <protein>NF-kappa B</protein> that directly bound to the <dna>LT-kappa B site</dna> .


Tax co-transfected with reporter constructs into Jurkat cells maximally activated HTLV-I-LTR-CAT and kappa B-fos-CAT and also activated LT-293 to a lesser extent .

<protein>Tax</protein> co-transfected with <dna>reporter constructs</dna> into <cell_line>Jurkat cells</cell_line> maximally activated <protein>HTLV-I-LTR-CAT</protein> and <protein>kappa B-fos-CAT</protein> and also activated <dna>LT-293</dna> to a lesser extent .


In JM T cells , tax induced LT-293 activity by two- to four-fold , though there was no induction of M1-CAT .

In <cell_line>JM T cells</cell_line> , <protein>tax</protein> induced <dna>LT-293</dna> activity by two- to four-fold , though there was no induction of <protein>M1-CAT</protein> .


The increase in LT-293 CAT activity mirrored the increase in LT biologic activity seen under these conditions .

The increase in <dna>LT-293</dna> <protein>CAT</protein> activity mirrored the increase in <protein>LT</protein> biologic activity seen under these conditions .


These studies , the first to demonstrate induction of LT promoter activity over basal levels , indicate that HTLV-I tax causes low-level activation of both endogenous LT and the LT promoter , at least in part through activation of NF-kappa B .

These studies , the first to demonstrate induction of <dna>LT promoter</dna> activity over basal levels , indicate that <protein>HTLV-I tax</protein> causes low-level activation of both endogenous <protein>LT</protein> and the <dna>LT promoter</dna> , at least in part through activation of <protein>NF-kappa B</protein> .


A concatenated form of Epstein-Barr viral DNA in lymphoblastoid cell lines induced by transfection with BZLF1 .

A concatenated form of <dna>Epstein-Barr viral DNA</dna> in <cell_line>lymphoblastoid cell lines</cell_line> induced by transfection with <protein>BZLF1</protein> .


The replicative form of Epstein-Barr virus ( EBV ) DNA was studied using two lymphoblastoid cell lines , X50-7 and 6F11 , which are latently infected by Epstein-Barr virus .

The replicative form of Epstein-Barr virus ( EBV ) DNA was studied using two <cell_line>lymphoblastoid cell lines</cell_line> , X50-7 and 6F11 , which are latently infected by Epstein-Barr virus .


The lytic cycle of EBV infection was induced by transfection of the cells with the BRLF1/BZLF1 coding region of the P3HR-1 defective genome .

The lytic cycle of EBV infection was induced by transfection of the cells with the <dna>BRLF1/BZLF1 coding region</dna> of the <dna>P3HR-1 defective genome</dna> .


We combined two techniques to identify the productive replicative form of Epstein-Barr viral DNA in the lytic cycle-induced cells .

We combined two techniques to identify the productive replicative form of <dna>Epstein-Barr viral DNA</dna> in the <cell_line>lytic cycle-induced cells</cell_line> .


Restriction enzyme analysis followed by Southern blot hybridization identified a significant increase in the fused fragment encompassing both ends of EBV DNA .

Restriction enzyme analysis followed by Southern blot hybridization identified a significant increase in the fused fragment encompassing both ends of <dna>EBV DNA</dna> .


This indicates an increase in either episomal DNA or concatameric linear DNA .

This indicates an increase in either <dna>episomal DNA</dna> or <dna>concatameric linear DNA</dna> .


Southern blot analysis of in situ lysing gels revealed that the cellular content of linear EBV DNA was also increased significantly after the initiation of the viral lytic cycle , while the amount of circular DNA remained approximately constant .

Southern blot analysis of in situ lysing gels revealed that the cellular content of <dna>linear EBV DNA</dna> was also increased significantly after the initiation of the viral lytic cycle , while the amount of circular DNA remained approximately constant .


We propose from these results that the source of the fused fragment encompassing both ends of EBV DNA is a concatenated linear EBV DNA molecule , and that such a concatenated molecule most likely represents a replicative form of EBV DNA in productively infected cells .

We propose from these results that the source of the fused fragment encompassing both ends of <dna>EBV DNA</dna> is a <dna>concatenated linear EBV DNA molecule</dna> , and that such a concatenated molecule most likely represents a replicative form of <dna>EBV DNA</dna> in productively infected cells .


Expression levels of the thyrotropin receptor gene in autoimmune thyroid disease : coregulation with parameters of thyroid function and inverse relation to major histocompatibility complex classes I and II .

Expression levels of the <dna>thyrotropin receptor gene</dna> in autoimmune thyroid disease : coregulation with parameters of thyroid function and inverse relation to <protein>major histocompatibility complex classes I and II</protein> .


Using a human TSH receptor ( TSH-R ) cDNA probe , we investigated TSH-R transcript levels in 13 human thyroid fragments by Northern blot analysis ; 7 Graves ' disease , 2 Hashimoto 's disease , 3 endemic goiter , and 1 healthy thyroid gland were studied .

Using a <dna>human TSH receptor ( TSH-R ) cDNA probe</dna> , we investigated <protein>TSH-R</protein> transcript levels in 13 human thyroid fragments by Northern blot analysis ; 7 Graves ' disease , 2 Hashimoto 's disease , 3 endemic goiter , and 1 healthy thyroid gland were studied .


TSH-R expression levels were variable , but displayed a close correlation to the expression of thyroid peroxidase ( r = 0.703 ; P < 0.05 ) , thyroglobulin ( r = 0.817 ; P < 0.01 ) , and the nuclear oncogene c-fos ( r = 0.935 ; P < 0.001 ) , but not c-myc .

<protein>TSH-R</protein> expression levels were variable , but displayed a close correlation to the expression of <protein>thyroid peroxidase</protein> ( r = 0.703 ; P < 0.05 ) , <protein>thyroglobulin</protein> ( r = 0.817 ; P < 0.01 ) , and the <dna>nuclear oncogene c-fos</dna> ( r = 0.935 ; P < 0.001 ) , but not <protein>c-myc</protein> .


Overall , TSH-R transcript levels were low or absent in those thyroids in which expression of the major histocompatibility complex class I or II ( MHC I or II ) was high , thus establishing an inverse relation ( MHC I , r = -0.791 ; P < 0.01 ; MHC II , r = -0.784 ; P < 0.01 ) .

Overall , <protein>TSH-R</protein> transcript levels were low or absent in those thyroids in which expression of the <protein>major histocompatibility complex class I or II</protein> ( <protein>MHC I or II</protein> ) was high , thus establishing an inverse relation ( <protein>MHC I</protein> , r = -0.791 ; P < 0.01 ; <protein>MHC II</protein> , r = -0.784 ; P < 0.01 ) .


In situ hybridization showed that apart from lymphocytes , thyroid cells themselves were the source of MHC II transcripts .

In situ hybridization showed that apart from <cell_type>lymphocytes</cell_type> , <cell_type>thyroid cells</cell_type> themselves were the source of <protein>MHC II transcripts</protein> .


gamma-Interferon expression was only detectable in 1 Hashimoto 's goiter .

<protein>gamma-Interferon</protein> expression was only detectable in 1 Hashimoto 's goiter .


Our findings suggest that next to lymphocyte infiltration , active regulatory events in the thyrocyte are responsible for the inverse relation between functional parameters ( TSH-R , thyroid peroxidase , thyroglobulin , and c-fos ) and immunological markers ( MHC I and II ) .

Our findings suggest that next to lymphocyte infiltration , active regulatory events in the <cell_type>thyrocyte</cell_type> are responsible for the inverse relation between functional parameters ( <protein>TSH-R</protein> , <protein>thyroid peroxidase</protein> , <protein>thyroglobulin</protein> , and c-fos ) and immunological markers ( <protein>MHC I and II</protein> ) .


Functional antagonism between vitamin D3 and retinoic acid in the regulation of CD14 and CD23 expression during monocytic differentiation of U-937 cells .

Functional antagonism between vitamin D3 and retinoic acid in the regulation of CD14 and CD23 expression during monocytic differentiation of <cell_line>U-937 cells</cell_line> .


1 , 25 alpha-Dihydroxicholecalciferol ( VitD3 ) and retinoic acid ( RA ) are important regulators of the proliferation and differentiation of several cell types .


This paper describes how the expression of the monocyte-macrophage Ag , CD14 , and the low affinity Fc receptor for IgE , CD23 , were inversely regulated during VitD3 -and RA-induced monocytic differentiation of human U-937 monoblasts .

This paper describes how the expression of the <protein>monocyte-macrophage Ag</protein> , <protein>CD14</protein> , and the low <protein>affinity Fc receptor</protein> for <protein>IgE</protein> , <protein>CD23</protein> , were inversely regulated during VitD3 -and RA-induced monocytic differentiation of <cell_line>human U-937 monoblasts</cell_line> .


PMA induced the expression of both CD14 and CD23 mRNA and protein .

PMA induced the expression of both <protein>CD14</protein> and <rna>CD23 mRNA</rna> and protein .


Exposure to VitD3 rapidly induced the de novo expression of CD14 mRNA and protein .

Exposure to VitD3 rapidly induced the de novo expression of <rna>CD14 mRNA</rna> and protein .


The addition of cycloheximide completely blocked the VitD3 induction of CD14 mRNA expression , indicating that the induction was dependent on ongoing protein synthesis .

The addition of cycloheximide completely blocked the VitD3 induction of <rna>CD14 mRNA</rna> expression , indicating that the induction was dependent on ongoing protein synthesis .


While inducing CD14 expression , VitD3 concomitantly suppressed the basal , PMA- , and RA-inducible CD23 expression in a dose-dependent manner .

While inducing <protein>CD14</protein> expression , VitD3 concomitantly suppressed the basal , PMA- , and RA-inducible <protein>CD23</protein> expression in a dose-dependent manner .


In contrast , U-937 cells induced by RA strongly increased their expression of CD23 mRNA and protein , whereas they completely lacked detectable CD14 cell surface or mRNA expression .

In contrast , <cell_line>U-937 cells</cell_line> induced by RA strongly increased their expression of <rna>CD23 mRNA</rna> and protein , whereas they completely lacked detectable CD14 cell surface or mRNA expression .


Furthermore , the VitD3 -and the PMA-induced CD14 expression was inhibited as a temporal consequence of the RA-induced differentiation .

Furthermore , the VitD3 -and the PMA-induced <protein>CD14</protein> expression was inhibited as a temporal consequence of the RA-induced differentiation .


The results suggest that there exists a functional antagonism between VitD3 and RA that may have important implications for the regulation of certain immune and inflammatory responses through their inverse effects on CD14 and CD23 gene expression .


Cell-specific bifunctional role of Jun oncogene family members on glucocorticoid receptor -dependent transcription .

Cell-specific bifunctional role of <dna>Jun oncogene family members</dna> on <protein>glucocorticoid receptor</protein> -dependent transcription .


Interaction between protein kinase C ( PKC ) - and glucocorticoid receptor ( GR ) -mediated signaling is suggested by the ability of the PKC activating phorbol ester 12-O-tetradecanoylphorbol-13-acetate ( TPA ) to inhibit GR -dependent transcription of the mouse mammary tumor virus ( MMTV ) long terminal repeat ( LTR ) .

Interaction between <protein>protein kinase C</protein> ( <protein>PKC</protein> ) - and <protein>glucocorticoid receptor</protein> ( <protein>GR</protein> ) -mediated signaling is suggested by the ability of the <protein>PKC</protein> activating phorbol ester 12-O-tetradecanoylphorbol-13-acetate ( TPA ) to inhibit <protein>GR</protein> -dependent transcription of the mouse mammary tumor virus ( MMTV ) <dna>long terminal repeat</dna> ( <dna>LTR</dna> ) .


Here we report that this interference is cell specific , as TPA augmented dexamethasone-induced transcriptional activation of the MMTV LTR in several T cell lines but was inhibitory in NIH-3T3 fibroblasts .

Here we report that this interference is cell specific , as TPA augmented dexamethasone-induced transcriptional activation of the <dna>MMTV LTR</dna> in several <cell_line>T cell lines</cell_line> but was inhibitory in <cell_line>NIH-3T3 fibroblasts</cell_line> .


TPA-GR synergism was determined to have occurred at the GR-responsive element ( GRE ) level by functional analysis of deletion mutants or synthetic GRE oligonucleotides driving chloramphenicol acetyl-transferase expression .

TPA-GR synergism was determined to have occurred at the <dna>GR-responsive element</dna> ( <dna>GRE</dna> ) level by functional analysis of <dna>deletion mutants</dna> or <dna>synthetic GRE oligonucleotides</dna> driving <protein>chloramphenicol acetyl-transferase</protein> expression .


Synergism required an intact GR DNA-binding domain , whereas amino- or carboxyl-terminal domains were dispensable .

Synergism required an intact <protein>GR DNA-binding domain</protein> , whereas <protein>amino- or carboxyl-terminal domains</protein> were dispensable .


The effect was abrogated by the PKC inhibitor staurosporine , suggesting a role for PKC .

The effect was abrogated by the <protein>PKC</protein> inhibitor staurosporine , suggesting a role for <protein>PKC</protein> .


Increased c-jun , jun-B , and jun-D expression above basal levels and increased transcriptional activity of AP-1/TPA responsive elements fused to chloramphenicol acetyl-transferase vectors were observed in T cells treated with TPA alone or in combination with dexamethasone .

Increased <protein>c-jun</protein> , <protein>jun-B</protein> , and <protein>jun-D</protein> expression above basal levels and increased transcriptional activity of <dna>AP-1/TPA responsive elements</dna> fused to <dna>chloramphenicol acetyl-transferase vectors</dna> were observed in <cell_type>T cells</cell_type> treated with TPA alone or in combination with dexamethasone .


The ability of Jun proteins to cooperate with GR in T cells has been investigated after transfection of c-jun , jun-B , or jun-D expression vectors , which augmented GR -dependent transcription from either MMTV LTR or GRE .

The ability of <protein>Jun proteins</protein> to cooperate with <protein>GR</protein> in <cell_type>T cells</cell_type> has been investigated after transfection of <dna>c-jun , jun-B , or jun-D expression vectors</dna> , which augmented <protein>GR</protein> -dependent transcription from either <dna>MMTV LTR</dna> or <dna>GRE</dna> .


Conversely , c-jun and jun-B transfection blunted GR -dependent transcription in HeLa cells .

Conversely , <protein>c-jun</protein> and <protein>jun-B</protein> transfection blunted <protein>GR</protein> -dependent transcription in <cell_line>HeLa cells</cell_line> .


The presence of c-fos had a negative influence on GR function and correlated with the cell-specific synergistic or antagonistic activity of Jun with respect to GR ; high basal expression of c-fos as well as AP-1 DNA binding and transcriptional activity were observed in HeLa cells , but not in T cells .

The presence of <protein>c-fos</protein> had a negative influence on <protein>GR</protein> function and correlated with the cell-specific synergistic or antagonistic activity of <protein>Jun</protein> with respect to <protein>GR</protein> ; high basal expression of <protein>c-fos</protein> as well as <protein>AP-1</protein> DNA binding and transcriptional activity were observed in <cell_line>HeLa cells</cell_line> , but not in <cell_type>T cells</cell_type> .


Furthermore overexpression of exogenous c-fos has an inhibitory effect on GR -dependent transcription from GRE in T cells .

Furthermore overexpression of <protein>exogenous c-fos</protein> has an inhibitory effect on <protein>GR</protein> -dependent transcription from <dna>GRE</dna> in <cell_type>T cells</cell_type> .


We propose that Jun plays a bifunctional role on GR -dependent transcriptional activation of GRE , selecting either synergistic or antagonistic activity depending on the cell-specific microenvironment .

We propose that <protein>Jun</protein> plays a bifunctional role on <protein>GR</protein> -dependent transcriptional activation of <dna>GRE</dna> , selecting either synergistic or antagonistic activity depending on the cell-specific microenvironment .


In this regard , intracellular levels of c-fos appear to be influential .

In this regard , intracellular levels of <protein>c-fos</protein> appear to be influential .


Cell type- and stage-specific expression of the CD20/B1 antigen correlates with the activity of a diverged octamer DNA motif present in its promoter .

Cell type- and stage-specific expression of the <protein>CD20/B1 antigen</protein> correlates with the activity of a diverged octamer DNA motif present in its <dna>promoter</dna> .


The CD20 ( B1 ) gene encodes a B cell-specific protein involved in the regulation of human B cell proliferation and differentiation .

The <dna>CD20 ( B1 ) gene</dna> encodes a <protein>B cell-specific protein</protein> involved in the regulation of human B cell proliferation and differentiation .


Studies with 5 ' deletion CD20 promoter-CAT constructs have previously revealed two regions of the promoter between bases -186 and -280 and between bases -280 and -454 which contained positive regulatory elements .

Studies with <dna>5 ' deletion CD20 promoter-CAT constructs</dna> have previously revealed two regions of the <dna>promoter</dna> between bases -186 and -280 and between bases -280 and -454 which contained <dna>positive regulatory elements</dna> .


In this study we identified a sequence element present in the most proximal region located between bases -214 and -201 , TTCTTCTAATTAA , which is important in the high constitutive expression of CD20 in mature B cells and the induction of CD20 in pre-B cells .

In this study we identified a <dna>sequence element</dna> present in the most proximal region located between bases -214 and -201 , TTCTTCTAATTAA , which is important in the high constitutive expression of <protein>CD20</protein> in mature B cells and the induction of <protein>CD20</protein> in <cell_type>pre-B cells</cell_type> .


This sequence element was referred to as the BAT box and its deletion significantly reduced the activity of a CD20 promoter-CAT construct in B cells .

This <dna>sequence element</dna> was referred to as the <dna>BAT box</dna> and its deletion significantly reduced the activity of a CD20 promoter-CAT construct in B cells .


Mobility shift assays with various mutant probes and B cell nuclear extracts demonstrated that the core sequence TAAT was essential for binding to this site .


Cross competition experiments with an octamer sequence from the Ig heavy chain promoter , the BAT box , and a TA-rich sequence present in the CD21 promoter revealed that all three sequences bound the same nuclear proteins suggesting that the BAT box binding proteins were Oct-1 and Oct-2 .

Cross competition experiments with an octamer sequence from the Ig heavy chain promoter , the <dna>BAT box</dna> , and a TA-rich sequence present in the <dna>CD21 promoter</dna> revealed that all three sequences bound the same <protein>nuclear proteins</protein> suggesting that the <protein>BAT box binding proteins</protein> were <protein>Oct-1</protein> and <protein>Oct-2</protein> .


Southwestern blotting and UV cross-linking studies confirmed that the BAT box binding proteins were Oct-1 and Oct-2 .

Southwestern blotting and UV cross-linking studies confirmed that the <protein>BAT box binding proteins</protein> were <protein>Oct-1</protein> and <protein>Oct-2</protein> .


The affinity of the BAT box binding proteins for the BAT box was approximately 25-fold less than for the octamer sequence and the BAT box binding proteins dissociated from the BAT box 10-fold more rapidly than from the octamer sequence .

The affinity of the <protein>BAT box binding proteins</protein> for the <dna>BAT box</dna> was approximately 25-fold less than for the <dna>octamer sequence</dna> and the <protein>BAT box binding proteins</protein> dissociated from the <dna>BAT box</dna> 10-fold more rapidly than from the <dna>octamer sequence</dna> .


Despite this lower affinity , a trimer of the BAT box sequence was as efficiently transactivated by an Oct-2 expression vector as was a trimer of the octamer sequence in HeLa cells .

Despite this lower affinity , a trimer of the <dna>BAT box sequence</dna> was as efficiently transactivated by an <dna>Oct-2 expression vector</dna> as was a trimer of the <dna>octamer sequence</dna> in <cell_line>HeLa cells</cell_line> .


The BAT box and Oct-2 were also implicated in the induction of CD20 in the pre-B cell line , PB-697 , via phorbol esters .

The <dna>BAT box</dna> and <protein>Oct-2</protein> were also implicated in the induction of <protein>CD20</protein> in the <cell_line>pre-B cell line</cell_line> , <cell_line>PB-697</cell_line> , via phorbol esters .


The induction of CD20 mRNA was temporally associated with induction of Oct-2 mRNA and a BAT box-deleted CD20-CAT construct , in contrast to the wild type , was poorly induced by phorbol esters .

The induction of <rna>CD20 mRNA</rna> was temporally associated with induction of <rna>Oct-2 mRNA</rna> and a <dna>BAT box-deleted CD20-CAT construct</dna> , in contrast to the wild type , was poorly induced by phorbol esters .


Together these results suggest that the BAT box binding proteins are important in the B cell specific expression of CD20 and perhaps CD21 .

Together these results suggest that the <protein>BAT box binding proteins</protein> are important in the B cell specific expression of <protein>CD20</protein> and perhaps <protein>CD21</protein> .


Human CD4 lymphocytes specifically recognize a peptide representing the fusion region of the hybrid protein pml/RAR alpha present in acute promyelocytic leukemia cells .

<cell_type>Human CD4 lymphocytes</cell_type> specifically recognize a peptide representing the fusion region of the <protein>hybrid protein</protein> <protein>pml/RAR alpha</protein> present in <cell_type>acute promyelocytic leukemia cells</cell_type> .


Fusion proteins present in leukemic cells frequently contain a new amino acid at the fusion point .

Fusion proteins present in <cell_type>leukemic cells</cell_type> frequently contain a new amino acid at the <protein>fusion point</protein> .


We tested whether a peptide ( BCR1/25 ) encompassing the fusion region of the hybrid molecule pml/RAR alpha , which is selectively expressed by acute promyelocytic leukemia ( APL ) cells , can be recognized by human T lymphocytes in vitro .

We tested whether a peptide ( BCR1/25 ) encompassing the <protein>fusion region</protein> of the hybrid molecule <protein>pml/RAR alpha</protein> , which is selectively expressed by <cell_type>acute promyelocytic leukemia ( APL ) cells</cell_type> , can be recognized by <cell_type>human T lymphocytes</cell_type> in vitro .


CD4+ lymphocytes , at both polyclonal and clonal level , recognized peptide BCR1/25 in an HLA-DR -- restricted fashion on presentation by autologous antigen-presenting cell ( APC ) or by APC expressing the HLA-DR11 restricting molecule .

<cell_type>CD4+ lymphocytes</cell_type> , at both polyclonal and clonal level , recognized peptide BCR1/25 in an <protein>HLA-DR</protein> -- restricted fashion on presentation by <cell_type>autologous antigen-presenting cell</cell_type> ( <cell_type>APC</cell_type> ) or by <cell_type>APC</cell_type> expressing the <protein>HLA-DR11 restricting molecule</protein> .


Control peptides corresponding to the normal pml and RAR alpha proteins were not recognized .

Control peptides corresponding to the normal <protein>pml</protein> and <protein>RAR alpha proteins</protein> were not recognized .


One clone ( DEG5 ) also exerted a high and specific cytotoxicity against autologous cells pulsed with BCR1/25 .

One clone ( <cell_line>DEG5</cell_line> ) also exerted a high and specific cytotoxicity against <cell_line>autologous cells</cell_line> pulsed with BCR1/25 .


The autologous DE LCL containing a transduced pml/RAR alpha fusion gene and expressing a bcr1 type of the pml/RAR alpha hybrid protein induced the proliferation of DE anti-BCR1/25 T cell clones .

The <cell_line>autologous DE LCL</cell_line> containing a transduced <dna>pml/RAR alpha fusion gene</dna> and expressing a bcr1 type of the <protein>pml/RAR alpha</protein> hybrid protein induced the proliferation of <cell_line>DE anti-BCR1/25 T cell clones</cell_line> .


It is concluded that the bcr1 type-pml/RAR alpha fusion protein of APL contains an antigenic site , absent from the normal parent molecules and recognized by human CD4+ lymphocytes .

It is concluded that the <protein>bcr1 type-pml/RAR alpha fusion protein</protein> of <cell_line>APL</cell_line> contains an antigenic site , absent from the normal parent molecules and recognized by <cell_line>human CD4+ lymphocytes</cell_line> .


The zinc finger transcription factor Egr-1 is essential for and restricts differentiation along the macrophage lineage .

The <protein>zinc finger transcription factor</protein> <protein>Egr-1</protein> is essential for and restricts differentiation along the <cell_type>macrophage lineage</cell_type> .


We have isolated cDNA clones of myeloid differentiation primary response ( MyD ) genes , activated in the absence of de novo protein synthesis following induction for differentiation along either the macrophage or granulocyte lineage in human myeloblastic leukemia HL-60 cells .

We have isolated <dna>cDNA clones</dna> of <dna>myeloid differentiation primary response ( MyD ) genes</dna> , activated in the absence of de novo protein synthesis following induction for differentiation along either the <cell_type>macrophage</cell_type> or <cell_type>granulocyte lineage</cell_type> in human <cell_line>myeloblastic leukemia HL-60 cells</cell_line> .


One cDNA clone of a primary response gene , expressed upon macrophage differentiation , encoded for Egr-1 , a zinc finger transcription factor .

One <dna>cDNA clone</dna> of a primary response gene , expressed upon macrophage differentiation , encoded for <protein>Egr-1</protein> , a <protein>zinc finger transcription factor</protein> .


The Egr-1 gene was observed to be transcriptionally silent in HL-60 cells , but active in U-937 and M1 cells , the latter two being predetermined for macrophage differentiation .

The <dna>Egr-1 gene</dna> was observed to be transcriptionally silent in <cell_line>HL-60 cells</cell_line> , but active in <cell_line>U-937</cell_line> and <cell_line>M1 cells</cell_line> , the latter two being predetermined for macrophage differentiation .


Egr-1 antisense oligomers in the culture media blocked macrophage differentiation in both myeloid leukemia cell lines and normal myeloblasts .

<protein>Egr-1</protein> antisense oligomers in the culture media blocked macrophage differentiation in both <cell_line>myeloid leukemia cell lines</cell_line> and normal <cell_type>myeloblasts</cell_type> .


HL-60 cells constitutively expressing an Egr-1 transgene ( HL-60Egr-1 ) could be induced for macrophage , but not granulocyte , differentiation .

<cell_line>HL-60 cells</cell_line> constitutively expressing an <dna>Egr-1 transgene</dna> ( <dna>HL-60Egr-1</dna> ) could be induced for <cell_type>macrophage</cell_type> , but not <cell_type>granulocyte</cell_type> , differentiation .


These observations indicate that expression of Egr-1 is essential for and restricts differentiation of myeloblasts along the macrophage lineage .

These observations indicate that expression of <protein>Egr-1</protein> is essential for and restricts differentiation of <cell_type>myeloblasts</cell_type> along the <cell_type>macrophage lineage</cell_type> .


The Epstein-Barr virus nuclear antigen 2 interacts with an EBNA2 responsive cis-element of the terminal protein 1 gene promoter .

The <protein>Epstein-Barr virus nuclear antigen 2</protein> interacts with an <dna>EBNA2 responsive cis-element</dna> of the <dna>terminal protein 1 gene promoter</dna> .


The Epstein-Barr virus protein EBNA2 acts as a transcriptional activator of cellular and viral genes and plays a crucial role in the immortalization of human primary B-cells by EBV .

The <protein>Epstein-Barr virus protein EBNA2</protein> acts as a <protein>transcriptional activator</protein> of <dna>cellular and viral genes</dna> and plays a crucial role in the immortalization of <cell_type>human primary B-cells</cell_type> by EBV .


We have shown previously that EBNA2 transactivates the promoters of the latent membrane antigens LMP , TP1 and TP2 .

We have shown previously that <protein>EBNA2</protein> transactivates the promoters of the <protein>latent membrane antigens</protein> <protein>LMP</protein> , <protein>TP1</protein> and <protein>TP2</protein> .


The promoter of the TP1 gene was chosen as a model system to study the molecular mechanism of EBNA2 mediated transactivation .

The <dna>promoter</dna> of the <dna>TP1 gene</dna> was chosen as a model system to study the molecular mechanism of <protein>EBNA2</protein> mediated transactivation .


To identify an EBNA2 dependent cis-acting element , various TP1 promoter-reporter gene constructs were transfected in the absence and presence of an EBNA2 expression vector into the established B-cell line BL41-P3HR1 .

To identify an <dna>EBNA2 dependent cis-acting element</dna> , various <dna>TP1 promoter-reporter gene constructs</dna> were transfected in the absence and presence of an <dna>EBNA2 expression vector</dna> into the established <cell_line>B-cell line BL41-P3HR1</cell_line> .


We were able to delineate an 81 bp EBNA2 responsive region between -258 and -177 relative to the TP1 RNA start site .

We were able to delineate an <dna>81 bp EBNA2 responsive region</dna> between -258 and -177 relative to the <dna>TP1 RNA start site</dna> .


The element worked in either orientation and could mediate EBNA2 dependent transactivation on a heterologous promoter .

The element worked in either orientation and could mediate <protein>EBNA2</protein> dependent transactivation on a <dna>heterologous promoter</dna> .


Electrophoretic mobility shift assays revealed three specific protein-DNA complexes formed with sequences of the EBNA2 responsive element .

Electrophoretic mobility shift assays revealed three specific <protein>protein-DNA complexes</protein> formed with sequences of the <dna>EBNA2 responsive element</dna> .


Two of these were not cell type specific , but the third was detected only in EBNA2 positive cell extracts .

Two of these were not cell type specific , but the third was detected only in <protein>EBNA2</protein> positive cell extracts .


Gel-shift analysis in the presence of EBNA2 specific monoclonal antibodies revealed that EBNA2 is a component of the third complex .

Gel-shift analysis in the presence of <protein>EBNA2</protein> specific monoclonal antibodies revealed that <protein>EBNA2</protein> is a component of the third complex .


Thus , these experiments demonstrate that EBNA2 interacts with an EBNA2 responsive cis-element of the TP1 promoter

Thus , these experiments demonstrate that <protein>EBNA2</protein> interacts with an <dna>EBNA2 responsive cis-element</dna> of the <dna>TP1 promoter</dna>


Minimally modified low density lipoprotein -induced inflammatory responses in endothelial cells are mediated by cyclic adenosine monophosphate .

Minimally modified low density <protein>lipoprotein</protein> -induced inflammatory responses in <cell_type>endothelial cells</cell_type> are mediated by cyclic adenosine monophosphate .


We have previously shown that minimally oxidized LDL ( MM-LDL ) activated endothelial cells to increase their interaction with monocytes but not neutrophils , inducing monocyte but not neutrophil binding and synthesis of monocyte chemotactic protein-1 and monocyte colony-stimulating factor ( M-CSF ) .

We have previously shown that <cell_line>minimally oxidized LDL ( MM-LDL ) activated endothelial cells</cell_line> to increase their interaction with <cell_type>monocytes</cell_type> but not <cell_type>neutrophils</cell_type> , inducing monocyte but not neutrophil binding and synthesis of <protein>monocyte chemotactic protein-1</protein> and <protein>monocyte colony-stimulating factor</protein> ( <protein>M-CSF</protein> ) .


In the present studies we have examined the signaling pathways by which this monocyte-specific response is induced .


Both induction of monocyte binding and mRNA levels for M-CSF by MM-LDL were not inhibited in protein kinase C-depleted endothelial cells .

Both induction of monocyte binding and mRNA levels for <protein>M-CSF</protein> by <protein>MM-LDL</protein> were not inhibited in protein kinase C-depleted <cell_type>endothelial cells</cell_type> .


A number of our studies indicate that cAMP is the second messenger for the effects of MM-LDL cited above .

A number of our studies indicate that cAMP is the second messenger for the effects of <protein>MM-LDL</protein> cited above .


Incubation of endothelial cells with MM-LDL caused a 173 % increase in intracellular cAMP levels .

Incubation of <cell_type>endothelial cells</cell_type> with <protein>MM-LDL</protein> caused a 173 % increase in intracellular cAMP levels .


Agents which increased cAMP levels , including cholera toxin , pertussis toxin , dibutyryl cAMP , and isoproterenol mimicked the actions of MM-LDL .

Agents which increased cAMP levels , including cholera toxin , pertussis toxin , dibutyryl cAMP , and isoproterenol mimicked the actions of <protein>MM-LDL</protein> .


Agents which elevated cAMP were also shown to activate NF kappa B , suggesting a role for this transcription factor in activation of monocyte-endothelial interactions .

Agents which elevated cAMP were also shown to activate <protein>NF kappa B</protein> , suggesting a role for this transcription factor in activation of monocyte-endothelial interactions .


Although endothelial leukocyte adhesion molecule ( ELAM ) mRNA synthesis can be regulated by NF kappa B , ELAM was not expressed and ELAM mRNA was only slightly elevated in response to MM-LDL .

Although <rna>endothelial leukocyte adhesion molecule ( ELAM ) mRNA</rna> synthesis can be regulated by <protein>NF kappa B</protein> , <protein>ELAM</protein> was not expressed and <rna>ELAM mRNA</rna> was only slightly elevated in response to <protein>MM-LDL</protein> .


We present evidence that induction of neutrophil binding by LPS is actually suppressed by agents that elevated cAMP levels .

We present evidence that induction of <cell_type>neutrophil</cell_type> binding by LPS is actually suppressed by agents that elevated cAMP levels .


Human T cell transcription factor GATA-3 stimulates HIV-1 expression .

<protein>Human T cell transcription factor</protein> <protein>GATA-3</protein> stimulates HIV-1 expression .


A family of transcriptional activating proteins , the GATA factors , has been shown to bind to a consensus motif through a highly conserved C4 zinc finger DNA binding domain .

A family of transcriptional activating proteins , the <protein>GATA factors</protein> , has been shown to bind to a consensus motif through a <protein>highly conserved C4 zinc finger DNA binding domain</protein> .


One member of this multigene family , GATA-3 , is most abundantly expressed in T lymphocytes , a cellular target for human immunodeficiency virus type 1 ( HIV-1 ) infection and replication .

One member of this multigene family , <protein>GATA-3</protein> , is most abundantly expressed in <cell_type>T lymphocytes</cell_type> , a cellular target for human immunodeficiency virus type 1 ( HIV-1 ) infection and replication .


In vitro DNase I footprinting analysis revealed six hGATA-3 binding sites in the U3 region ( the transcriptional regulatory domain ) of the HIV-1 LTR .

In vitro <protein>DNase I</protein> footprinting analysis revealed six <dna>hGATA-3 binding sites</dna> in the <dna>U3 region</dna> ( the <dna>transcriptional regulatory domain</dna> ) of the <dna>HIV-1 LTR</dna> .


Cotransfection of an hGATA-3 expression plasmid with a reporter plasmid whose transcription is directed by the HIV-1 LTR resulted in 6- to 10-fold stimulation of LTR -mediated transcription , whereas site specific mutation of these GATA sites resulted in virtual abrogation of the activation by hGATA-3 .

Cotransfection of an <dna>hGATA-3 expression plasmid</dna> with a <dna>reporter plasmid</dna> whose transcription is directed by the <dna>HIV-1 LTR</dna> resulted in 6- to 10-fold stimulation of <dna>LTR</dna> -mediated transcription , whereas site specific mutation of these <dna>GATA sites</dna> resulted in virtual abrogation of the activation by <protein>hGATA-3</protein> .


Further , deletion of the hGATA-3 transcriptional activation domain abolished GATA-dependent HIV-1 trans-activation , showing that the stimulation of viral transcription observed is a direct effect of cotransfected hGATA-3 .

Further , deletion of the <dna>hGATA-3 transcriptional activation domain</dna> abolished GATA-dependent HIV-1 trans-activation , showing that the stimulation of viral transcription observed is a direct effect of <protein>cotransfected hGATA-3</protein> .


Introduction of the HIV-1 plasmids in which the GATA sites have been mutated into human T lymphocytes also caused a significant reduction in LTR -mediated transcription at both the basal level and in ( PHA- plus PMA- ) stimulated T cells .

Introduction of the <dna>HIV-1 plasmids</dna> in which the <dna>GATA sites</dna> have been mutated into human <cell_type>T lymphocytes</cell_type> also caused a significant reduction in <dna>LTR</dna> -mediated transcription at both the basal level and in ( PHA- plus PMA- ) <cell_line>stimulated T cells</cell_line> .


These observations suggest that in addition to its normal role in T lymphocyte gene regulation , hGATA-3 may also play a significant role in HIV-1 transcriptional activation .

These observations suggest that in addition to its normal role in <cell_type>T lymphocyte</cell_type> gene regulation , <protein>hGATA-3</protein> may also play a significant role in HIV-1 transcriptional activation .


Cytokine modulation of HIV expression .


Cytokines , the peptide hormones which control the homeostasis of the immune system and also play a fundamental role in inflammatory and immune mediated reactions , have been involved at multiple levels in the pathogenesis of the acquired immune deficiency syndrome ( AIDS ) .

<protein>Cytokines</protein> , the <protein>peptide hormones</protein> which control the homeostasis of the immune system and also play a fundamental role in inflammatory and immune mediated reactions , have been involved at multiple levels in the pathogenesis of the acquired immune deficiency syndrome ( AIDS ) .


Infection with the human immunodeficiency virus ( HIV ) has been shown to induce production of several cytokines both in vitro and in vivo .

Infection with the human immunodeficiency virus ( HIV ) has been shown to induce production of several <protein>cytokines</protein> both in vitro and in vivo .


Conversely , several cytokines modulate the levels of HIV expression in infected cells of both T lymphocytic and mononuclear phagocytic lineage .

Conversely , several <protein>cytokines</protein> modulate the levels of HIV expression in infected cells of both <cell_type>T lymphocytic and mononuclear phagocytic lineage</cell_type> .


Activated mononuclear cells , particularly B cells which are in a state of chronic activation in HIV infected individuals , release HIV-inductive cytokines and thus play a potentially important role in the pathogenesis of HIV infection .

<cell_type>Activated mononuclear cells</cell_type> , particularly <cell_type>B cells</cell_type> which are in a state of chronic activation in HIV infected individuals , release <protein>HIV-inductive cytokines</protein> and thus play a potentially important role in the pathogenesis of HIV infection .


Cloning and functional characterization of early B-cell factor , a regulator of lymphocyte-specific gene expression .

Cloning and functional characterization of <protein>early B-cell factor</protein> , a regulator of lymphocyte-specific gene expression .


Early B-cell factor ( EBF ) was identified previously as a tissue-specific and differentiation stage-specific DNA-binding protein that participates in the regulation of the pre-B and B lymphocyte-specific mb-1 gene .

<protein>Early B-cell factor</protein> ( <protein>EBF</protein> ) was identified previously as a tissue-specific and differentiation stage-specific <protein>DNA-binding protein</protein> that participates in the regulation of the <dna>pre-B and B lymphocyte-specific mb-1 gene</dna> .


Partial amino acid sequences obtained from purified EBF were used to isolate cDNA clones , which by multiple criteria encode EBF .

Partial amino acid sequences obtained from purified <protein>EBF</protein> were used to isolate <dna>cDNA clones</dna> , which by multiple criteria encode <protein>EBF</protein> .


The recombinant polypeptide formed sequence-specific complexes with the EBF-binding site in the mb-1 promoter .

The <protein>recombinant polypeptide</protein> formed sequence-specific complexes with the <dna>EBF-binding site</dna> in the <dna>mb-1 promoter</dna> .


The cDNA hybridized to multiple transcripts in pre-B and B-cell lines , but transcripts were not detected at significant levels in plasmacytoma , T-cell , and nonlymphoid cell lines .

The <dna>cDNA</dna> hybridized to multiple transcripts in <cell_line>pre-B and B-cell lines</cell_line> , but transcripts were not detected at significant levels in <cell_line>plasmacytoma</cell_line> , <cell_line>T-cell</cell_line> , and <cell_line>nonlymphoid cell lines</cell_line> .


Expression of recombinant EBF in transfected nonlymphoid cells strongly activated transcription from reporter plasmids containing functional EBF-binding sites .

Expression of recombinant <protein>EBF</protein> in <cell_line>transfected nonlymphoid cells</cell_line> strongly activated transcription from reporter plasmids containing functional <dna>EBF-binding sites</dna> .


Analysis of DNA binding by deletion mutants of EBF identified an amino-terminal cysteine-rich DNA-binding domain lacking obvious sequence similarity to known transcription factors .

Analysis of DNA binding by deletion mutants of <protein>EBF</protein> identified an <protein>amino-terminal cysteine-rich DNA-binding domain</protein> lacking obvious sequence similarity to known <protein>transcription factors</protein> .


DNA-binding assays with cotranslated wild-type and truncated forms of EBF indicated that the protein interacts with its site as a homodimer .

DNA-binding assays with cotranslated wild-type and truncated forms of <protein>EBF</protein> indicated that the protein interacts with its site as a <protein>homodimer</protein> .


Deletions delineated a carboxy-terminal dimerization region containing two repeats of 15 amino acids that show similarity with the dimerization domains of basic-helix-loop-helix proteins .

Deletions delineated a <protein>carboxy-terminal dimerization region</protein> containing two repeats of 15 amino acids that show similarity with the <protein>dimerization domains</protein> of <protein>basic-helix-loop-helix proteins</protein> .


Together , these data suggest that EBF represents a novel regulator of B lymphocyte-specific gene expression .

Together , these data suggest that <protein>EBF</protein> represents a novel regulator of B lymphocyte-specific gene expression .


Cell-specific expression of helix-loop-helix transcription factors encoded by the E2A gene .

Cell-specific expression of <protein>helix-loop-helix transcription factors</protein> encoded by the <dna>E2A gene</dna> .


The E2A gene encodes transcription factors of the helix-loop-helix family that are implicated in cell-specific gene expression as part of dimeric complexes that interact with E box enhancer elements .

The <dna>E2A gene</dna> encodes <protein>transcription factors</protein> of the <protein>helix-loop-helix family</protein> that are implicated in cell-specific gene expression as part of <protein>dimeric complexes</protein> that interact with <dna>E box enhancer elements</dna> .


It has previously been shown that transcripts of the E2A gene can be detected in a wide range of cell types .

It has previously been shown that transcripts of the <dna>E2A gene</dna> can be detected in a wide range of cell types .


We have now examined expression of the mouse E2A gene at the protein level using polyclonal antisera directed against distinct portions of the E2A protein to probe blots of cellular extracts .

We have now examined expression of the <dna>mouse E2A gene</dna> at the protein level using polyclonal antisera directed against distinct portions of the <protein>E2A protein</protein> to probe blots of cellular extracts .


A 73 kDa protein was identified by this analysis : this protein is highly enriched in cell lines of B lymphoid origin as compared to pancreatic beta-cells and fibroblast cells .

A <protein>73 kDa protein</protein> was identified by this analysis : this protein is highly enriched in <cell_line>cell lines of B lymphoid origin</cell_line> as compared to <cell_type>pancreatic beta-cells</cell_type> and <cell_type>fibroblast cells</cell_type> .


The detection of this protein selectively in extracts of lymphoid cells correlates with the presence of the E box -binding activity LEF1/BCF1 in these cells ; this binding activity was previously shown to be efficiently recognized by antiserum directed against E2A gene products .

The detection of this protein selectively in extracts of <cell_type>lymphoid cells</cell_type> correlates with the presence of the <dna>E box</dna> -binding activity <protein>LEF1/BCF1</protein> in these cells ; this binding activity was previously shown to be efficiently recognized by antiserum directed against <protein>E2A gene products</protein> .


Transfection of cells with full length E2A cDNA leads to appearance of protein co-migrating with the 73 kDa protein on SDS gel electrophoresis and co-migrating with LEF1/BCF1 on mobility shift analysis .

Transfection of cells with full length <dna>E2A cDNA</dna> leads to appearance of protein co-migrating with the <protein>73 kDa protein</protein> on SDS gel electrophoresis and co-migrating with <protein>LEF1/BCF1</protein> on mobility shift analysis .


Our results are consistent with the view that the DNA-binding activity LEF1/BCF1 is a homodimer of E2A proteins ; the selective appearance of this putative cell-specific transcription factor in B lymphoid cells seems to be attributable , at least in part , to the elevated E2A protein concentrations in these cells .

Our results are consistent with the view that the DNA-binding activity <protein>LEF1/BCF1</protein> is a <protein>homodimer of E2A proteins</protein> ; the selective appearance of this putative cell-specific transcription factor in <cell_type>B lymphoid cells</cell_type> seems to be attributable , at least in part , to the elevated <protein>E2A protein</protein> concentrations in these cells .


Hypertension in pregnancy .


Pregnancy-induced hypertension ( PIH ) is a frequent cause of maternal and neonatal morbidity and mortality .


In the present study we focused on the pathophysiology of PIH , mainly on the role of mineralocorticoids , reversed blood pressure patterns , and the resulting necessity of continuous monitoring of the preeclamptic mother .


Problems of antihypertensive therapy are discussed and the first results of a pilot study with Urapidil are presented .


To examine the role of mineralocorticoids in the pathophysiology of PIH , we studied plasma aldosterone and 18-hydroxy-corticosterone ( 18-OH-B ) levels in 25 women with PIH and in 25 healthy pregnant women .


Furthermore , we evaluated the mineralocorticoid receptor ( MR ) count in mononuclear leukocytes in the 2 groups .

Furthermore , we evaluated the <protein>mineralocorticoid receptor</protein> ( <protein>MR</protein> ) count in <cell_type>mononuclear leukocytes</cell_type> in the 2 groups .


The MR-count was significantly decreased in the PIH-group .


The values of plasma aldosterone and 18-OH-B were also low .


These results can not be explained by receptor down-regulation due to higher level of mineralocorticoids of the zona glomerulosa .


Perhaps deoxycorticosterone or a hitherto unknown mineralocorticoid is responsible for the hypertension and altered MR -status .

Perhaps deoxycorticosterone or a hitherto unknown mineralocorticoid is responsible for the hypertension and altered <protein>MR</protein> -status .


The first results of continuous blood pressure measurements with a noninvasive , real-time blood pressure monitor ( Finapres ) are presented .


The comparison of the obtained values with intraarterial measurements demonstrates a good correlation between the two methods .


We also report on the first experiences with Urapidil in the treatment of hypertension in severe preeclampsia .


The data show that hypertension in preeclamptic women can be treated by Urapidil without side effects or reflex-tachycardia .


Further studies will have to prove if Urapidil is suited for prepartal treatment of PIH as well .


Suppression of a cellular differentiation program by phorbol esters coincides with inhibition of binding of a cell-specific transcription factor ( NF-E2 ) to an enhancer element required for expression of an erythroid-specific gene .

Suppression of a cellular differentiation program by phorbol esters coincides with inhibition of binding of a <protein>cell-specific transcription factor</protein> ( <protein>NF-E2</protein> ) to an <dna>enhancer element</dna> required for expression of an <dna>erythroid-specific gene</dna> .


Induction by hemin increases , while induction with 12-O-tetradecanoylphorbol-13-acetate ( TPA ) represses , erythroid-specific gene expression in the human cell line K562 .

Induction by hemin increases , while induction with 12-O-tetradecanoylphorbol-13-acetate ( TPA ) represses , <dna>erythroid-specific gene</dna> expression in the <cell_line>human cell line K562</cell_line> .


We analyzed the effects of hemin or TPA induction on the binding and activity of transcription factors at a regulatory element found within the transcriptional regulatory sequences of many erythroid-specific genes .

We analyzed the effects of hemin or TPA induction on the binding and activity of <protein>transcription factors</protein> at a <dna>regulatory element</dna> found within the <dna>transcriptional regulatory sequences</dna> of many <dna>erythroid-specific genes</dna> .


TPA induction increases the binding of ubiquitous AP-1 factors to this element .

TPA induction increases the binding of <protein>ubiquitous AP-1 factors</protein> to this element .


TPA induction inhibits the binding of the lineage limited transcription factor NF-E2 to this transcriptional control element .

TPA induction inhibits the binding of the <protein>lineage limited transcription factor</protein> <protein>NF-E2</protein> to this <dna>transcriptional control element</dna> .


Hemin induction of K562 cells does not facilitate the binding of NF-E2 to its recognition site .

Hemin induction of <cell_line>K562 cells</cell_line> does not facilitate the binding of <protein>NF-E2</protein> to its recognition site .


Hemin induction appears to nonspecifically increase the expression of transiently transfected genes in K562 cells .

Hemin induction appears to nonspecifically increase the expression of transiently transfected genes in <cell_line>K562 cells</cell_line> .


Beyond this nonspecific increase in gene expression , hemin induction acts to increase the activity of the lineage limited transcription factor NF-E2 .

Beyond this nonspecific increase in gene expression , <protein>hemin</protein> induction acts to increase the activity of the <protein>lineage limited transcription factor</protein> NF-E2 .


The divergent effects of hemin and TPA on gene expression in K562 cells are mediated , in part , by their contrasting effects on the transcription factor NF-E2 .

The divergent effects of hemin and TPA on gene expression in <cell_line>K562 cells</cell_line> are mediated , in part , by their contrasting effects on the <protein>transcription factor</protein> <protein>NF-E2</protein> .


Interleukin-3 expression by activated T cells involves an inducible , T-cell-specific factor and an octamer binding protein .

<protein>Interleukin-3</protein> expression by <cell_type>activated T cells</cell_type> involves an inducible , <protein>T-cell-specific factor</protein> and an <protein>octamer binding protein</protein> .


Interleukin-3 ( IL-3 ) is exclusively expressed by activated T and natural killer cells , a function that is tightly controlled both in a lineage-specific and in a stimulation-dependent manner .

<protein>Interleukin-3</protein> ( <protein>IL-3</protein> ) is exclusively expressed by <cell_type>activated T</cell_type> and <cell_type>natural killer cells</cell_type> , a function that is tightly controlled both in a lineage-specific and in a stimulation-dependent manner .


We have investigated the protein binding characteristics and functional importance of the ACT-1-activating region of the IL-3 promoter .

We have investigated the protein binding characteristics and functional importance of the <dna>ACT-1-activating region</dna> of the <protein>IL-3</protein> promoter .


This region binds an inducible , T-cell-specific factor over its 5 ' end , a site that is necessary for the expression of IL-3 in the absence of other upstream elements .

This region binds an inducible , <protein>T-cell-specific factor</protein> over its <dna>5 ' end</dna> , a site that is necessary for the expression of <protein>IL-3</protein> in the absence of other upstream elements .


Over its 3 ' end , it binds a factor that is ubiquitously and constitutively expressed .

Over its <dna>3 ' end</dna> , it binds a factor that is ubiquitously and constitutively expressed .


This factor is Oct-1 or an immunologically related octamer-binding protein , and it plays a role in coordinating the activity of several regulatory elements .

This factor is <protein>Oct-1</protein> or an <protein>immunologically related octamer-binding protein</protein> , and it plays a role in coordinating the activity of several <dna>regulatory elements</dna> .


These characteristics make the ACT-1 site analogous to the activating ARRE-1 site in the IL-2 promoter .

These characteristics make the <dna>ACT-1 site</dna> analogous to the activating <dna>ARRE-1 site</dna> in the <dna>IL-2 promoter</dna> .


Furthermore , and despite a lack of sequence homology , the promoters of IL-3 and IL-2 share an organizational pattern of regulatory elements that is likely to be important for the T-cell-specific expression of these genes .

Furthermore , and despite a lack of sequence homology , the promoters of <protein>IL-3</protein> and <protein>IL-2</protein> share an organizational pattern of regulatory elements that is likely to be important for the T-cell-specific expression of these genes .


Interleukin-4 inhibits the lipopolysaccharide-induced expression of c-jun and c-fos messenger RNA and activator protein-1 binding activity in human monocytes .

<protein>Interleukin-4</protein> inhibits the lipopolysaccharide-induced expression of <rna>c-jun and c-fos messenger RNA</rna> and <protein>activator protein-1</protein> binding activity in <cell_type>human monocytes</cell_type> .