By searching protein Ag for clusters of amino acids containing cysteine and two of the other amino acids we were able to predict 17 out of 23 empirically known T-cell determinants in the Ag with a relatively low number of false ( positive ) predictions .

By searching protein <protein>Ag</protein> for clusters of amino acids containing cysteine and two of the other amino acids we were able to predict 17 out of 23 empirically known <protein>T-cell determinants</protein> in the <protein>Ag</protein> with a relatively low number of false ( positive ) predictions .


Furthermore , we present a new principle for searching Ag for potential amphipatic alpha-helical protein segments .

Furthermore , we present a new principle for searching <protein>Ag</protein> for potential <protein>amphipatic alpha-helical protein segments</protein> .


Such segments accord well with empirically known T-cell determinants and our algorithm produces a lower number of false positive predictions than the principle based on discrete Fourier transformations previously described .

Such segments accord well with empirically known <protein>T-cell determinants</protein> and our algorithm produces a lower number of false positive predictions than the principle based on discrete Fourier transformations previously described .


Contribution of NF-kappa B and Sp1 binding motifs to the replicative capacity of human immunodeficiency virus type 1 : distinct patterns of viral growth are determined by T-cell types .

Contribution of <protein>NF-kappa B</protein> and <dna>Sp1 binding motifs</dna> to the replicative capacity of human immunodeficiency virus type 1 : distinct patterns of viral growth are determined by <cell_type>T-cell types</cell_type> .


Starting with a replication-incompetent molecular clone of human immunodeficiency virus type 1 , lacking all the NF-kappa B and Sp1 binding sites present in the native long terminal repeat ( LTR ) , proviruses containing reconstructed LTRs with individual or combinations of NF-kappa B and Sp1 elements were generated and evaluated for their capacity to produce virus progeny following transfection-cocultivation .

Starting with a replication-incompetent molecular clone of human immunodeficiency virus type 1 , lacking all the <dna>NF-kappa B and Sp1 binding sites</dna> present in the <dna>native long terminal repeat</dna> ( <dna>LTR</dna> ) , proviruses containing <dna>reconstructed LTRs</dna> with individual or combinations of <dna>NF-kappa B and Sp1 elements</dna> were generated and evaluated for their capacity to produce virus progeny following transfection-cocultivation .


Virus stocks obtained from these experiments exhibited a continuum of replicative capacities in different human T-cell types depending on which element ( s ) was present in the LTR .

Virus stocks obtained from these experiments exhibited a continuum of replicative capacities in different <cell_type>human T-cell types</cell_type> depending on which <dna>element</dna> ( s ) was present in the <dna>LTR</dna> .


For example , in experiments involving proviral clones with LTRs containing one or two NF-kappa B elements ( and no Sp1 binding sites ) , a hierarchy of cellular permissivity to virus replication ( peripheral blood lymphocytes = MT4 greater than H9 greater than CEM greater than Jurkat ) was observed .

For example , in experiments involving proviral clones with <dna>LTRs</dna> containing one or two <dna>NF-kappa B elements</dna> ( and no <dna>Sp1 binding sites</dna> ) , a hierarchy of cellular permissivity to virus replication ( <cell_type>peripheral blood lymphocytes</cell_type> = <cell_line>MT4</cell_line> greater than <cell_line>H9</cell_line> greater than <cell_line>CEM</cell_line> greater than <cell_line>Jurkat</cell_line> ) was observed .


Of note was the associated emergence of second-site LTR revertants which involved an alteration of the TATA box .

Of note was the associated emergence of <dna>second-site LTR</dna> revertants which involved an alteration of the <dna>TATA box</dna> .


These results suggest that the human immunodeficiency virus type 1 LTR possesses functional redundancy which ensures virus replication in different T-cell types and is capable of changing depending on the particular combination of transcriptional factors present .

These results suggest that the <dna>human immunodeficiency virus type 1 LTR</dna> possesses functional redundancy which ensures virus replication in different <cell_type>T-cell types</cell_type> and is capable of changing depending on the particular combination of <protein>transcriptional factors</protein> present .


Stimulation of interferon beta gene transcription in vitro by purified NF-kappa B and a novel TH protein .

Stimulation of <dna>interferon beta gene</dna> transcription in vitro by purified <protein>NF-kappa B</protein> and a novel <protein>TH protein</protein> .


The human interferon beta ( IFN-beta ) regulatory element consists of multiple enhanson domains which are targets for transcription factors involved in inducible expression of the promoter .

The <dna>human interferon beta ( IFN-beta ) regulatory element</dna> consists of multiple <dna>enhanson domains</dna> which are targets for <protein>transcription factors</protein> involved in inducible expression of the <dna>promoter</dna> .


To further characterize the protein-DNA interactions mediating IFN-beta induction , positive regulatory domain ( PRD ) II binding proteins were purified from phorbol ester induced Jurkat T-cells and from IFN primed , cycloheximide/polyinosinic-polycytidylic acid treated HeLa S3 cells .

To further characterize the protein-DNA interactions mediating <protein>IFN-beta</protein> induction , <protein>positive regulatory domain ( PRD ) II binding proteins</protein> were purified from phorbol ester induced <cell_line>Jurkat T-cells</cell_line> and from <cell_line>IFN primed , cycloheximide/polyinosinic-polycytidylic acid treated HeLa S3 cells</cell_line> .


From HeLa cells , two major proteins of 52 and 45 kilodaltons ( kD ) copurified with DNA binding activity , whereas from T-cells , four proteins -- a major protein of 52 kD and three minor proteins of 82 , 67 , and 43-47 kD -- were purified .

From <cell_line>HeLa cells</cell_line> , two major proteins of <protein>52 and 45 kilodaltons ( kD )</protein> copurified with DNA binding activity , whereas from <cell_type>T-cells</cell_type> , four proteins -- a <protein>major protein</protein> of <protein>52 kD</protein> and three <protein>minor proteins</protein> of <protein>82</protein> , <protein>67</protein> , and <protein>43-47 kD</protein> -- were purified .


Also , an induction specific DNA binding protein was purified from HeLa cells that interacted with the ( AAGTGA ) 4 tetrahexamer sequence and the PRDI domain .

Also , an induction <protein>specific DNA binding protein</protein> was purified from <cell_line>HeLa cells</cell_line> that interacted with the ( AAGTGA ) 4 <dna>tetrahexamer sequence</dna> and the <dna>PRDI domain</dna> .


This protein is immunologically distinct from IRF-1/ISGF2 .

This protein is immunologically distinct from <protein>IRF-1/ISGF2</protein> .


Uninduced or Sendai virus induced HeLa extracts were used to examine transcription in vitro using a series of IFN beta promoter deletions .

Uninduced or Sendai virus induced HeLa extracts were used to examine transcription in vitro using a series of <dna>IFN beta promoter deletions</dna> .


Deletions upstream of the PRDII element increased transcription in the uninduced extract , indicating predominantly negative regulation of the promoter .

Deletions upstream of the <dna>PRDII element</dna> increased transcription in the uninduced extract , indicating predominantly negative regulation of the <dna>promoter</dna> .


A 2-4-fold increase in IFN-beta promoter transcription was observed in Sendai virus induced extracts , and deletion of PRDI and PRDII elements decreased this induced level of transcription .

A 2-4-fold increase in <dna>IFN-beta promoter</dna> transcription was observed in Sendai virus induced extracts , and deletion of <dna>PRDI</dna> and <dna>PRDII elements</dna> decreased this induced level of transcription .


When purified PRDII and tetrahexamer binding proteins were added to the induced extract , a 4-fold increase in transcription was observed .

When purified <protein>PRDII and tetrahexamer binding proteins</protein> were added to the induced extract , a 4-fold increase in transcription was observed .


These experiments demonstrate that it is possible to modulate IFN-beta transcription in vitro but indicate that additional proteins may be required to fully activate IFN-beta transcription .

These experiments demonstrate that it is possible to modulate IFN-beta transcription in vitro but indicate that additional proteins may be required to fully activate <protein>IFN-beta</protein> transcription .


The rhombotin family of cysteine-rich LIM-domain oncogenes : distinct members are involved in T-cell translocations to human chromosomes 11p15 and 11p13 .

The <dna>rhombotin family</dna> of <dna>cysteine-rich LIM-domain oncogenes</dna> : distinct members are involved in <dna>T-cell translocations</dna> to <dna>human chromosomes 11p15 and 11p13</dna> .


A chromosomal translocation in a T-cell leukemia involving the short arm of human chromosome 11 at band 11p15 disrupts the rhombotin gene .

A chromosomal translocation in a T-cell leukemia involving the <dna>short arm</dna> of <dna>human chromosome 11</dna> at <dna>band 11p15</dna> disrupts the <dna>rhombotin gene</dna> .


This gene encodes a protein with duplicated cysteine-rich regions called LIM domains , which show homology to zinc-binding proteins and to iron-sulfur centers of ferredoxins .

This gene encodes a protein with duplicated <protein>cysteine-rich regions</protein> called <protein>LIM domains</protein> , which show homology to <protein>zinc-binding proteins</protein> and to <protein>iron-sulfur centers</protein> of <protein>ferredoxins</protein> .


Two homologues of the rhombotin gene have now been isolated .

Two homologues of the <dna>rhombotin gene</dna> have now been isolated .


One of these , designated Rhom-2 , is located on human chromosome 11 at band 11p13 , where a cluster of T-cell leukemia-specific translocations occur ; all translocation breakpoints at 11p13 are upstream of the Rhom-2 gene .

One of these , designated <dna>Rhom-2</dna> , is located on <dna>human chromosome 11</dna> at <dna>band 11p13</dna> , where a cluster of <dna>T-cell leukemia-specific translocations</dna> occur ; all translocation breakpoints at <dna>11p13</dna> are upstream of the <dna>Rhom-2 gene</dna> .


Human and mouse Rhom-2 are highly conserved and , like rhombotin , encode two tandem cysteine-rich LIM domains .

<dna>Human and mouse Rhom-2</dna> are highly conserved and , like <dna>rhombotin</dna> , encode two <dna>tandem cysteine-rich LIM domains</dna> .


Rhom-2 mRNA is expressed in early mouse development in central nervous system , lung , kidney , liver , and spleen but only very low levels occur in thymus .

<rna>Rhom-2 mRNA</rna> is expressed in early mouse development in central nervous system , lung , kidney , liver , and spleen but only very low levels occur in thymus .


The other gene , designated Rhom-3 , is not on chromosome 11 but also retains homology to the LIM domain of rhombotin .

The other gene , designated <dna>Rhom-3</dna> , is not on chromosome 11 but also retains homology to the <dna>LIM domain</dna> of <dna>rhombotin</dna> .


Since the Rhom-2 gene is such a common site of chromosomal damage in T-cell tumors , the consistency of translocations near the rhombotin gene was further examined .

Since the <dna>Rhom-2 gene</dna> is such a common site of chromosomal damage in <cell_type>T-cell tumors</cell_type> , the consistency of translocations near the <dna>rhombotin gene</dna> was further examined .


A second translocation adjacent to rhombotin was found and at the same position as in the previous example .

A second translocation adjacent to <dna>rhombotin</dna> was found and at the same position as in the previous example .


Therefore , chromosome bands 11p15 ( rhombotin ) and 11p13 ( Rhom-2 ) are consistent sites of chromosome translocation in T-cell leukemia , with the 11p15 target more rarely involved .

Therefore , <dna>chromosome bands 11p15</dna> ( <dna>rhombotin</dna> ) and <dna>11p13</dna> ( <dna>Rhom-2</dna> ) are consistent sites of chromosome translocation in T-cell leukemia , with the <dna>11p15 target</dna> more rarely involved .


The results define the rhombotin gene family as a class of T-cell oncogenes with duplicated cysteine-rich LIM domains .

The results define the <dna>rhombotin</dna> gene family as a class of <dna>T-cell oncogenes</dna> with duplicated <dna>cysteine-rich LIM domains</dna> .


NF-kappa B activation by tumor necrosis factor alpha in the Jurkat T cell line is independent of protein kinase A , protein kinase C , and Ca ( 2+ ) -regulated kinases .

<protein>NF-kappa B</protein> activation by <protein>tumor necrosis factor alpha</protein> in the <cell_line>Jurkat T cell line</cell_line> is independent of <protein>protein kinase A</protein> , <protein>protein kinase C</protein> , and <protein>Ca ( 2+ ) -regulated kinases</protein> .


NF-kappa B is a DNA-binding regulatory factor able to control transcription of a number of genes , including human immunodeficiency virus ( HIV ) genes .

<protein>NF-kappa B</protein> is a <protein>DNA-binding regulatory factor</protein> able to control transcription of a number of genes , including <dna>human immunodeficiency virus ( HIV ) genes</dna> .


In T cells , NF-kappa B is activated upon cellular treatment by phorbol esters and the cytokine tumor necrosis factor alpha ( TNF alpha ) .

In <cell_type>T cells</cell_type> , <protein>NF-kappa B</protein> is activated upon cellular treatment by phorbol esters and the cytokine <protein>tumor necrosis factor alpha</protein> ( <protein>TNF alpha</protein> ) .


In the present work , we investigated the molecular events leading to NF-kappa B activation by TNF alpha in a human T cell line ( Jurkat ) and its subclone JCT6 , which presents a deficiency in the PKA transduction pathway .

In the present work , we investigated the molecular events leading to <protein>NF-kappa B</protein> activation by <protein>TNF alpha</protein> in a <cell_line>human T cell line</cell_line> ( <cell_line>Jurkat</cell_line> ) and its subclone <cell_line>JCT6</cell_line> , which presents a deficiency in the <protein>PKA</protein> transduction pathway .


We found that in both cell lines , both phorbol ester and TNF alpha were able to activate NF-kappa B .

We found that in both cell lines , both phorbol ester and <protein>TNF alpha</protein> were able to activate <protein>NF-kappa B</protein> .


Phorbol activation was positively modulated by Ca2+ influx while TNF alpha activation was not .

Phorbol activation was positively modulated by Ca2+ influx while <protein>TNF alpha</protein> activation was not .


Furthermore , while PMA activation was inhibited by the PKC inhibitor staurosporin , the TNF alpha effect was unchanged .

Furthermore , while PMA activation was inhibited by the <protein>PKC</protein> inhibitor staurosporin , the <protein>TNF alpha</protein> effect was unchanged .


TNF alpha did not activate cAMP production and its signal was not modulated by cAMP activators .

<protein>TNF alpha</protein> did not activate cAMP production and its signal was not modulated by cAMP activators .


Moreover , cAMP activators did not activate NF-kappa B in Jurkat cells .

Moreover , cAMP activators did not activate <protein>NF-kappa B</protein> in <cell_line>Jurkat cells</cell_line> .


Thus , TNF alpha -induced NF-kappa B activation was found to be mediated by none of the major signal-mediating kinases such as protein kinase C ( PKC ) , protein kinase A , or Ca ( 2+ ) -regulated kinases .

Thus , <protein>TNF alpha</protein> -induced <protein>NF-kappa B</protein> activation was found to be mediated by none of the major <protein>signal-mediating kinases</protein> such as <protein>protein kinase C</protein> ( <protein>PKC</protein> ) , <protein>protein kinase A</protein> , or <protein>Ca ( 2+ ) -regulated kinases</protein> .


Furthermore , we found that cytoplasmic acidification facilitated NF-kappa B activation by both TNF alpha and PKC , by a mechanism that increases NF-kappa B /I kappa B dissociation without affecting the NF-kappa B translocation step .

Furthermore , we found that cytoplasmic acidification facilitated <protein>NF-kappa B</protein> activation by both <protein>TNF alpha</protein> and <protein>PKC</protein> , by a mechanism that increases <protein>NF-kappa B</protein> <protein>/I kappa B</protein> dissociation without affecting the <protein>NF-kappa B</protein> translocation step .


The functional domains of the murine Thy-1 gene promoter .

The functional domains of the <dna>murine Thy-1 gene promoter</dna> .


The Thy-1 gene promoter resembles a `` housekeeping '' promoter in that it is located within a methylation-free island , lacks a canonical TATA box , and displays heterogeneity in the 5'-end termini of the mRNA .

The <dna>Thy-1 gene promoter</dna> resembles a <dna>`` housekeeping '' promoter</dna> in that it is located within a <dna>methylation-free island</dna> , lacks a <dna>canonical TATA box</dna> , and displays heterogeneity in the <rna>5'-end termini</rna> of the <rna>mRNA</rna> .


Using transgenic mice , we show that this promoter does not confer any tissue specificity and is active only in a position-dependent manner .

Using transgenic mice , we show that this <dna>promoter</dna> does not confer any tissue specificity and is active only in a position-dependent manner .


It can only be activated in a tissue-specific manner by elements that lie downstream of the initiation site .

It can only be activated in a tissue-specific manner by elements that lie downstream of the <dna>initiation site</dna> .


We have analyzed the functional domains of the minimal Thy-1 promoter and show that the dominant promoter elements consist of multiple binding sites for the transcription factor Sp1 , an inverted CCAAT box , and sequences proximal to the transcription start site .

We have analyzed the functional domains of the <dna>minimal Thy-1 promoter</dna> and show that the <dna>dominant promoter elements</dna> consist of <dna>multiple binding sites</dna> for the <protein>transcription factor</protein> <protein>Sp1</protein> , an inverted <dna>CCAAT box</dna> , and sequences proximal to the <dna>transcription start site</dna> .


DNase I and gel mobility shift assays show the binding of a number of nuclear factors to these elements , including Sp1 and CP1 .

DNase I and gel mobility shift assays show the binding of a number of <protein>nuclear factors</protein> to these <dna>elements</dna> , including <protein>Sp1</protein> and <protein>CP1</protein> .


Our results show that the structure of this promoter only permits productive interactions of the two transcription factors Sp1 and CP1 with the basal transcription machinery in the presence of enhancer sequences .

Our results show that the structure of this <dna>promoter</dna> only permits productive interactions of the two <protein>transcription factors</protein> <protein>Sp1</protein> and <protein>CP1</protein> with the basal transcription machinery in the presence of <dna>enhancer sequences</dna> .


Nuclear factor kappa B activates proenkephalin transcription in T lymphocytes .

<protein>Nuclear factor kappa B</protein> activates proenkephalin transcription in <cell_type>T lymphocytes</cell_type> .


Upon activation , T lymphocytes accumulate high levels of the neuropeptide enkephalin which correlate with high levels of proenkephalin mRNA in the cells .

Upon activation , <cell_type>T lymphocytes</cell_type> accumulate high levels of the neuropeptide enkephalin which correlate with high levels of <rna>proenkephalin mRNA</rna> in the cells .


Here we investigated the transcriptional basis for these changes .


The proenkephalin promoter contains a sequence GGGGACGTCCCC , named B2 , which is similar to the kappa B sequence GGGGACTTTCC , the binding site of the transcription factor nuclear factor ( NF ) -kappa B .

The proenkephalin promoter contains a sequence GGGGACGTCCCC , named <dna>B2</dna> , which is similar to the <dna>kappa B sequence</dna> GGGGACTTTCC , the binding site of the <protein>transcription factor</protein> <protein>nuclear factor ( NF ) -kappa B</protein> .


Activation of T lymphocytes induces an NF-kappa B -like binding activity to the B2 site , concomitant with activation of the proenkephalin promoter .

Activation of <cell_type>T lymphocytes</cell_type> induces an <protein>NF-kappa B</protein> -like binding activity to the <dna>B2</dna> site , concomitant with activation of the <dna>proenkephalin promoter</dna> .


Mutations at the B2 site abolish this transcriptional activation .

Mutations at the <dna>B2</dna> site abolish this transcriptional activation .


The purified homodimer ( two p50s ) of the DNA-binding subunit of NF-kappa B binds the B2 site of proenkephalin relatively better than does the heterotetramer ( two p65s plus two p50s ) form of the factor .

The purified <protein>homodimer</protein> ( two <protein>p50s</protein> ) of the <protein>DNA-binding subunit</protein> of <protein>NF-kappa B</protein> binds the <dna>B2</dna> site of proenkephalin relatively better than does the <protein>heterotetramer</protein> ( two <protein>p65s</protein> plus two <protein>p50s</protein> ) form of the factor .


Thus , it appears that the T-cell-specific activation of the proenkephalin promoter is mediated by NF-kappa B .

Thus , it appears that the T-cell-specific activation of the <dna>proenkephalin promoter</dna> is mediated by <protein>NF-kappa B</protein> .


However , as NF-kappa B is ubiquitous and the transcriptional activation through the B2 site is T cell specific , yet another T-cell-specific factor which synergizes with NF-kappa B should be considered .

However , as <protein>NF-kappa B</protein> is ubiquitous and the transcriptional activation through the <dna>B2</dna> site is T cell specific , yet another <protein>T-cell-specific factor</protein> which synergizes with <protein>NF-kappa B</protein> should be considered .


Induction of NF-KB during monocyte differentiation by HIV type 1 infection .

Induction of <protein>NF-KB</protein> during <cell_type>monocyte</cell_type> differentiation by HIV type 1 infection .


The production of human immunodeficiency virus type 1 ( HIV-1 ) progeny was followed in the U937 promonocytic cell line after stimulation either with retinoic acid or PMA , and in purified human monocytes and macrophages .

The production of human immunodeficiency virus type 1 ( HIV-1 ) progeny was followed in the <cell_line>U937 promonocytic cell line</cell_line> after stimulation either with retinoic acid or PMA , and in <cell_type>purified human monocytes and macrophages</cell_type> .


Electrophoretic mobility shift assays and Southwestern blotting experiments were used to detect the binding of cellular transactivation factor NF-KB to the double repeat-KB enhancer sequence located in the long terminal repeat .

Electrophoretic mobility shift assays and Southwestern blotting experiments were used to detect the binding of <protein>cellular transactivation factor</protein> <protein>NF-KB</protein> to the <dna>double repeat-KB enhancer sequence</dna> located in the <dna>long terminal repeat</dna> .


PMA treatment , and not retinoic acid treatment of the U937 cells acts in inducing NF-KB expression in the nuclei .

PMA treatment , and not retinoic acid treatment of the <cell_line>U937 cells</cell_line> acts in inducing <protein>NF-KB</protein> expression in the nuclei .


In nuclear extracts from monocytes or macrophages , induction of NF-KB occurred only if the cells were previously infected with HIV-1 .

In nuclear extracts from <cell_type>monocytes</cell_type> or <cell_type>macrophages</cell_type> , induction of <protein>NF-KB</protein> occurred only if the cells were previously infected with HIV-1 .


When U937 cells were infected with HIV-1 , no induction of NF-KB factor was detected , whereas high level of progeny virions was produced , suggesting that this factor was not required for viral replication .

When <cell_line>U937 cells</cell_line> were infected with HIV-1 , no induction of <protein>NF-KB factor</protein> was detected , whereas high level of progeny virions was produced , suggesting that this factor was not required for viral replication .


These results indicate that in monocytic cell lineage , HIV-1 could mimic some differentiation/activation stimuli allowing nuclear NF-KB expression .

These results indicate that in <cell_line>monocytic cell lineage</cell_line> , HIV-1 could mimic some differentiation/activation stimuli allowing nuclear <protein>NF-KB</protein> expression .


Disruption of the human SCL locus by `` illegitimate '' V- ( D ) -J recombinase activity .

Disruption of the <dna>human SCL locus</dna> by `` illegitimate '' V- ( D ) -J recombinase activity .


A fusion complementary DNA in the T cell line HSB-2 elucidates a provocative mechanism for the disruption of the putative hematopoietic transcription factor SCL .

A <dna>fusion complementary DNA</dna> in the <cell_line>T cell line HSB-2</cell_line> elucidates a provocative mechanism for the disruption of the putative <protein>hematopoietic transcription factor</protein> <protein>SCL</protein> .


The fusion cDNA results from an interstitial deletion between a previously unknown locus , SIL ( SCL interrupting locus ) , and the 5 ' untranslated region of SCL .

The <dna>fusion cDNA</dna> results from an interstitial deletion between a previously <dna>unknown locus</dna> , <dna>SIL</dna> ( <dna>SCL interrupting locus</dna> ) , and the <dna>5 ' untranslated region</dna> of <protein>SCL</protein> .


Similar to 1 ; 14 translocations , this deletion disrupts the SCL 5 ' regulatory region .

Similar to 1 ; 14 translocations , this deletion disrupts the <dna>SCL 5 ' regulatory region</dna> .


This event is probably mediated by V- ( D ) -J recombinase activity , although neither locus is an immunoglobulin or a T cell receptor .

This event is probably mediated by V- ( D ) -J recombinase activity , although neither locus is an <protein>immunoglobulin</protein> or a <protein>T cell receptor</protein> .


Two other T cell lines , CEM and RPMI 8402 , have essentially identical deletions .

Two other <cell_line>T cell lines</cell_line> , <cell_line>CEM</cell_line> and <cell_line>RPMI 8402</cell_line> , have essentially identical deletions .


Thus , in lymphocytes , growth-affecting genes other than immune receptors risk rearrangements .

Thus , in <cell_type>lymphocytes</cell_type> , <dna>growth-affecting genes</dna> other than <protein>immune receptors</protein> risk rearrangements .


Thyroid hormone receptors form distinct nuclear protein-dependent and independent complexes with a thyroid hormone response element .

<protein>Thyroid hormone receptors</protein> form distinct <protein>nuclear protein-dependent and independent complexes</protein> with a <dna>thyroid hormone response element</dna> .


We have examined the binding of nuclear proteins and recombinant thyroid hormone receptors ( TRs ) to the palindromic thyroid hormone responsive element AGGTCATGACCT ( TREp ) using a gel electrophoretic mobility shift assay .

We have examined the binding of <protein>nuclear proteins</protein> and <protein>recombinant thyroid hormone receptors</protein> ( <protein>TRs</protein> ) to the <dna>palindromic thyroid hormone responsive element</dna> AGGTCATGACCT ( <dna>TREp</dna> ) using a gel electrophoretic mobility shift assay .


Four specific protein-DNA complexes were detected after incubation of nuclear extracts ( NE ) from T3-responsive pituitary ( GH3 ) cells with a TREp-containing DNA fragment .

Four specific <protein>protein-DNA complexes</protein> were detected after incubation of nuclear extracts ( NE ) from <cell_line>T3-responsive pituitary ( GH3 ) cells</cell_line> with a <dna>TREp-containing DNA fragment</dna> .


This was compared with the TREp binding of reticulocyte lysate-synthesized TRs .

This was compared with the <dna>TREp</dna> binding of <protein>reticulocyte lysate-synthesized TRs</protein> .


TR alpha 1 and TR beta 2 each formed a single major TR : TREp complex which comigrated with the least retarded complex formed by GH3 NE , while TR beta 1 formed multiple complexes suggesting that it can bind to TREp as an oligomer .

<protein>TR alpha 1</protein> and <protein>TR beta 2</protein> each formed a single major <protein>TR : TREp complex</protein> which comigrated with the least retarded complex formed by GH3 NE , while <protein>TR beta 1</protein> formed multiple complexes suggesting that it can bind to <dna>TREp</dna> as an <protein>oligomer</protein> .


Interestingly , coincubation of 35S-TR alpha 1 , GH3 NE , and unlabeled TREp resulted in not only the 35S-TR : TREp complex , but in two additional more greatly retarded complexes containing 35S-TR alpha 1 and comigrating with those formed by GH3 extract alone .

Interestingly , coincubation of <protein>35S-TR alpha 1</protein> , GH3 NE , and unlabeled <dna>TREp</dna> resulted in not only the <protein>35S-TR : TREp complex</protein> , but in two additional more greatly retarded complexes containing <protein>35S-TR alpha 1</protein> and comigrating with those formed by GH3 extract alone .


Incubation of each of the TRs with NE from COS-7 cells , which do not possess sufficient endogenous TRs to mediate T3-responses , resulted in formation of a new , more greatly shifted complex .

Incubation of each of the <protein>TRs</protein> with NE from <cell_line>COS-7 cells</cell_line> , which do not possess sufficient endogenous <protein>TRs</protein> to mediate T3-responses , resulted in formation of a new , more <protein>greatly shifted complex</protein> .


A similar , heat labile activity which altered mobility of the TR : TRE complex was also present in NE from T3-unresponsive JEG-3 cells .

A similar , heat labile activity which altered mobility of the <protein>TR : TRE complex</protein> was also present in NE from <cell_line>T3-unresponsive JEG-3 cells</cell_line> .


At high concentration of NE , all of the TR bound to TREp was more greatly retarded than in the absence of NE .

At high concentration of NE , all of the <protein>TR</protein> bound to <dna>TREp</dna> was more greatly retarded than in the absence of NE .


Truncation of TR alpha 1 at amino acid 210 prevented additional complex formation in the presence of NE without affecting DNA binding , suggesting that the carboxyl-terminus of the TRs is essential for interaction with nuclear proteins .

Truncation of <protein>TR alpha 1</protein> at <protein>amino acid 210</protein> prevented additional complex formation in the presence of NE without affecting DNA binding , suggesting that the <protein>carboxyl-terminus</protein> of the <protein>TRs</protein> is essential for interaction with <protein>nuclear proteins</protein> .


( ABSTRACT TRUNCATED AT 250 WORDS )


Cell-specific differences in activation of NF-kappa B regulatory elements of human immunodeficiency virus and beta interferon promoters by tumor necrosis factor .

Cell-specific differences in activation of <dna>NF-kappa B regulatory elements</dna> of <dna>human immunodeficiency virus and beta interferon promoters</dna> by <protein>tumor necrosis factor</protein> .


Three aspects of the involvement of tumor necrosis factor in human immunodeficiency virus ( HIV ) pathogenesis were examined .

Three aspects of the involvement of <protein>tumor necrosis factor</protein> in human immunodeficiency virus ( HIV ) pathogenesis were examined .


Tumor necrosis factor alpha ( TNF-alpha ) mRNA production was analyzed by polymerase chain reaction amplification in monocytic U937 cells and in a chronically HIV infected U937 cell line ( U9-IIIB ) .

<rna>Tumor necrosis factor alpha ( TNF-alpha ) mRNA</rna> production was analyzed by polymerase chain reaction amplification in <cell_line>monocytic U937 cells</cell_line> and in a <cell_line>chronically HIV infected U937 cell line</cell_line> ( <cell_line>U9-IIIB</cell_line> ) .


TNF-alpha RNA was undetectable in U937 cells , whereas a low constitutive level was detected in U9-IIIB cells .

<rna>TNF-alpha RNA</rna> was undetectable in <cell_line>U937 cells</cell_line> , whereas a low constitutive level was detected in <cell_line>U9-IIIB cells</cell_line> .


Paramyxovirus infection induced a 5- to 10-fold increase in the steady-state level of TNF-alpha RNA in U9-IIIB cells compared with U937 cells , suggesting that HIV-infected monocytic cells produced higher levels of TNF-alpha than did normal cells after a secondary virus infection .

Paramyxovirus infection induced a 5- to 10-fold increase in the steady-state level of <rna>TNF-alpha RNA</rna> in <cell_line>U9-IIIB cells</cell_line> compared with <cell_line>U937 cells</cell_line> , suggesting that <cell_line>HIV-infected monocytic cells</cell_line> produced higher levels of <protein>TNF-alpha</protein> than did normal cells after a secondary virus infection .


The effects of TNF-alpha on gene expression were examined by transient expression assays using reporter chloramphenicol acetyltransferase plasmids linked to regulatory elements from the HIV long terminal repeat ( LTR ) and the beta interferon promoter .

The effects of <protein>TNF-alpha</protein> on gene expression were examined by transient expression assays using <dna>reporter chloramphenicol acetyltransferase plasmids</dna> linked to <dna>regulatory elements</dna> from the <dna>HIV long terminal repeat</dna> ( <dna>LTR</dna> ) and the <dna>beta interferon promoter</dna> .


In U937 and Jurkat T lymphoid cells , the inducibility of the different hybrid promoters by TNF-alpha or phorbol ester varied in a cell type- and promoter context-specific manner ; the levels of gene activity of NF-kappa B-containing plasmids correlated directly with induction of NF-kappa B DNA-binding activity .

In <cell_line>U937 and Jurkat T lymphoid cells</cell_line> , the inducibility of the different <dna>hybrid promoters</dna> by <protein>TNF-alpha</protein> or phorbol ester varied in a cell type- and promoter context-specific manner ; the levels of gene activity of <dna>NF-kappa B-containing plasmids</dna> correlated directly with induction of <protein>NF-kappa B</protein> DNA-binding activity .


Although the intact beta interferon promoter was only weakly stimulated by phorbol ester or TNF-alpha , multimers of the PRDII NF-kappa B-binding domain were inducible by both agents .

Although the intact <dna>beta interferon promoter</dna> was only weakly stimulated by phorbol ester or <protein>TNF-alpha</protein> , multimers of the <dna>PRDII NF-kappa B-binding domain</dna> were inducible by both agents .


TNF-alpha was able to increase expression of the HIV LTR in T cells , but in monocytic cells , TNF-alpha did not induce the HIV LTR above a constitutive level of activity .

<protein>TNF-alpha</protein> was able to increase expression of the <dna>HIV LTR</dna> in <cell_type>T cells</cell_type> , but in <cell_type>monocytic cells</cell_type> , <protein>TNF-alpha</protein> did not induce the <dna>HIV LTR</dna> above a constitutive level of activity .


This level of NF-kappa B -independent activity appears to be sufficient for virus multiplication , since TNF-alpha treatment had no effect on the kinetics of de novo HIV type 1 ( HIV-1 ) infection and viral RNA production in U937 cells .

This level of <protein>NF-kappa B</protein> -independent activity appears to be sufficient for virus multiplication , since <protein>TNF-alpha</protein> treatment had no effect on the kinetics of de novo HIV type 1 ( HIV-1 ) infection and <rna>viral RNA</rna> production in <cell_line>U937 cells</cell_line> .


However , in Jurkat cells , TNF-alpha dramatically enhanced the spread of HIV-1 through the cell population and increased viral RNA synthesis , indicating that in T cells HIV-1 multiplication was stimulated by TNF-alpha treatment .

However , in <cell_line>Jurkat cells</cell_line> , <protein>TNF-alpha</protein> dramatically enhanced the spread of HIV-1 through the cell population and increased <rna>viral RNA</rna> synthesis , indicating that in <cell_type>T cells</cell_type> HIV-1 multiplication was stimulated by <protein>TNF-alpha</protein> treatment .


Functional analysis of cis-linked regulatory sequences in the HLA DRA promoter by transcription in vitro .

Functional analysis of <dna>cis-linked regulatory sequences</dna> in the <dna>HLA DRA promoter</dna> by transcription in vitro .


Two consensus sequences , called X and Y boxes , capable of binding nuclear proteins and regulating expression in B cells have been defined within the immediate upstream region of major histocompatibility complex ( MHC ) class II promoters .

Two consensus sequences , called <dna>X and Y boxes</dna> , capable of binding <protein>nuclear proteins</protein> and regulating expression in <cell_type>B cells</cell_type> have been defined within the immediate upstream region of <dna>major histocompatibility complex ( MHC ) class II promoters</dna> .


Unlike other class II promoters , the HLA-DR alpha ( DRA ) promoter also contains one element identical to the `` octamer '' motif of immunoglobulin variable region promoters that is responsible for B cell-specific transcription .

Unlike other <dna>class II promoters</dna> , the <dna>HLA-DR alpha ( DRA ) promoter</dna> also contains one element identical to the <dna>`` octamer '' motif</dna> of <dna>immunoglobulin variable region promoters</dna> that is responsible for B cell-specific transcription .


This `` octamer `` in the context of DRA appears capable of binding both the ubiquitous ( OTF-1 ) and lymphoid-specific ( OTF-2 ) `` octamer '' binding proteins , but at least one other distinct `` octamer '' complex was found .

This `` <dna>octamer</dna> `` in the context of <protein>DRA</protein> appears capable of binding both the <protein>ubiquitous</protein> ( <protein>OTF-1</protein> ) and <protein>lymphoid-specific ( OTF-2 ) `` octamer '' binding proteins</protein> , but at least one other distinct <protein>`` octamer '' complex</protein> was found .


In order to characterize the function of cis-acting elements , we have developed an in vitro system in which a DRA promoter construct is transcribed more efficiently in extracts from B cells than in extracts from class II-negative HeLa cells .

In order to characterize the function of <dna>cis-acting elements</dna> , we have developed an in vitro system in which a <dna>DRA promoter construct</dna> is transcribed more efficiently in extracts from <cell_type>B cells</cell_type> than in extracts from <cell_line>class II-negative HeLa cells</cell_line> .


5 ' deletion constructs which lacked the Y box , but retained the `` octamer '' motif and TATA box were completely inactive , and internal deletion of the Y box reduced transcription by 95 % .

5 ' deletion constructs which lacked the <dna>Y box</dna> , but retained the <dna>`` octamer '' motif</dna> and <dna>TATA box</dna> were completely inactive , and internal deletion of the <dna>Y box</dna> reduced transcription by 95 % .


Using supercoiled , but not linear templates , we observed differences in transcription efficiencies from templates lacking or disrupting the X consensus element that reflect effects of random replacement of X box sequences in transient expression assays .

Using supercoiled , but not linear templates , we observed differences in transcription efficiencies from templates lacking or disrupting the <dna>X consensus element</dna> that reflect effects of random replacement of <dna>X box sequences</dna> in transient expression assays .


Demonstration of the complete dependence on the Y box in this system suggests that , despite its demonstrated importance in the DRA promoter , the DRA `` octamer '' does not utilize OTF-2 in a manner analogous to immunoglobulin promoters in B cells .

Demonstration of the complete dependence on the <dna>Y box</dna> in this system suggests that , despite its demonstrated importance in the <dna>DRA promoter</dna> , the <dna>DRA `` octamer ''</dna> does not utilize <protein>OTF-2</protein> in a manner analogous to <dna>immunoglobulin promoters</dna> in <cell_type>B cells</cell_type> .


Lipopolysaccharide is a potent monocyte/macrophage-specific stimulator of human immunodeficiency virus type 1 expression .


Lipopolysaccharide ( LPS ) potently stimulates human immunodeficiency virus type 1-long terminal repeat ( HIV-1-LTR ) CAT constructs transfected into monocyte/macrophage-like cell lines but not a T cell line .

Lipopolysaccharide ( LPS ) potently stimulates <dna>human immunodeficiency virus type 1-long terminal repeat ( HIV-1-LTR ) CAT constructs</dna> transfected into <cell_line>monocyte/macrophage-like cell lines</cell_line> but not a <cell_line>T cell line</cell_line> .


This effect appears to be mediated through the induction of nuclear factor kappa B ( NF-kappa B ) .

This effect appears to be mediated through the induction of <protein>nuclear factor kappa B</protein> ( <protein>NF-kappa B</protein> ) .


Electrophoretic mobility shift assays demonstrate that LPS induces a DNA binding activity indistinguishable from NF-kappa B in U937 and THP-1 cells .

Electrophoretic mobility shift assays demonstrate that LPS induces a DNA binding activity indistinguishable from <protein>NF-kappa B</protein> in <cell_line>U937</cell_line> and <cell_line>THP-1 cells</cell_line> .


LPS is also shown to dramatically increase HIV-1 production from a chronically infected monocyte/macrophage-like cloned cell line , U1 , which produces very low levels of HIV-1 at baseline .

LPS is also shown to dramatically increase HIV-1 production from a <cell_line>chronically infected monocyte/macrophage-like cloned cell line</cell_line> , <cell_line>U1</cell_line> , which produces very low levels of HIV-1 at baseline .


The stimulation of viral production from this cell line occurs only if these cells are treated with granulocyte/macrophage colony-stimulating factor ( GM-CSF ) before treatment with LPS .

The stimulation of viral production from this cell line occurs only if these cells are treated with <protein>granulocyte/macrophage colony-stimulating factor</protein> ( <protein>GM-CSF</protein> ) before treatment with LPS .


This stimulation of HIV-1 production is correlated with an increase in the level of HIV-1 RNA and and activation of NF-kappa B .

This stimulation of HIV-1 production is correlated with an increase in the level of <rna>HIV-1 RNA</rna> and and activation of <protein>NF-kappa B</protein> .


LPS is not able to induce HIV-1 production in a cloned T cell line .

LPS is not able to induce HIV-1 production in a cloned <cell_line>T cell line</cell_line> .


The effect of LPS on HIV-1 replication occurs at picogram per milliliter concentrations and may be clinically significant in understanding the variability of the natural history of HIV-1 infection .


Steroid dose sparing : pharmacodynamic responses to single versus divided doses of methylprednisolone in man .


Inhibitory drug interactions affecting the metabolism of methylprednisolone ( MP ) may produce either steroid sparing or adverse effects partly by increasing the exposure time to the steroid .


This phenomenon can be mimicked by administering MP in divided doses .


Two types of responses were compared after a single MP dose ( 40 mg bolus ) and a divided regimen ( 20 mg bolus and a 5 mg bolus 8 hours later ) in six healthy male volunteers .


The suppression of basophils measured as whole blood histamine and plasma cortisol concentrations was assessed during 32 hours .

The suppression of <cell_type>basophils</cell_type> measured as whole blood histamine and plasma cortisol concentrations was assessed during 32 hours .


The 37.5 % reduction in dose produced a 23 % overall decreased blood histamine response .


A pharmacodynamic model for basophil cell distribution to and from an extravascular compartment describes the effects of MP after both regimens .


A slower initial decline in blood histamine after the divided regimen may be related to incomplete suppression of basophil cell return to blood .

A slower initial decline in blood histamine after the divided regimen may be related to incomplete suppression of <cell_type>basophil cell</cell_type> return to blood .


The 50 % inhibitory concentrations of MP of about 5 ng/ml were similar for both regimens .


The decline and return of cortisol concentrations were similar between MP treatments with suppression continuing for 24 hours .


The 50 % inhibitory concentrations of MP values for adrenal suppression were about 1 ng/ml .


Pharmacodynamic modeling is useful in quantitating corticosteroid responses and generally predicted the `` dose-sparing '' effects that were achieved by prolonging MP plasma concentrations .


This study supports previous clinical observations that patients may require morning through evening exposure to MP to optimize efficacy while adrenal suppression is being minimized .


1 , 25 ( OH ) 2D2 production by T lymphocytes and alveolar macrophages recovered by lavage from normocalcemic patients with tuberculosis .

1 , 25 ( OH ) 2D2 production by <cell_type>T lymphocytes</cell_type> and <cell_type>alveolar macrophages</cell_type> recovered by lavage from normocalcemic patients with tuberculosis .


To compare extra-renal 1 , 25 ( OH ) 2D3 production in different types of granulomatous disease , and to identify the cell types responsible , we have evaluated the conversion of 25 ( OH ) D3 in 1 , 25 ( OH ) 2D3 by uncultured cells recovered by bronchoalveolar lavage and blood mononuclear cells from normocalcemic patients with sarcoidosis and tuberculosis .

To compare extra-renal 1 , 25 ( OH ) 2D3 production in different types of granulomatous disease , and to identify the cell types responsible , we have evaluated the conversion of 25 ( OH ) D3 in 1 , 25 ( OH ) 2D3 by <cell_type>uncultured cells</cell_type> recovered by bronchoalveolar lavage and <cell_type>blood mononuclear cells</cell_type> from normocalcemic patients with sarcoidosis and tuberculosis .


1 , 25 ( OH ) 2D3 was produced both by lavage cells ( 12/12 tuberculosis patients , 2/6 sarcoidosis patients ) and blood mononuclear cells ( 3/5 tuberculosis patients , 0/3 sarcoidosis patients ) from patients but not controls , but significantly greater amounts were produced by lavage cells from tuberculosis patients than those of sarcoidosis patients ( P less than 0.001 ) .

1 , 25 ( OH ) 2D3 was produced both by <cell_type>lavage cells</cell_type> ( 12/12 tuberculosis patients , 2/6 sarcoidosis patients ) and <cell_type>blood mononuclear cells</cell_type> ( 3/5 tuberculosis patients , 0/3 sarcoidosis patients ) from patients but not controls , but significantly greater amounts were produced by lavage cells from tuberculosis patients than those of sarcoidosis patients ( P less than 0.001 ) .


1 , 25 ( OH ) 2D3 production by lavage cells from tuberculosis patients correlated with the number of CD8+ T lymphocytes present but not other cell types .

1 , 25 ( OH ) 2D3 production by <cell_type>lavage cells</cell_type> from tuberculosis patients correlated with the number of CD8+ <cell_type>T lymphocytes</cell_type> present but not other cell types .


T lymphocytes appeared to be an important source of 1 , 25 ( OH ) 2D3 production , since purified T lymphocytes from all patients with tuberculosis produced 1 , 25 ( OH ) 2D3 , and 1 , 25 ( OH ) 2D3 production by these cells correlated closely with that produced by unseparated lavage cells .

<cell_type>T lymphocytes</cell_type> appeared to be an important source of 1 , 25 ( OH ) 2D3 production , since purified <cell_type>T lymphocytes</cell_type> from all patients with tuberculosis produced 1 , 25 ( OH ) 2D3 , and 1 , 25 ( OH ) 2D3 production by these cells correlated closely with that produced by unseparated <cell_type>lavage cells</cell_type> .


Because 1 , 25 ( OH ) 2D3 can improve the capacity of macrophages to kill mycobacteria , our results support the conclusion that macrophage-lymphocyte interactions , mediated at least in part by 1 , 25 ( OH ) 2D3 , may be an important component of a successful antituberculous immune response .

Because 1 , 25 ( OH ) 2D3 can improve the capacity of <cell_type>macrophages</cell_type> to kill mycobacteria , our results support the conclusion that macrophage-lymphocyte interactions , mediated at least in part by 1 , 25 ( OH ) 2D3 , may be an important component of a successful antituberculous immune response .


Megakaryocytic and erythrocytic lineages share specific transcription factors .

<cell_line>Megakaryocytic and erythrocytic lineages</cell_line> share specific <protein>transcription factors</protein> .


Erythroid-specific genes contain binding sites for NF-E1 ( also called GF-1 and Eryf-1 ; refs 1-3 respectively ) , the principal DNA-binding protein of the erythrocytic lineage .

<dna>Erythroid-specific genes</dna> contain binding sites for <protein>NF-E1</protein> ( also called <protein>GF-1</protein> and <protein>Eryf-1</protein> ; refs 1-3 respectively ) , the principal <protein>DNA-binding protein</protein> of the <cell_type>erythrocytic lineage</cell_type> .


NF-E1 expression seems to be restricted to the erythrocytic lineage .

<protein>NF-E1</protein> expression seems to be restricted to the <cell_type>erythrocytic lineage</cell_type> .


A closely related ( if not identical ) protein is found in both a human megakaryocytic cell line and purified human megakaryocytes ; it binds to promoter regions of two megakaryocytic-specific genes .

A closely related ( if not identical ) protein is found in both a <cell_line>human megakaryocytic cell line</cell_line> and <cell_line>purified human megakaryocytes</cell_line> ; it binds to <dna>promoter regions</dna> of two <dna>megakaryocytic-specific genes</dna> .


The binding sites and partial proteolysis profile of this protein are indistinguishable from those of the erythroid protein ; also , NF-E1 messenger RNA is the same size in both the megakaryocytic and erythroid cell lines .

The binding sites and partial proteolysis profile of this protein are indistinguishable from those of the <protein>erythroid protein</protein> ; also , <rna>NF-E1 messenger RNA</rna> is the same size in both the <cell_line>megakaryocytic and erythroid cell lines</cell_line> .


Furthermore , point mutations that abolish binding of NF-E1 result in a 70 % decrease in the transcriptional activity of a megakaryocytic-specific promoter .

Furthermore , point mutations that abolish binding of <protein>NF-E1</protein> result in a 70 % decrease in the transcriptional activity of a <dna>megakaryocytic-specific promoter</dna> .


We also find that NF-E2 , another trans-acting factor of the erythrocytic lineage , is present in megakaryocytes .

We also find that <protein>NF-E2</protein> , another <protein>trans-acting factor</protein> of the <cell_type>erythrocytic lineage</cell_type> , is present in <cell_line>megakaryocytes</cell_line> .


Transcriptional effects in both lineages might then be mediated in part by the same specific trans-acting factors .

Transcriptional effects in both lineages might then be mediated in part by the same specific <protein>trans-acting factors</protein> .


Our data strengthen the idea of a close association between the erythrocytic and the megakaryocytic lineages and could also explain the expression of markers specific to the erythrocytic and megakaryocytic lineages in most erythroblastic and megakaryoblastic permanent cell lines .

Our data strengthen the idea of a close association between the <cell_line>erythrocytic and the megakaryocytic lineages</cell_line> and could also explain the expression of markers specific to the <cell_type>erythrocytic and megakaryocytic lineages</cell_type> in most <cell_line>erythroblastic and megakaryoblastic permanent cell lines</cell_line> .


Transcriptional down-regulation of c-myc expression by protein synthesis-dependent and -independent pathways in a human T lymphoblastic tumor cell line .

Transcriptional down-regulation of <dna>c-myc</dna> expression by protein synthesis-dependent and -independent pathways in a <cell_line>human T lymphoblastic tumor cell line</cell_line> .


We show that in the human T lymphoblastic tumor cell line Molt4 c-myc mRNA and protein expression is down-regulated after exposure to dimethyl sulfoxide , to phorbol myristate acetate , or to the calcium ionophore A23187 , which raises the intracellular calcium concentration .

We show that in the <cell_line>human T lymphoblastic tumor cell line</cell_line> <rna>Molt4 c-myc mRNA</rna> and protein expression is down-regulated after exposure to dimethyl sulfoxide , to phorbol myristate acetate , or to the calcium ionophore A23187 , which raises the intracellular calcium concentration .


A block to RNA elongation is largely responsible for decreased c-myc transcription .

A block to RNA elongation is largely responsible for decreased <dna>c-myc</dna> transcription .


Although negative regulation by dimethyl sulfoxide takes place even when protein synthesis is inhibited by cycloheximide , the phorbol myristate acetate effect is blocked to some extent only by cycloheximide .


The calcium ionophore-induced c-myc suppression , however , strictly requires de novo protein synthesis .

The calcium ionophore-induced <dna>c-myc</dna> suppression , however , strictly requires de novo protein synthesis .


Therefore , two different negative regulatory pathways are involved in c-myc regulation : one which is independent and one which depends on de novo protein synthesis .

Therefore , two different negative regulatory pathways are involved in <dna>c-myc</dna> regulation : one which is independent and one which depends on de novo protein synthesis .


The latter one appears to be mediated by a rapidly calcium-dependent induced gene product .

The latter one appears to be mediated by a rapidly <protein>calcium-dependent induced gene product</protein> .


Oestrogen receptor ( ER ) analysis in B-cell chronic lymphocytic leukemia : correlation of biochemical and immunocytochemical methods .

<protein>Oestrogen receptor</protein> ( <protein>ER</protein> ) analysis in B-cell chronic lymphocytic leukemia : correlation of biochemical and immunocytochemical methods .


Oestrogen receptors ( ER ) are present in neoplastic lymphoid cells and have been considered a physiological marker of growth rate or differentiation .

<protein>Oestrogen receptors</protein> ( <protein>ER</protein> ) are present in <cell_type>neoplastic lymphoid cells</cell_type> and have been considered a physiological marker of growth rate or differentiation .


Tamoxifen , an oestrogen antagonist , has been given in some patients with CLL and Hodgkin 's disease , with dramatic response in single cases .


Until now , ER status has been assessed using a steroid binding assay ( SBA ) which has many inherent problems .

Until now , <protein>ER</protein> status has been assessed using a steroid binding assay ( SBA ) which has many inherent problems .


Recently , the development of monoclonal antibodies directed against ER has been applied to the study of breast carcinomas and results obtained show good correlation with the quantitative SBA .

Recently , the development of monoclonal antibodies directed against <protein>ER</protein> has been applied to the study of breast carcinomas and results obtained show good correlation with the quantitative SBA .


We studied 49 cases of B-cell chronic lymphocytic leukemia ( CLL ) using immunostaining of cytospin preparations .


In 30 of these cases ER enzyme immunoassay ( ER -EIA ) was also performed .

In 30 of these cases <protein>ER</protein> enzyme immunoassay ( <protein>ER</protein> -EIA ) was also performed .


Cultured MCF-7 cells , derived from a pleural effusion of a breast cancer patient , known to contain high levels of ER were used as a positive control ( 40-48 % ER positive cells by immunocytochemistry ; 200 fmol/mg protein by EIA ) .

<cell_line>Cultured MCF-7 cells</cell_line> , derived from a pleural effusion of a breast cancer patient , known to contain high levels of <protein>ER</protein> were used as a positive control ( 40-48 % <cell_type>ER positive cells</cell_type> by immunocytochemistry ; 200 fmol/mg protein by EIA ) .


All of the CLL cases except two ( 96 % ) were negative for ER ( less than 1 % staining ; less than 4 fmol/mg protein ) .

All of the CLL cases except two ( 96 % ) were negative for <protein>ER</protein> ( less than 1 % staining ; less than 4 fmol/mg protein ) .


The two positive cases expressed granular ER staining over the nucleus ( 9.2 and 12.1 % positive cells ) and were positive by EIA and SBA .

The two positive cases expressed granular <protein>ER</protein> staining over the nucleus ( 9.2 and 12.1 % positive cells ) and were positive by EIA and SBA .


It is concluded that ( i ) patients with CLL rarely express ER and ( ii ) immunocytochemical staining of cytospin preparations is a valid technique for the measurement of ER .

It is concluded that ( i ) patients with CLL rarely express <protein>ER</protein> and ( ii ) immunocytochemical staining of cytospin preparations is a valid technique for the measurement of <protein>ER</protein> .


It is of interest that one of the positive cases was diagnosed as CLL with Richter 's transformation confirming earlier findings .


Type-II estrogen binding sites in a lymphoblastoid cell line and growth-inhibitory effect of estrogen , anti-estrogen and bioflavonoids .

<protein>Type-II estrogen binding sites</protein> in a <cell_line>lymphoblastoid cell line</cell_line> and growth-inhibitory effect of estrogen , anti-estrogen and bioflavonoids .


Type-II estrogen-binding sites ( type-II EBS ) have been demonstrated in the human lymphoblastoid cell line IM-9 using a whole-cell assay with ( 6 , 7-3H ) estradiol ( 3H-E2 ) as tracer .

<protein>Type-II estrogen-binding sites</protein> ( <protein>type-II EBS</protein> ) have been demonstrated in the <cell_line>human lymphoblastoid cell line</cell_line> <cell_line>IM-9</cell_line> using a whole-cell assay with ( 6 , 7-3H ) estradiol ( 3H-E2 ) as tracer .


Competition analysis showed that the anti-estrogen tamoxifen and the flavonoids quercetin and rutin competed for ( 3H ) -E2 binding to type-II EBS .

Competition analysis showed that the anti-estrogen tamoxifen and the flavonoids quercetin and rutin competed for ( 3H ) -E2 binding to <protein>type-II EBS</protein> .


Growth experiments demonstrated that diethylstilbestrol ( DES ) tamoxifen ( TAM ) , quercetin and rutin exerted a reversible dose-dependent inhibition of cell proliferation in the range of concentrations between 10 nM and 10 microM .


The relative binding affinity of quercetin , rutin , DES and TAM for type-II EBS correlated well with their potency as cell growth inhibitors .

The relative binding affinity of quercetin , rutin , DES and TAM for <protein>type-II EBS</protein> correlated well with their potency as cell growth inhibitors .


Moreover , hesperidin , a flavonoid which does not bind to type-II EBS , was ineffective in inhibiting cell growth .

Moreover , hesperidin , a flavonoid which does not bind to <protein>type-II EBS</protein> , was ineffective in inhibiting cell growth .


Cell-cycle analysis showed that the growth-inhibitory effect of DES , TAM or quercetin was due to a blocking effect in the G0-G1 phases .


Our results suggest that high estrogen and anti-estrogen concentrations and flavonoids may regulate IM-9 cell growth through a common mechanism involving a binding interaction with type-II EBS .

Our results suggest that high estrogen and anti-estrogen concentrations and flavonoids may regulate <cell_line>IM-9</cell_line> cell growth through a common mechanism involving a binding interaction with <protein>type-II EBS</protein> .


[ Glucocorticoid receptors in peripheral blood lymphocytes of patients with bronchial asthma ]

[ <protein>Glucocorticoid receptors</protein> in <cell_type>peripheral blood lymphocytes</cell_type> of patients with bronchial asthma ]


Quantitation of glucocorticoid receptors ( GCR ) and the study of their affinity for glucocorticosteroids ( GCS ) were made in peripheral blood lymphocytes of bronchial asthma ( BA ) patients in consideration of GCR treatment and serum levels of endogenous cortisol .

Quantitation of <protein>glucocorticoid receptors</protein> ( <protein>GCR</protein> ) and the study of their affinity for glucocorticosteroids ( GCS ) were made in <cell_type>peripheral blood lymphocytes</cell_type> of bronchial asthma ( BA ) patients in consideration of <protein>GCR</protein> treatment and serum levels of endogenous cortisol .


It is stated that GCR of healthy controls and GCS-untreated patients outnumbered those of cortisol-dependent BA patients on hormone therapy .

It is stated that <protein>GCR</protein> of healthy controls and GCS-untreated patients outnumbered those of cortisol-dependent BA patients on hormone therapy .


Following discontinuation of glucocorticoid drugs GCR count in cortisol-dependent BA tends to rise .

Following discontinuation of glucocorticoid drugs <protein>GCR</protein> count in cortisol-dependent BA tends to rise .


Endogenous cortisol has no effect on GCR level estimated by 3H-triamcinolone acetonide .

Endogenous cortisol has no effect on <protein>GCR</protein> level estimated by 3H-triamcinolone acetonide .


Two glucocorticoid binding sites on the human glucocorticoid receptor .

Two <protein>glucocorticoid binding sites</protein> on the <protein>human glucocorticoid receptor</protein> .


Glucocorticoids are known to have a lytic effect in leukemic cells via interactions with the glucocorticoid receptor ( GR ) .

Glucocorticoids are known to have a lytic effect in <cell_type>leukemic cells</cell_type> via interactions with the <protein>glucocorticoid receptor</protein> ( <protein>GR</protein> ) .


Cortisol and various synthetic glucocorticoids bind to the GR with one-site kinetics .

Cortisol and various synthetic glucocorticoids bind to the <protein>GR</protein> with one-site kinetics .


Cortivazol ( CVZ ) is a unique , high potency synthetic glucocorticoid , which has a phenylpyrazol fused to the A-ring of the steroid nucleus and displays binding consistent with two or more sites in the cytosol from CEM C7 cells ( a human acute lymphoblastic T-cell line ) .

Cortivazol ( CVZ ) is a unique , high potency synthetic glucocorticoid , which has a phenylpyrazol fused to the A-ring of the steroid nucleus and displays binding consistent with two or more sites in the cytosol from <cell_line>CEM C7 cells</cell_line> ( a <cell_line>human acute lymphoblastic T-cell line</cell_line> ) .


It has previously been shown that the lower affinity class of sites are similar in affinity and site molarity to those recognized by dexamethasone .


The higher affinity sites bind CVZ with 20- to 50-fold greater affinity , consistent with CVZ 's enhanced biological effects .


In mutant leukemic cells resistant to the lytic effects of dexamethasone , CVZ both lyses the cells and recognizes a single class of sites similar to the high affinity site in CEM C7 cells .

In mutant <cell_type>leukemic cells</cell_type> resistant to the lytic effects of dexamethasone , CVZ both lyses the cells and recognizes a single class of sites similar to the high affinity site in <cell_line>CEM C7 cells</cell_line> .


We have carried out experiments to define the nature of the higher affinity CVZ binding site .

We have carried out experiments to define the nature of the <protein>higher affinity CVZ binding site</protein> .


We now show that : 1 ) CVZ has more than one binding site in a second , independent , B-cell line , IM-9 ; 2 ) the antiglucocorticoid RU 38486 is able to block both CVZ 's higher and lower affinity sites ; 3 ) all of CVZ 's binding sites are on a protein immunologically indistinguishable from the human GR ; and 4 ) freshly isolated clones of CVZ-resistant cells have lost all binding sites for CVZ .

We now show that : 1 ) CVZ has more than one binding site in a second , independent , <cell_line>B-cell line</cell_line> , <cell_line>IM-9</cell_line> ; 2 ) the antiglucocorticoid RU 38486 is able to block both CVZ 's higher and lower affinity sites ; 3 ) all of <protein>CVZ 's binding sites</protein> are on a protein immunologically indistinguishable from the human <protein>GR</protein> ; and 4 ) freshly isolated clones of CVZ-resistant cells have lost all binding sites for CVZ .


These data indicate that CVZ is recognizing two glucocorticoid binding sites on the human GR or a protein very similar to it .

These data indicate that CVZ is recognizing two <protein>glucocorticoid binding sites</protein> on the human <protein>GR</protein> or a protein very similar to it .


Retroviral mediated transfer and expression of exogenous genes in primary lymphoid cells : assaying for a viral transactivator activity in normal and malignant cells .

Retroviral mediated transfer and expression of <dna>exogenous genes</dna> in <cell_type>primary lymphoid cells</cell_type> : assaying for a viral <protein>transactivator</protein> activity in <cell_type>normal and malignant cells</cell_type> .


In this report we describe the use of recombinant retroviruses to characterize the activity of an exogenous promoter in primary cells obtained from patients with lymphoproliferative disorders .

In this report we describe the use of recombinant retroviruses to characterize the activity of an <dna>exogenous promoter</dna> in primary cells obtained from patients with lymphoproliferative disorders .


The infection of a variety of cultured and primary lymphoid cells with a recombinant retrovirus containing a histone promoter-driven beta-galactosidase gene is shown to result in the expression of beta-galactosidase in 50 % to 100 % of the cells .

The infection of a variety of cultured and <cell_type>primary lymphoid cells</cell_type> with a recombinant retrovirus containing a <dna>histone promoter-driven beta-galactosidase gene</dna> is shown to result in the expression of <protein>beta-galactosidase</protein> in 50 % to 100 % of the cells .


A similar infection with a recombinant retrovirus containing the beta-galactosidase gene with an adenovirus E2 promoter , results in beta-galactosidase activity in a limited number of cultured and primary cells .

A similar infection with a recombinant retrovirus containing the <dna>beta-galactosidase gene</dna> with an <dna>adenovirus E2 promoter</dna> , results in <protein>beta-galactosidase</protein> activity in a limited number of <cell_line>cultured</cell_line> and <cell_type>primary cells</cell_type> .


Since the adenovirus E2 promoter has been well characterized and is known to be regulated by transactivators encoded by many viruses , the activity of this promoter in specific cell types is discussed in reference to both the biology of the cell and the possible presence of as yet undetected viral gene products .

Since the <dna>adenovirus E2 promoter</dna> has been well characterized and is known to be regulated by <protein>transactivators</protein> encoded by many viruses , the activity of this promoter in specific cell types is discussed in reference to both the biology of the cell and the possible presence of as yet undetected <protein>viral gene products</protein> .


[ The effect of 24 , 25-dihydroxyvitamin D3 ( dioxyvit ) on Ca metabolism and immune status during chronic kidney failure ]


Active metabolite of vitamin D3 , 24R , 25 ( OH ) 2D3 ( dioxyvit ) was used at a daily dose of 100 micrograms in treatment of children affected with tubulointerstitial disease of kidney and with chronic glomerulonephritis under conditions of kidney insufficiency .


The drug exhibited distinct normalizing effect on patterns of calcium metabolism : increase of total and ionized Ca2+ and of 25-OHD , decrease in concentration of parath hormone and osteocalcine in blood serum as well as on immunological parameters : restoration of decreased content of T- and 0-lymphocytes .

The drug exhibited distinct normalizing effect on patterns of calcium metabolism : increase of total and ionized Ca2+ and of 25-OHD , decrease in concentration of parath hormone and osteocalcine in blood serum as well as on immunological parameters : restoration of decreased content of <cell_type>T- and 0-lymphocytes</cell_type> .


Concentration of receptors of hormonal form of 1 , 25 ( OH ) 2D3 was found to be minimal in lymphocytes under conditions of chronic kidney insufficiency , while their expression , after the dioxyvit action , was detected only in patients with glomerulonephritis .

Concentration of receptors of hormonal form of 1 , 25 ( OH ) 2D3 was found to be minimal in <cell_type>lymphocytes</cell_type> under conditions of chronic kidney insufficiency , while their expression , after the dioxyvit action , was detected only in patients with glomerulonephritis .


Specific calcitropic effect of dioxyvit with simultaneous correction of vitamin D deficiency were apparently responsible for high efficacy of the drug in treatment of calcium metabolism and immunity impairments in children with renal deteriorations at the step of chronic kidney insufficiency .


[ The role of glucocorticoid receptors and HLA antigens in the pathogenesis of Cushing 's syndrome ]

[ The role of <protein>glucocorticoid receptors</protein> and <protein>HLA antigens</protein> in the pathogenesis of Cushing 's syndrome ]


Lymphocytic levels of glucocorticoid receptors were evaluated in 114 patients suffering from Icenko-Cushing 's syndrome .

Lymphocytic levels of <protein>glucocorticoid receptors</protein> were evaluated in 114 patients suffering from Icenko-Cushing 's syndrome .


Incidence of HLA antigens was determined in 94 of them .

Incidence of <protein>HLA antigens</protein> was determined in 94 of them .


A significant rise of A10 and B27 antigen incidence compared to that in normal subjects allows these antigens to be considered genetic markers of Icenko-Cushing 's syndrome .

A significant rise of <protein>A10</protein> and <protein>B27 antigen</protein> incidence compared to that in normal subjects allows these antigens to be considered genetic markers of Icenko-Cushing 's syndrome .


The levels of glucocorticoid receptors in lymphocytes of the patients are lower than in normal subjects both in the active stage of the disease and following bilateral total adrenalectomy .

The levels of <protein>glucocorticoid receptors</protein> in <cell_type>lymphocytes</cell_type> of the patients are lower than in normal subjects both in the active stage of the disease and following bilateral total adrenalectomy .


The patients carrying B27 antigen had lymphocytic receptor concentrations under the levels of such in patients free of the antigen carriage .

The patients carrying <protein>B27 antigen</protein> had lymphocytic receptor concentrations under the levels of such in patients free of the antigen carriage .


Antigen B27 seems to be a cause of lower levels of glucocorticoid receptors in blood lymphocytes .

<protein>Antigen B27</protein> seems to be a cause of lower levels of <protein>glucocorticoid receptors</protein> in <cell_type>blood lymphocytes</cell_type> .


Effects of 1 alpha , 25-dihydroxyvitamin D3 on the human chronic myelogenous leukemia cell line RWLeu-4 .

Effects of 1 alpha , 25-dihydroxyvitamin D3 on the <cell_line>human chronic myelogenous leukemia cell line</cell_line> <cell_line>RWLeu-4</cell_line> .


The effects of 1 alpha , 25-dihydroxyvitamin D3 ( VD3 ) on proliferation , differentiation , and macromolecular synthesis in the new Philadelphia chromosome-positive chronic myelogenous leukemia cell line , RWLeu-4 , were investigated .

The effects of 1 alpha , 25-dihydroxyvitamin D3 ( VD3 ) on proliferation , differentiation , and macromolecular synthesis in the new <cell_line>Philadelphia chromosome-positive chronic myelogenous leukemia cell line</cell_line> , <cell_line>RWLeu-4</cell_line> , were investigated .


Binding of [ 3H ] VD3 was saturable , with approximately 2000-3000 sites/cell , and half-maximal binding occurring at 0.21-0.33 nM .


Treatment of RWLeu-4 cells with VD3 induced 24R-hydroxylase activity , a marker of vitamin D3 responsiveness in many tissues .

Treatment of <cell_line>RWLeu-4 cells</cell_line> with VD3 induced <protein>24R-hydroxylase</protein> activity , a marker of vitamin D3 responsiveness in many tissues .


Exposure of RWLeu-4 cells to VD3 also inhibited proliferation and DNA synthesis with a 50 % effective dose of 3.5-10 nM within 72 h ; in addition , protein and RNA synthesis were inhibited by VD3 treatment .

Exposure of <cell_line>RWLeu-4 cells</cell_line> to VD3 also inhibited proliferation and DNA synthesis with a 50 % effective dose of 3.5-10 nM within 72 h ; in addition , protein and RNA synthesis were inhibited by VD3 treatment .


Exposure of RWLeu-4 cells to 5 nM VD3 for 72 h caused 50 % of the cells to differentiate into macrophage/monocyte type cells as judged by nitroblue tetrazolium staining and adherence to plastic .

Exposure of <cell_line>RWLeu-4 cells</cell_line> to 5 nM VD3 for 72 h caused 50 % of the cells to differentiate into <cell_type>macrophage/monocyte type cells</cell_type> as judged by nitroblue tetrazolium staining and adherence to plastic .


Progressive expression of cell surface maturation-specific antigens of the monocyte/macrophage lineage was induced by treatment of RWLeu-4 cells with VD3 for 24 to 72 h at doses that inhibited cellular proliferation .

Progressive expression of <protein>cell surface maturation-specific antigens</protein> of the <cell_type>monocyte/macrophage lineage</cell_type> was induced by treatment of <cell_line>RWLeu-4 cells</cell_line> with VD3 for 24 to 72 h at doses that inhibited cellular proliferation .


c-myc RNA , which is constitutively expressed in RWLeu-4 cells , increased after 0.5 h of treatment with 50 nM VD3 and then rapidly decreased to barely detectable levels after 4 h of treatment .

<rna>c-myc RNA</rna> , which is constitutively expressed in <cell_line>RWLeu-4 cells</cell_line> , increased after 0.5 h of treatment with 50 nM VD3 and then rapidly decreased to barely detectable levels after 4 h of treatment .


Finally , the in vitro tyrosine kinase activity associated with the p210bcr-abl oncogene product was decreased approximately 50 % by VD3 treatment .

Finally , the in vitro tyrosine kinase activity associated with the <protein>p210bcr-abl oncogene product</protein> was decreased approximately 50 % by VD3 treatment .


Because of the presence of a functional receptor-effector system for VD3 and multiple biological responses to the hormone , these cells provide a unique model system with which to probe the specific effects of VD3 on cell growth and differentiation in chronic myelogenous leukemia .


A new member of the leucine zipper class of proteins that binds to the HLA DR alpha promoter .

A new member of the <protein>leucine zipper class</protein> of proteins that binds to the <dna>HLA DR alpha promoter</dna> .


Several mutants derived from transformed human B cell lines are defective in expressing major histocompatibility complex ( MHC ) class II genes .

Several mutants derived from <cell_line>transformed human B cell lines</cell_line> are defective in expressing <dna>major histocompatibility complex ( MHC ) class II genes</dna> .


The failure to express a class II gene in at least one such mutant line has been mapped to the MHC class II X box , a conserved transcriptional element in the promoter region .

The failure to express a <dna>class II gene</dna> in at least one such <cell_line>mutant line</cell_line> has been mapped to the <dna>MHC class II X box</dna> , a <dna>conserved transcriptional element</dna> in the <dna>promoter region</dna> .


A complementary DNA encoding a DNA-binding protein ( human X box binding protein , hXBP-1 ) whose target is the human DR alpha X box and the 3 ' flanking region has now been cloned .

A <dna>complementary DNA</dna> encoding a <protein>DNA-binding protein</protein> ( <protein>human X box binding protein</protein> , <protein>hXBP-1</protein> ) whose target is the <dna>human DR alpha X box</dna> and the <dna>3 ' flanking region</dna> has now been cloned .


This complementary DNA encoded a protein with structural similarities to the c-jun proto-oncogene product , and its target sequence was closely related to the palindromic target sequence of c-jun .

This <dna>complementary DNA</dna> encoded a protein with structural similarities to the <protein>c-jun proto-oncogene product</protein> , and its target sequence was closely related to the <dna>palindromic target sequence</dna> of <dna>c-jun</dna> .


Mutation of the hXBP-1 DNA target sequence decreased DR alpha promoter activity in vivo .

Mutation of the <dna>hXBP-1 DNA target sequence</dna> decreased <dna>DR alpha promoter</dna> activity in vivo .


These studies suggest that the hXBP-1 protein acts as a transcription factor in B cells .

These studies suggest that the <protein>hXBP-1 protein</protein> acts as a <protein>transcription factor</protein> in <cell_type>B cells</cell_type> .


Pseudohypoaldosteronism in eight families : different forms of inheritance are evidence for various genetic defects .


Pseudohypoaldosteronism is a rare hereditary disorder presenting in early infancy with renal salt loss leading to hyponatremia and hyperkalemia despite high levels of plasma aldosterone .


The patients are insensitive to mineralocorticoids ; however , sodium supplementation is able to correct electrolyte abnormalities .


Absent or greatly diminished type I aldosterone receptors in peripheral mononuclear leucocytes have been recently demonstrated and explain the lack of response to mineralocorticoids .

Absent or greatly diminished type <protein>I aldosterone receptors</protein> in <cell_type>peripheral mononuclear leucocytes</cell_type> have been recently demonstrated and explain the lack of response to mineralocorticoids .


We have studied the mode of inheritance in eight families with a total of nine patients .


There was evidence for an autosomal recessive form of inheritance in four families , while the other four families appeared to have an autosomal dominant mode of transmission .


In three families the autosomal recessive form was characterized by normal receptor as well as hormone data in both parents , while in one family receptor levels in both parents were greatly reduced , but hormone levels were normal .

In three families the autosomal recessive form was characterized by <protein>normal receptor</protein> as well as hormone data in both parents , while in one family receptor levels in both parents were greatly reduced , but hormone levels were normal .


In the four families with an autosomal dominant mode of transmission there was always one parent with reduced receptor binding in peripheral mononuclear leucocytes and elevated serum hormone levels .

In the four families with an autosomal dominant mode of transmission there was always one parent with reduced receptor binding in <cell_type>peripheral mononuclear leucocytes</cell_type> and elevated serum hormone levels .


These parents were entirely asymptomatic .


In an extended family we were able to study an aunt and her newborn daughter , who were both also biochemically affected but clinically asymptomatic .


It , therefore , appears that this dual pattern of genetic transmission may indicate differing genetic defects which cause the same clinical picture of pseudohypoaldosteronism .


Perceived social support and tumor estrogen/progesterone receptor status as predictors of natural killer cell activity in breast cancer patients .

Perceived social support and tumor <protein>estrogen/progesterone receptor</protein> status as predictors of <cell_type>natural killer cell</cell_type> activity in breast cancer patients .


This report is concerned with the prediction of natural killer ( NK ) cell activity in 61 Stage I and II breast cancer patients , between the ages of 25 and 70 , who were accrued to this project .

This report is concerned with the prediction of natural <cell_type>killer ( NK ) cell</cell_type> activity in 61 Stage I and II breast cancer patients , between the ages of 25 and 70 , who were accrued to this project .


All baseline interview and testing data were obtained either just before patients were discharged from the hospital , or at their first outpatient visit , within two weeks of discharge .


A major interest of this project is the predictive value of perceived social support , as a potential `` stress '' buffer , related to NK activity .


In the main model reported here , we found that a significant amount of NK activity variance could be explained by five variables .


Higher NK activity could be predicted by the perception of high quality emotional support from a spouse or intimate other , perceived social support from the patient 's physician , estrogen receptor -negative tumor status , having an excisional biopsy as surgical treatment , and actively seeking social support as a major coping strategy ( R2 = 0.33 , F ( 5 , 55 ) = 5.5 , p less than 0.0004 ) .

Higher NK activity could be predicted by the perception of high quality emotional support from a spouse or intimate other , perceived social support from the patient 's physician , <protein>estrogen receptor</protein> -negative tumor status , having an excisional biopsy as surgical treatment , and actively seeking social support as a major coping strategy ( R2 = 0.33 , F ( 5 , 55 ) = 5.5 , p less than 0.0004 ) .


Findings are discussed in terms of host interaction with tumor endocrine status , and the role that social support might play in modulating such activity .


[ Estrogen receptor content of peripheral blood lymphocytes in patients with systemic lupus erythematosus ]

[ <protein>Estrogen receptor</protein> content of <cell_type>peripheral blood lymphocytes</cell_type> in patients with systemic lupus erythematosus ]


ER content in lymphocytes of peripheral blood from 27 SLE patients and 20 healthy controls were determined by dextran-coated charcoal assay .

ER content in <cell_type>lymphocytes</cell_type> of peripheral blood from 27 SLE patients and 20 healthy controls were determined by dextran-coated charcoal assay .


ER content in lymphocytes of each sample was expressed by both fmol/mg of lymphocyte cytosolic protein and fmol/micrograms of lymphocyte DNA .

<protein>ER</protein> content in <cell_type>lymphocytes</cell_type> of each sample was expressed by both fmol/mg of <protein>lymphocyte cytosolic protein</protein> and fmol/micrograms of <dna>lymphocyte DNA</dna> .


The results showed that there was no significant difference between the ER content of lymphocytes from the controls and that from patients with SLE .

The results showed that there was no significant difference between the <protein>ER</protein> content of <cell_type>lymphocytes</cell_type> from the controls and that from patients with SLE .


But the logarithmic mean of ER content in lymphocytes , expressed by fmol/mg of cytosolic protein , in 14 patients with active SLE ( 0.9356 +/- 0.31 ) was significantly higher than that in 13 patients with inactive SLE ( 0.2979 +/- 0.23 , P less than 0.001 ) and in the controls ( 0.6204 +/- 0.52 , P less than 0.001 ) .

But the logarithmic mean of <protein>ER</protein> content in <cell_type>lymphocytes</cell_type> , expressed by fmol/mg of <protein>cytosolic protein</protein> , in 14 patients with active SLE ( 0.9356 +/- 0.31 ) was significantly higher than that in 13 patients with inactive SLE ( 0.2979 +/- 0.23 , P less than 0.001 ) and in the controls ( 0.6204 +/- 0.52 , P less than 0.001 ) .


The normal upper limit of ER content in lymphocytes , expressed by fmol/micrograms of DNA , was 0.136 .

The normal upper limit of <protein>ER</protein> content in <cell_type>lymphocytes</cell_type> , expressed by fmol/micrograms of DNA , was 0.136 .


The elevated rate of ER content in lymphocytes in 14 active SLE ( 92.9 % ) was also higher than that in quieiescent patients ( 23.1 % , P less than 0.001 ) and in the controls ( 10 % , P less than 0.001 ) .

The elevated rate of <protein>ER</protein> content in <cell_type>lymphocytes</cell_type> in 14 active SLE ( 92.9 % ) was also higher than that in quieiescent patients ( 23.1 % , P less than 0.001 ) and in the controls ( 10 % , P less than 0.001 ) .


Moreover , the elevated level of ER content was found to be related to the positive antidsDNA antibody and hypocomplementemia .

Moreover , the elevated level of <protein>ER</protein> content was found to be related to the positive <protein>antidsDNA antibody</protein> and hypocomplementemia .


An in vitro globin gene switching model based on differentiated embryonic stem cells .

An in vitro <dna>globin gene</dna> switching model based on <cell_type>differentiated embryonic stem cells</cell_type> .


We used mouse embryonic stem ( ES ) cells to study globin gene expression and switching in vitro .

We used <cell_type>mouse embryonic stem ( ES ) cells</cell_type> to study <dna>globin gene</dna> expression and switching in vitro .


We show that ES-derived embryoid bodies express the full complement of mouse embryonic globin genes in the correct temporal order and that on further differentiation , a switch occurs to the fetal/adult genes .

We show that <cell_type>ES-derived embryoid bodies</cell_type> express the full complement of <dna>mouse embryonic globin genes</dna> in the correct temporal order and that on further differentiation , a switch occurs to the <dna>fetal/adult genes</dna> .


In addition , the erythroid-specific transcription factor NF-E1 was shown to be expressed coordinately with that of globin in embryoid bodies .

In addition , the <protein>erythroid-specific transcription factor</protein> <protein>NF-E1</protein> was shown to be expressed coordinately with that of <protein>globin</protein> in <cell_type>embryoid bodies</cell_type> .


We conclude from these experiments that the ES cell system provides a good model to study hematopoietic development .


When the human epsilon- or beta-globin genes driven by the dominant control region ( DCR ) are introduced into this system , the human epsilon-globin gene , in contrast to the beta-globin gene , is not deregulated by the presence of the DCR and is expressed strictly as an embryonic gene .

When the <dna>human epsilon- or beta-globin genes</dna> driven by the <dna>dominant control region</dna> ( <dna>DCR</dna> ) are introduced into this system , the <dna>human epsilon-globin gene</dna> , in contrast to the <dna>beta-globin gene</dna> , is not deregulated by the presence of the <dna>DCR</dna> and is expressed strictly as an <dna>embryonic gene</dna> .


We conclude from this that the epsilon-globin gene is not regulated by competition with other genes in the human beta-globin locus .

We conclude from this that the <dna>epsilon-globin gene</dna> is not regulated by competition with other genes in the <dna>human beta-globin locus</dna> .


Cloning of a mitogen-inducible gene encoding a kappa B DNA-binding protein with homology to the rel oncogene and to cell-cycle motifs .

Cloning of a <dna>mitogen-inducible gene</dna> encoding a <protein>kappa B DNA-binding protein</protein> with homology to the <dna>rel oncogene</dna> and to <dna>cell-cycle motifs</dna> .


We have cloned and characterized a mitogen-inducible gene isolated from human T cells that predicts a protein of 968 amino acids .

We have cloned and characterized a <dna>mitogen-inducible gene</dna> isolated from <cell_type>human T cells</cell_type> that predicts a protein of <protein>968 amino acids</protein> .


The amino-terminal domain has regions homologous to the oncogene rel and to the developmentally important gene dorsal of Drosophila .

The <protein>amino-terminal domain</protein> has regions homologous to the <dna>oncogene rel</dna> and to the developmentally important gene <dna>dorsal</dna> of Drosophila .


The carboxy-terminal domain contains repeat structures found in a variety of proteins that are involved in cell-cycle control of yeast and in tissue differentiation in Drosophila and Ceanorhabditis elegans , as well as in the putative human oncogene bcl-3 and in the ankyrin protein .

The <protein>carboxy-terminal domain</protein> contains repeat structures found in a variety of proteins that are involved in cell-cycle control of yeast and in tissue differentiation in Drosophila and Ceanorhabditis elegans , as well as in the <dna>putative human oncogene bcl-3</dna> and in the <protein>ankyrin protein</protein> .


A truncated form of the product of this gene translated in vitro is a DNA-binding protein which interacts specifically with the kappa B binding site found in many inducible genes , including the enhancer in human immunodeficiency virus .

A truncated form of the product of this gene translated in vitro is a <protein>DNA-binding protein</protein> which interacts specifically with the <dna>kappa B binding site</dna> found in many <dna>inducible genes</dna> , including the enhancer in human immunodeficiency virus .


This gene is yet another in a growing list of important regulatory molecules whose expression is transcriptionally induced upon cellular activation .


Extrarenal receptor-effector-mechanisms for aldosterone : the sequence of effects on the cellular electrolyte transport in human lymphocytes and their implications for disorders of the water and electrolyte balances .

Extrarenal receptor-effector-mechanisms for aldosterone : the sequence of effects on the cellular electrolyte transport in <cell_type>human lymphocytes</cell_type> and their implications for disorders of the water and electrolyte balances .


High affinity aldosterone binding sites have not only been described in the classic target tissues such as the renal tubules , but also in non-classic target tissues such as the hippocampus , mammary gland , endothelial cells and , recently , human mononuclear leukocytes .

High affinity aldosterone binding sites have not only been described in the classic target tissues such as the renal tubules , but also in non-classic target tissues such as the hippocampus , mammary gland , <cell_type>endothelial cells</cell_type> and , recently , <cell_type>human mononuclear leukocytes</cell_type> .


An in vitro effect of aldosterone on intracellular sodium , potassium and calcium concentrations and cell volume was shown in human mononuclear leukocytes .

An in vitro effect of aldosterone on intracellular sodium , potassium and calcium concentrations and cell volume was shown in <cell_type>human mononuclear leukocytes</cell_type> .


In the absence of aldosterone , the intracellular Na+ , K+ and Ca2+ concentrations and the cell volume decreased significantly , but remained constant when aldosterone ( 1.4 nmol/l ) was added to the incubation medium .


These effects of aldosterone were blocked by the aldosterone antagonist canrenone ( 140 nmol/l ) .


The sodium/proton exchanger of the cell membrane could be identified as the primary target of the aldosterone action , possibly non-genomically mediated through membrane receptors .

The <protein>sodium/proton exchanger</protein> of the cell membrane could be identified as the primary target of the aldosterone action , possibly non-genomically mediated through <protein>membrane receptors</protein> .


The clinical significance of this model was underlined by the demonstration of absent or a decreased number of mineralocorticoid receptors and the lack of electrolyte response to aldosterone in human mononuclear leukocytes of patients with pseudohypoaldosteronism and aldosteronism .

The clinical significance of this model was underlined by the demonstration of absent or a decreased number of <protein>mineralocorticoid receptors</protein> and the lack of electrolyte response to aldosterone in <cell_type>human mononuclear leukocytes</cell_type> of patients with pseudohypoaldosteronism and aldosteronism .


Additionally , an abnormal effector mechanism could be demonstrated in human mononuclear leukocytes from essential hypertensives .

Additionally , an abnormal effector mechanism could be demonstrated in <cell_type>human mononuclear leukocytes</cell_type> from essential hypertensives .


These studies are the first to demonstrate the significance of extrarenal , nonepithelial mineralocorticoid receptors and the related effector mechanism in different disorders of the water and electrolyte balance in man .

These studies are the first to demonstrate the significance of <protein>extrarenal , nonepithelial mineralocorticoid receptors</protein> and the related effector mechanism in different disorders of the water and electrolyte balance in man .


Immunohistochemical study of steroid hormones and an estrogen binding assay in malignant soft tissue tumors .

Immunohistochemical study of steroid hormones and an estrogen binding assay in <cell_type>malignant soft tissue tumors</cell_type> .


Immunohistochemically , the immunoreaction against 5 steroid hormone anti-sera ( estradiol , estriol , cortisol , progesterone and testosterone ) was examined in 39 cases with the malignant soft tissue tumors ( fibrosarcoma : 8 , malignant fibrous histiocytoma : 6 , rhabdomyosarcoma : 10 , leiomyosarcoma : 10 , liposarcoma : 5 ) .

Immunohistochemically , the immunoreaction against 5 steroid hormone anti-sera ( estradiol , estriol , cortisol , progesterone and testosterone ) was examined in 39 cases with the <cell_type>malignant soft tissue tumors</cell_type> ( fibrosarcoma : 8 , malignant fibrous histiocytoma : 6 , rhabdomyosarcoma : 10 , leiomyosarcoma : 10 , liposarcoma : 5 ) .


Seventeen cases revealed distinct immunostaining against at least 1 of the 5 steroid hormones .


Immunostained tumor cells were more frequently distributed in the area where tumor cell infiltration was more invasive .

<cell_type>Immunostained tumor cells</cell_type> were more frequently distributed in the area where tumor cell infiltration was more invasive .


The majority of the positive cases occurred in female cases .


Furthermore , the existence of estrogen receptor ( estrogen binding activity ) was examined histochemically in 39 cases and it was detected in 8 .

Furthermore , the existence of <protein>estrogen receptor</protein> ( estrogen binding activity ) was examined histochemically in 39 cases and it was detected in 8 .


We concluded that steroid hormones might be closely related to tumor cell infiltration of some malignant soft tissue tumors .

We concluded that steroid hormones might be closely related to tumor cell infiltration of some <cell_type>malignant soft tissue tumors</cell_type> .


Involvement of cyclic AMP-dependent protein kinases in the signal transduction pathway for interleukin-1 .

Involvement of <protein>cyclic AMP-dependent protein kinases</protein> in the signal transduction pathway for <protein>interleukin-1</protein> .


Expression of a highly specific protein inhibitor for cyclic AMP-dependent protein kinases in interleukin-1 ( IL-1 ) -responsive cells blocked IL-1-induced gene transcription that was driven by the kappa immunoglobulin enhancer or the human immunodeficiency virus long terminal repeat .

Expression of a highly specific protein inhibitor for <protein>cyclic AMP-dependent protein kinases</protein> in <cell_line>interleukin-1 ( IL-1 ) -responsive cells</cell_line> blocked <dna>IL-1-induced gene</dna> transcription that was driven by the <dna>kappa immunoglobulin enhancer</dna> or the <dna>human immunodeficiency virus long terminal repeat</dna> .


This inhibitor did not affect protein kinase C -mediated gene transcription , suggesting that cyclic AMP-dependent protein kinases are involved in the signal transduction pathway for IL-1 in a number of responsive cell types .

This inhibitor did not affect <protein>protein kinase C</protein> -mediated gene transcription , suggesting that <protein>cyclic AMP-dependent protein kinases</protein> are involved in the signal transduction pathway for <protein>IL-1</protein> in a number of <cell_type>responsive cell types</cell_type> .


The Epstein-Barr virus ( EBV ) ORI1yt enhancer is not B-cell specific and does not respond synergistically to the EBV transcription factors R and Z .

The <dna>Epstein-Barr virus ( EBV ) ORI1yt enhancer</dna> is not B-cell specific and does not respond synergistically to the <protein>EBV transcription factors R and Z</protein> .


The Epstein-Barr virus DR promoter is located upstream of the PstI repeats , and in addition to the TATA box , it contains an upstream region ( positions -69 to -220 ) responsive to EB1 ( Z ) ( the BZLF1-encoded transcription factor ) and an enhancer with two functionally distinct domains , A and B .

The <dna>Epstein-Barr virus DR promoter</dna> is located upstream of the <dna>PstI repeats</dna> , and in addition to the <dna>TATA box</dna> , it contains an <dna>upstream region</dna> ( positions -69 to -220 ) responsive to <protein>EB1 ( Z )</protein> ( the <protein>BZLF1-encoded transcription factor</protein> ) and an <dna>enhancer</dna> with two functionally distinct domains , A and <dna>B</dna> .


Domain B has been described as a B-cell-specific EB1-responsive element ( P.M.Lieberman , J.M.Hardwick , and S.D.Hayward , J.Virol.63 : 3040-3050 , 1989 ) activated synergistically by EB1 and R , an EBV early product encoded by the open reading frame BRLF1 ( M.A. Cox , J.Leahy , and J.M.Hardwick , J.Virol.64 : 313-321 , 1990 ) .

<dna>Domain B</dna> has been described as a <dna>B-cell-specific EB1-responsive element</dna> ( P.M.Lieberman , J.M.Hardwick , and S.D.Hayward , J.Virol.63 : 3040-3050 , 1989 ) activated synergistically by <protein>EB1</protein> and <protein>R</protein> , an <protein>EBV early product</protein> encoded by the <dna>open reading frame BRLF1</dna> ( M.A. Cox , J.Leahy , and J.M.Hardwick , J.Virol.64 : 313-321 , 1990 ) .


We show here that domain B is an R-responsive element in HeLa cells and is therefore not an EB1-responsive B-cell-specific element .

We show here that <dna>domain B</dna> is an <dna>R-responsive element</dna> in <cell_line>HeLa cells</cell_line> and is therefore not an <dna>EB1-responsive B-cell-specific element</dna> .


However , there is an EB1-binding site ( ZRE-B ) located within the R-responsive enhancer region .

However , there is an <dna>EB1-binding site</dna> ( <dna>ZRE-B</dna> ) located within the <dna>R-responsive enhancer region</dna> .


ZRE-B can be deleted without affecting the R-dependent enhancer activity .

<dna>ZRE-B</dna> can be deleted without affecting the R-dependent enhancer activity .