We studied the effect of interleukin-4 ( IL-4 ) on the lipopolysaccharide ( LPS ) induction of two immediate early genes c-fos and c-jun .

We studied the effect of <protein>interleukin-4</protein> ( <protein>IL-4</protein> ) on the lipopolysaccharide ( LPS ) induction of two immediate early genes <dna>c-fos</dna> and <dna>c-jun</dna> .


These genes encode proteins that form the dimeric complex activator protein-1 ( AP-1 ) , which is active as a transcriptional factor .

These genes encode proteins that form the <protein>dimeric complex</protein> <protein>activator protein-1</protein> ( <protein>AP-1</protein> ) , which is active as a <protein>transcriptional factor</protein> .


Maximal accumulation of either c-fos and c-jun messenger RNA ( mRNA ) occurred 30 minutes after LPS addition .

Maximal accumulation of either <rna>c-fos and c-jun messenger RNA</rna> ( mRNA ) occurred 30 minutes after LPS addition .


When cells were treated with IL-4 for 5 hours before LPS activation , both the c-fos and the c-jun mRNA expression was decreased .

When cells were treated with <protein>IL-4</protein> for 5 hours before LPS activation , both the c-fos and the c-jun mRNA expression was decreased .


The inhibition of c-fos and c-jun expression by IL-4 in LPS-treated cells was shown to be due to a lower transcription rate of the c-fos and c-jun genes .

The inhibition of <dna>c-fos</dna> and c-jun expression by <protein>IL-4</protein> in <cell_type>LPS-treated cells</cell_type> was shown to be due to a lower transcription rate of the <dna>c-fos and c-jun genes</dna> .


IL-4 did not affect the stability of the c-fos and c-jun transcripts .

<protein>IL-4</protein> did not affect the stability of the <protein>c-fos</protein> and <protein>c-jun transcripts</protein> .


Finally , using electrophoretic mobility shift assays , evidence was obtained that IL-4 inhibits LPS-induced expression of AP-1 protein .

Finally , using electrophoretic mobility shift assays , evidence was obtained that <protein>IL-4</protein> inhibits LPS-induced expression of <protein>AP-1</protein> protein .


These data indicate that IL-4 suppresses the induction of transcription factors in human activated monocytes .

These data indicate that <protein>IL-4</protein> suppresses the induction of <protein>transcription factors</protein> in <cell_type>human activated monocytes</cell_type> .


Transient pseudohypoaldosteronism in obstructive renal disease with transient reduction of lymphocytic aldosterone receptors .

Transient pseudohypoaldosteronism in obstructive renal disease with transient reduction of <protein>lymphocytic aldosterone receptors</protein> .


Results in two affected infants .


We report two patients with transient pseudohypoaldosteronism due to obstructive renal disease .


Both patients presented with a salt-losing episode simulating adrenal insufficiency .


In one patient , transient reduction of aldosterone receptors could be documented , while in the second patient the clinical and biochemical parameters were consistent with transient pseudohypoaldosteronism .

In one patient , transient reduction of <protein>aldosterone receptors</protein> could be documented , while in the second patient the clinical and biochemical parameters were consistent with transient pseudohypoaldosteronism .


Aldosterone receptors were normal in both patients

<protein>Aldosterone receptors</protein> were normal in both patients


Aldosterone-specific membrane receptors and rapid non-genomic actions of mineralocorticoids .

<protein>Aldosterone-specific membrane receptors</protein> and rapid non-genomic actions of mineralocorticoids .


Functional studies in extrarenal , non-epithelial cells such as smooth muscle cells and more recently circulating human lymphocytes have provided increasing evidence that aldosterone produces not only classical genomic effects , but also rapid , non-genomic effects on transmembrane electrolyte movements .

Functional studies in <cell_type>extrarenal , non-epithelial cells</cell_type> such as <cell_type>smooth muscle cells</cell_type> and more recently <cell_type>circulating human lymphocytes</cell_type> have provided increasing evidence that aldosterone produces not only classical genomic effects , but also rapid , non-genomic effects on transmembrane electrolyte movements .


These involve activation of the sodium/proton exchanger of the cell membrane at very low , physiological concentrations of aldosterone with an acute onset within 1-2 min .

These involve activation of the <protein>sodium/proton exchanger</protein> of the cell membrane at very low , physiological concentrations of aldosterone with an acute onset within 1-2 min .


A second messenger cascade involved is the inositol 1 , 4 , 5-trisphosphate/calcium pathway which responds over the same rapid time course .


Such changes clearly can not be explained by genomic mechanisms , which are responsible for later effects than the membrane related rapid responses .


The mechanisms underlying these rapid effects of aldosterone on electrolytes have been extensively studied in human lymphocytes , which thus may represent valuable tools in the delineation of the receptor-effector mechanisms involved .

The mechanisms underlying these rapid effects of aldosterone on electrolytes have been extensively studied in <cell_type>human lymphocytes</cell_type> , which thus may represent valuable tools in the delineation of the receptor-effector mechanisms involved .


The unique characteristics of this new pathway for steroid action include its rapid time course , 10 , 000-fold selectivity for aldosterone over cortisol and the ineffectiveness of spironolactones , classical mineralocorticoid antagonists , as antagonists of the response .


Human immunodeficiency virus type 1 Nef protein inhibits NF-kappa B induction in human T cells .

<protein>Human immunodeficiency virus type 1 Nef protein</protein> inhibits <protein>NF-kappa B</protein> induction in <cell_type>human T cells</cell_type> .


Human immunodeficiency virus type 1 ( HIV-1 ) can establish a persistent and latent infection in CD4+ T lymphocytes ( W.C.Greene , N.Engl.J. Med.324 : 308-317 , 1991 ; S.M.Schnittman , M.C.Psallidopoulos , H.C. Lane , L.Thompson , M.Baseler , F.Massari , C.H.Fox , N.P.Salzman , and A.S.Fauci , Science 245 : 305-308 , 1989 ) .

Human immunodeficiency virus type 1 ( HIV-1 ) can establish a persistent and latent infection in <cell_type>CD4+ T lymphocytes</cell_type> ( W.C.Greene , N.Engl.J. Med.324 : 308-317 , 1991 ; S.M.Schnittman , M.C.Psallidopoulos , H.C. Lane , L.Thompson , M.Baseler , F.Massari , C.H.Fox , N.P.Salzman , and A.S.Fauci , Science 245 : 305-308 , 1989 ) .


Production of HIV-1 from latently infected cells requires host cell activation by T-cell mitogens ( T.Folks , D.M.Powell , M.M.Lightfoote , S.Benn , M.A. Martin , and A.S.Fauci , Science 231 : 600-602 , 1986 ; D.Zagury , J. Bernard , R.Leonard , R.Cheynier , M.Feldman , P.S.Sarin , and R.C. Gallo , Science 231 : 850-853 , 1986 ) .

Production of HIV-1 from latently infected cells requires host cell activation by <protein>T-cell mitogens</protein> ( T.Folks , D.M.Powell , M.M.Lightfoote , S.Benn , M.A. Martin , and A.S.Fauci , Science 231 : 600-602 , 1986 ; D.Zagury , J. Bernard , R.Leonard , R.Cheynier , M.Feldman , P.S.Sarin , and R.C. Gallo , Science 231 : 850-853 , 1986 ) .


This activation is mediated by the host transcription factor NF-kappa B [ G.Nabel and D.Baltimore , Nature ( London ) 326 : 711-717 , 1987 ] .

This activation is mediated by the <protein>host transcription factor</protein> <protein>NF-kappa B</protein> [ G.Nabel and D.Baltimore , Nature ( London ) 326 : 711-717 , 1987 ] .


We report here that the HIV-1-encoded Nef protein inhibits the induction of NF-kappa B DNA-binding activity by T- cell mitogens .

We report here that the <protein>HIV-1-encoded Nef protein</protein> inhibits the induction of <protein>NF-kappa B</protein> DNA-binding activity by <protein>T- cell mitogens</protein> .


However , Nef does not affect the DNA-binding activity of other transcription factors implicated in HIV-1 regulation , including SP-1 , USF , URS , and NF-AT .

However , <protein>Nef</protein> does not affect the DNA-binding activity of other <protein>transcription factors</protein> implicated in HIV-1 regulation , including <protein>SP-1</protein> , <protein>USF</protein> , <protein>URS</protein> , and <protein>NF-AT</protein> .


Additionally , Nef inhibits the induction of HIV-1- and interleukin 2-directed gene expression , and the effect on HIV-1 transcription depends on an intact NF-kappa B-binding site .

Additionally , <protein>Nef</protein> inhibits the induction of HIV-1- and interleukin 2-directed gene expression , and the effect on HIV-1 transcription depends on an intact <dna>NF-kappa B-binding site</dna> .


These results indicate that defective recruitment of NF-kappa B may underlie Nef 's negative transcriptional effects on the HIV-1 and interleukin 2 promoters .

These results indicate that defective recruitment of <protein>NF-kappa B</protein> may underlie <protein>Nef</protein> 's negative transcriptional effects on the <dna>HIV-1 and interleukin 2 promoters</dna> .


Further evidence suggests that Nef inhibits NF-kappa B induction by interfering with a signal derived from the T-cell receptor complex .

Further evidence suggests that <protein>Nef</protein> inhibits <protein>NF-kappa B</protein> induction by interfering with a signal derived from the <protein>T-cell receptor complex</protein> .


Expression of c-fos , c-jun and jun B in peripheral blood lymphocytes from young and elderly adults .

Expression of <dna>c-fos</dna> , <dna>c-jun</dna> and <dna>jun B</dna> in peripheral blood lymphocytes from young and elderly adults .


The expression of c-fos , c-jun and jun B proto-oncogenes was studied in phytohemagglutinin ( PHA ) activated peripheral blood lymphocytes ( PBL ) from young and aged humans .

The expression of <dna>c-fos , c-jun and jun B proto-oncogenes</dna> was studied in <cell_line>phytohemagglutinin ( PHA ) activated peripheral blood lymphocytes</cell_line> ( <cell_type>PBL</cell_type> ) from young and aged humans .


Specific mRNAs for c-fos and c-jun were detectable within 30 min after cell activation and reached maximal levels within 2 h .

Specific <rna>mRNAs</rna> for <dna>c-fos</dna> and <dna>c-jun</dna> were detectable within 30 min after cell activation and reached maximal levels within 2 h .


Both c-fos and jun B mRNAs decreased to pre-activation levels within 6 h , while c-jun mRNA remained elevated .

Both <rna>c-fos and jun B mRNAs</rna> decreased to pre-activation levels within 6 h , while <rna>c-jun mRNA</rna> remained elevated .


In PHA-activated PBL , no age-related differences were observed in c-fos or jun B mRNA expression .

In <cell_line>PHA-activated PBL</cell_line> , no age-related differences were observed in c-fos or jun B mRNA expression .


However , c-jun mRNA levels decreased significantly ( 1.73 +/- 0.08 vs. 1.16 +/- 0.09 arbitrary units , P < 0.01 , young vs. old ) in PBL from elderly individuals activated with PHA .

However , <rna>c-jun mRNA</rna> levels decreased significantly ( 1.73 +/- 0.08 vs. 1.16 +/- 0.09 arbitrary units , P < 0.01 , young vs. old ) in <cell_type>PBL</cell_type> from elderly individuals activated with <protein>PHA</protein> .


Because previous work has demonstrated that T cells from elderly individuals may display normal proliferative responses when activated via the anti-CD2 pathway , c-jun and jun B mRNA expression was also studied in anti-CD2-activated purified T cells .

Because previous work has demonstrated that <cell_type>T cells</cell_type> from elderly individuals may display normal proliferative responses when activated via the <protein>anti-CD2</protein> pathway , c-jun and jun B mRNA expression was also studied in <cell_line>anti-CD2-activated purified T cells</cell_line> .


No age-related differences were found in the expression of either of these two proto-oncogenes by anti-CD2 activated T cells .

No age-related differences were found in the expression of either of these two <dna>proto-oncogenes</dna> by anti-CD2 activated T cells .


These results suggest that the decreased IL-2 production and proliferative response displayed by PHA-activated PBL from elderly adults may be related to age-related changes in c-jun mRNA expression and in the ratio of c-fos to c-jun mRNA .

These results suggest that the decreased <protein>IL-2</protein> production and proliferative response displayed by <cell_line>PHA-activated PBL</cell_line> from elderly adults may be related to age-related changes in <rna>c-jun mRNA</rna> expression and in the ratio of c-fos to <rna>c-jun mRNA</rna> .


Oct2 transactivation from a remote enhancer position requires a B-cell-restricted activity .

<protein>Oct2</protein> transactivation from a <dna>remote enhancer position</dna> requires a B-cell-restricted activity .


Previous cotransfection experiments had demonstrated that ectopic expression of the lymphocyte-specific transcription factor Oct2 could efficiently activate a promoter containing an octamer motif .

Previous cotransfection experiments had demonstrated that ectopic expression of the <protein>lymphocyte-specific transcription factor</protein> <protein>Oct2</protein> could efficiently activate a <dna>promoter</dna> containing an octamer motif .


Oct2 expression was unable to stimulate a multimerized octamer enhancer element in HeLa cells , however .

<protein>Oct2</protein> expression was unable to stimulate a <dna>multimerized octamer enhancer element</dna> in <cell_line>HeLa cells</cell_line> , however .


We have tested a variety of Oct2 isoforms generated by alternative splicing for the capability to activate an octamer enhancer in nonlymphoid cells and a B-cell line .

We have tested a variety of <protein>Oct2 isoforms</protein> generated by alternative splicing for the capability to activate an <dna>octamer enhancer</dna> in <cell_type>nonlymphoid cells</cell_type> and a <cell_line>B-cell line</cell_line> .


Our analyses show that several Oct2 isoforms can stimulate from a remote position but that this stimulation is restricted to B cells .

Our analyses show that several <protein>Oct2 isoforms</protein> can stimulate from a remote position but that this stimulation is restricted to <cell_type>B cells</cell_type> .


This result indicates the involvement of either a B-cell-specific cofactor or a specific modification of a cofactor or the Oct2 protein in Oct2 -mediated enhancer activation .

This result indicates the involvement of either a <protein>B-cell-specific cofactor</protein> or a specific modification of a <protein>cofactor</protein> or the <protein>Oct2 protein</protein> in <protein>Oct2</protein> -mediated enhancer activation .


Mutational analyses indicate that the carboxy-terminal domain of Oct2 is critical for enhancer activation .

Mutational analyses indicate that the <protein>carboxy-terminal domain</protein> of <protein>Oct2</protein> is critical for enhancer activation .


Moreover , this domain conferred enhancing activity when fused to the Oct1 protein , which by itself was unable to stimulate from a remote position .

Moreover , this domain conferred enhancing activity when fused to the <protein>Oct1 protein</protein> , which by itself was unable to stimulate from a remote position .


The glutamine-rich activation domain present in the amino-terminal portion of Oct2 and the POU domain contribute only marginally to the transactivation function from a distal position .

The <protein>glutamine-rich activation domain</protein> present in the <protein>amino-terminal portion of Oct2</protein> and the <protein>POU domain</protein> contribute only marginally to the transactivation function from a distal position .


The promoter of the CD19 gene is a target for the B-cell-specific transcription factor BSAP .

The <dna>promoter</dna> of the <dna>CD19 gene</dna> is a target for the <protein>B-cell-specific transcription factor</protein> <protein>BSAP</protein> .


The CD19 protein is expressed on the surface of all B-lymphoid cells with the exception of terminally differentiated plasma cells and has been implicated as a signal-transducing receptor in the control of proliferation and differentiation .

The <protein>CD19 protein</protein> is expressed on the surface of all <cell_type>B-lymphoid cells</cell_type> with the exception of <cell_type>terminally differentiated plasma cells</cell_type> and has been implicated as a signal-transducing receptor in the control of proliferation and differentiation .


Here we demonstrate complete correlation between the expression pattern of the CD19 gene and the B-cell-specific transcription factor BSAP in a large panel of B-lymphoid cell lines .

Here we demonstrate complete correlation between the expression pattern of the <dna>CD19 gene</dna> and the <protein>B-cell-specific transcription factor</protein> <protein>BSAP</protein> in a large panel of <cell_line>B-lymphoid cell lines</cell_line> .


The human CD19 gene has been cloned , and several BSAP-binding sites have been mapped by in vitro protein-DNA binding studies .

The <dna>human CD19 gene</dna> has been cloned , and several <dna>BSAP-binding sites</dna> have been mapped by in vitro protein-DNA binding studies .


In particular , a high-affinity BSAP-binding site instead of a TATA sequence is located in the -30 promoter region upstream of a cluster of heterogeneous transcription start sites .

In particular , a <dna>high-affinity BSAP-binding site</dna> instead of a <dna>TATA sequence</dna> is located in the <dna>-30 promoter region</dna> upstream of a cluster of heterogeneous transcription start sites .


Moreover , this site is occupied by BSAP in vivo in a CD19-expressing B-cell line but not in plasma or HeLa cells .

Moreover , this site is occupied by <protein>BSAP</protein> in vivo in a <cell_line>CD19-expressing B-cell line</cell_line> but not in <cell_type>plasma</cell_type> or <cell_line>HeLa cells</cell_line> .


This high-affinity site has been conserved in the promoters of both human and mouse CD19 genes and was furthermore shown to confer B-cell specificity to a beta-globin reporter gene in transient transfection experiments .

This <dna>high-affinity site</dna> has been conserved in the <dna>promoters</dna> of both <dna>human and mouse CD19 genes</dna> and was furthermore shown to confer B-cell specificity to a beta-globin reporter gene in transient transfection experiments .


In addition , BSAP was found to be the only abundant DNA-binding activity of B-cell nuclear extracts that interacts with the CD19 promoter .

In addition , <protein>BSAP</protein> was found to be the only abundant DNA-binding activity of B-cell nuclear extracts that interacts with the <dna>CD19 promoter</dna> .


Together , this evidence strongly implicates BSAP in the regulation of the CD19 gene .

Together , this evidence strongly implicates <protein>BSAP</protein> in the regulation of the <dna>CD19 gene</dna> .


Eicosanoids in breast cancer patients before and after mastectomy .


In 19 patients with a malignant breast tumor , tumor tissue and blood were taken to determine the eicosanoid profile and platelet aggregation .

In 19 patients with a malignant breast tumor , tumor tissue and blood were taken to determine the eicosanoid profile and <cell_type>platelet</cell_type> aggregation .


Values were compared with those of patients with benign tumors ( n = 4 ) , or undergoing a mammary reduction ( n = 7 ) .


Postoperatively , blood was taken as well in order to compare pre- and postoperative values .


Eicosanoids were measured in peripheral blood monocytes and mammary tissue by means of HPLC ; furthermore , TXA2 , 6-keto-PGF1 alpha , and PGE2 were determined by RIA .

Eicosanoids were measured in <cell_type>peripheral blood monocytes</cell_type> and mammary tissue by means of HPLC ; furthermore , TXA2 , 6-keto-PGF1 alpha , and PGE2 were determined by RIA .


Differences in pre- and postoperative values of cancer patients were seen in plasma RIA values : PGE2 and 6-k-PGF1 alpha were significantly higher preoperatively when compared with postoperatively , however , such differences were seen in the control groups as well .


Compared to benign tumor or mammary reduction test material the eicosanoid profile of tissue obtained from malignant mammary tumors showed important differences .


Except for PGF2 alpha , HHT and 15-HETE no detectable quantities of eicosanoids were found in the non-tumor material , whereas in the malignant tumor material substantial quantities of a number of eicosanoid metabolites were present .


Statistically significant correlations could be established between patient/histopathology data and the results of the platelet aggregation assays , e.g. between menopausal status and ADP aggregation ; oestrogen receptor ( +/- ) and collagen and arachidonic acid aggregation , inflammatory cell infiltration score and arachidonic acid aggregation and fibrosis score and ADP aggregation .

Statistically significant correlations could be established between patient/histopathology data and the results of the <cell_type>platelet</cell_type> aggregation assays , e.g. between menopausal status and ADP aggregation ; <protein>oestrogen receptor</protein> ( +/- ) and <protein>collagen</protein> and arachidonic acid aggregation , inflammatory cell infiltration score and arachidonic acid aggregation and fibrosis score and ADP aggregation .


The results show that eicosanoid synthesis in material from mammary cancer patients is different from that in benign mammary tissue .


The implications , in particular , in relation to future prognosis of the patient , remain obscure .


Mineralocorticoids and mineralocorticoid receptors in mononuclear leukocytes in patients with pregnancy-induced hypertension .

Mineralocorticoids and <protein>mineralocorticoid receptors</protein> in <cell_type>mononuclear leukocytes</cell_type> in patients with pregnancy-induced hypertension .


To examine the role of mineralocorticoids in the pathophysiology of pregnancy-induced hypertension ( PIH ) , we studied plasma aldosterone and 18-hydroxycorticosterone levels in 25 women with PIH and 25 normal pregnant women , as controls .


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

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


MR count was significantly ( P less than 0.0005 ) decreased in the PIH group ( 148 +/- 9 binding sites/cell ) compared with the control group ( 300 +/- 17 binding sites/cell ; mean +/- SEM ) .

<protein>MR</protein> count was significantly ( P less than 0.0005 ) decreased in the PIH group ( 148 +/- 9 binding sites/cell ) compared with the control group ( 300 +/- 17 binding sites/cell ; mean +/- SEM ) .


Plasma aldosterone in women with PIH was 281 +/- 61 pmol/L ; in normal pregnant women it was 697 +/- 172 pmol/L ( P less than 0.025 ) .


Plasma 18-hydroxycorticosterone was also significantly ( P less than 0.025 ) lower ( PIH , 1071 +/- 149 pmol/L ; controls , 1907 +/- 318 pmol/L ) .


These values were determined at the onset of clinical symptoms of PIH .


These results can not be explained by receptor down-regulation due to higher levels of mineralocorticoids in PIH ; a hitherto unknown mineralocorticoid may , thus , be responsible for the hypertension and altered MR status .

These results can not be explained by receptor down-regulation due to higher levels of mineralocorticoids in PIH ; a hitherto unknown mineralocorticoid may , thus , be responsible for the hypertension and altered <protein>MR</protein> status .


Structure function analysis of vitamin D analogs with C-ring modifications .


Analogs of 1 alpha , 25-dihydroxyvitamin D3 ( 1 alpha , 25- ( OH ) 2D3 ) with substitutions on C-11 were synthesized .


Small apolar substitutions ( 11 alpha-methyl , 11 alpha-fluoromethyl ) did not markedly decrease the affinity for the vitamin D receptor , but larger ( 11 alpha-chloromethyl or 11 alpha- or 11 beta-phenyl ) or more polar substitutions ( 11 alpha-hydroxymethyl , 11 alpha- ( 2-hydroxyethyl ] decreased the affinity to less than 5 % of that of 1 alpha , 25-OH ) 2D3 .

Small apolar substitutions ( 11 alpha-methyl , 11 alpha-fluoromethyl ) did not markedly decrease the affinity for the <protein>vitamin D receptor</protein> , but larger ( 11 alpha-chloromethyl or 11 alpha- or 11 beta-phenyl ) or more polar substitutions ( 11 alpha-hydroxymethyl , 11 alpha- ( 2-hydroxyethyl ] decreased the affinity to less than 5 % of that of 1 alpha , 25-OH ) 2D3 .


Their affinity for the vitamin D-binding protein , however , increased up to 4-fold .

Their affinity for the <protein>vitamin D-binding protein</protein> , however , increased up to 4-fold .


The biological activity of 11 alpha-methyl-1 alpha , 25- ( OH ) 2D3 closely resembled that of the natural hormone on normal and leukemic cell proliferation and bone resorption , whereas its in vivo effect on calcium metabolism of the rachitic chick was about 50 % of that of 1 alpha , 25- ( OH ) 2D3 .

The biological activity of 11 alpha-methyl-1 alpha , 25- ( OH ) 2D3 closely resembled that of the natural hormone on normal and <cell_type>leukemic cell</cell_type> proliferation and bone resorption , whereas its in vivo effect on calcium metabolism of the rachitic chick was about 50 % of that of 1 alpha , 25- ( OH ) 2D3 .


The 11 beta-methyl analog had a greater than 10-fold lower activity .


The differentiating effects of the other C-11 analogs on human promyeloid leukemia cells ( HL-60 ) agreed well with their bone-resorbing activity and receptor affinity , but they demonstrated lower calcemic effects in vivo .

The differentiating effects of the other C-11 analogs on <cell_line>human promyeloid leukemia cells</cell_line> ( <cell_line>HL-60</cell_line> ) agreed well with their bone-resorbing activity and receptor affinity , but they demonstrated lower calcemic effects in vivo .


Large or polar substitutions on C-11 of 1 alpha , 25- ( OH ) 2D3 thus impair the binding of the vitamin D receptor but increase the affinity to vitamin D-binding protein .

Large or polar substitutions on C-11 of 1 alpha , 25- ( OH ) 2D3 thus impair the binding of the <protein>vitamin D receptor</protein> but increase the affinity to <protein>vitamin D-binding protein</protein> .


The effects of many C-11-substituted 1 alpha , 25- ( OH ) 2D3 analogs on HL-60 cell differentiation exceeded their activity on calcium metabolism .

The effects of many C-11-substituted 1 alpha , 25- ( OH ) 2D3 analogs on <cell_line>HL-60</cell_line> cell differentiation exceeded their activity on calcium metabolism .


Glucocorticoid receptor binding in three different cell types in major depressive disorder : lack of evidence of receptor binding defect .

<protein>Glucocorticoid receptor</protein> binding in three different cell types in major depressive disorder : lack of evidence of receptor binding defect .


1 .


In order to further understand the apparent glucocorticoid resistance in major depressive disorder , circadian variation in cortisol concentration , dexamethasone suppression and glucocorticoid receptor binding in mononuclear leukocytes , polymorphonuclear leukocytes and cultured skin fibroblasts were measured in rigidly defined major depressive disorder patients and non-depressed psychiatric controls .

In order to further understand the apparent glucocorticoid resistance in major depressive disorder , circadian variation in cortisol concentration , dexamethasone suppression and glucocorticoid receptor binding in <cell_type>mononuclear leukocytes</cell_type> , <cell_type>polymorphonuclear leukocytes</cell_type> and <cell_line>cultured skin fibroblasts</cell_line> were measured in rigidly defined major depressive disorder patients and non-depressed psychiatric controls .


2 .


Mononuclear leukocytes binding to glucocorticoid correlated significantly with polymorphonuclear leukocytes binding to glucocorticoid , but both determinations failed to differentiate major depressive disorder and control subjects .

<cell_type>Mononuclear leukocytes</cell_type> binding to glucocorticoid correlated significantly with <cell_type>polymorphonuclear leukocytes</cell_type> binding to glucocorticoid , but both determinations failed to differentiate major depressive disorder and control subjects .


3 .


Initial and post-dexamethasone in vitro fibroblast binding to glucocorticoid was not different between major depressive disorder and non-depressed control subjects .


4 .


The phenomenon of glucocorticoid resistance in major depressive disorder remains unexplained .


High affinity aldosterone binding to plasma membrane rich fractions from mononuclear leukocytes : is there a membrane receptor for mineralocorticoids ?

High affinity aldosterone binding to plasma membrane rich fractions from <cell_type>mononuclear leukocytes</cell_type> : is there a <protein>membrane receptor</protein> for mineralocorticoids ?


In vitro effects of aldosterone on the intracellular concentrations of sodium , potassium and calcium , cell volume and the sodium-proton-antiport have been described in intact human mononuclear leukocytes ( HML ) .

In vitro effects of aldosterone on the intracellular concentrations of sodium , potassium and calcium , cell volume and the <protein>sodium-proton-antiport</protein> have been described in intact <cell_type>human mononuclear leukocytes</cell_type> ( <cell_type>HML</cell_type> ) .


In the present paper , the binding of a [ 125I ] -labeled aldosterone derivative to plasma membrane rich fractions of HML was studied .

In the present paper , the binding of a [ 125I ] -labeled aldosterone derivative to plasma membrane rich fractions of <cell_type>HML</cell_type> was studied .


High affinity binding of the radioligand with an apparent Kd of approximately 0.1 nM was found .


Aldosterone displaced the tracer at a similar Kd .


Both canrenone and cortisol were inactive as ligands up to concentrations of 0.1 microM .


The findings are the first to demonstrate membrane binding sites with a high affinity for aldosterone , but not for cortisol .


These data are perfectly compatible with major properties of steroidal effects on the sodium-proton-antiport in HML and thus very likely represent membrane receptors for aldosterone .

These data are perfectly compatible with major properties of steroidal effects on the <protein>sodium-proton-antiport</protein> in <cell_type>HML</cell_type> and thus very likely represent <protein>membrane receptors</protein> for aldosterone .


Natural variants of the HIV-1 long terminal repeat : analysis of promoters with duplicated DNA regulatory motifs .

Natural variants of the <dna>HIV-1 long terminal repeat</dna> : analysis of <dna>promoters</dna> with duplicated <dna>DNA regulatory motifs</dna> .


Sequence variation in the long terminal repeat ( LTR ) region of HIV-1 was analyzed in viral isolates of 17 infected individuals .

Sequence variation in the <dna>long terminal repeat ( LTR ) region</dna> of HIV-1 was analyzed in viral isolates of 17 infected individuals .


Two classes of LTR size variants were found .


One HIV-1 variant was detected containing an additional binding site for the transcription factor Sp1 .


Another LTR size variation was observed in four patients in a region just upstream of the NF-kappa B enhancer .

Another <dna>LTR size variation</dna> was observed in four patients in a region just upstream of the <dna>NF-kappa B enhancer</dna> .


This variation was the result of a duplication of a short DNA sequence ( CTG-motif ) .

This variation was the result of a duplication of a <dna>short DNA sequence</dna> ( <dna>CTG-motif</dna> ) .


Cell culture experiments demonstrated that the natural variant with four Sp1 sites had a slightly higher promoter activity and viral replication rate than the isogenic control LTR with three Sp1 sites .

Cell culture experiments demonstrated that the natural variant with four <dna>Sp1 sites</dna> had a slightly higher promoter activity and viral replication rate than the <dna>isogenic control LTR</dna> with three <dna>Sp1 sites</dna> .


No positive effect of the duplicated CTG-motif could be detected .

No positive effect of the duplicated <dna>CTG-motif</dna> could be detected .


In order to measure small differences in virus production more accurately , equal amounts of a size variant and the wild-type plasmid were cotransfected into T-cells .

In order to measure small differences in virus production more accurately , equal amounts of a size variant and the <dna>wild-type plasmid</dna> were cotransfected into <cell_type>T-cells</cell_type> .


The virus with four Sp1 sites did outgrow the three Sp1 virus in 35 days of culture and CTG-monomer virus outcompeted the CTG-dimer virus in 42 days .


Based on these results we estimate a 5-10 % difference in virus production of the LTR variants when compared to that of wild-type .

Based on these results we estimate a 5-10 % difference in virus production of the <dna>LTR variants</dna> when compared to that of wild-type .


A novel B cell-derived coactivator potentiates the activation of immunoglobulin promoters by octamer-binding transcription factors .

A <protein>novel B cell-derived coactivator</protein> potentiates the activation of <dna>immunoglobulin promoters</dna> by <protein>octamer-binding transcription factors</protein> .


A novel B cell-restricted activity , required for high levels of octamer / Oct -dependent transcription from an immunoglobulin heavy chain ( IgH ) promoter , was detected in an in vitro system consisting of HeLa cell -derived extracts complemented with fractionated B cell nuclear proteins .

A novel B cell-restricted activity , required for high levels of <dna>octamer</dna> / <dna>Oct</dna> -dependent transcription from an <dna>immunoglobulin heavy chain ( IgH ) promoter</dna> , was detected in an in vitro system consisting of <cell_line>HeLa cell</cell_line> -derived extracts complemented with <protein>fractionated B cell nuclear proteins</protein> .


The factor responsible for this activity was designated Oct coactivator from B cells ( OCA-B ) .

The factor responsible for this activity was designated <protein>Oct coactivator</protein> from <cell_type>B cells</cell_type> ( <protein>OCA-B</protein> ) .


OCA-B stimulates the transcription from an IgH promoter in conjunction with either Oct-1 or Oct-2 but shows no significant effect on the octamer / Oct -dependent transcription of the ubiquitously expressed histone H2B promoter and the transcription of USF- and Sp1-regulated promoters .

<protein>OCA-B</protein> stimulates the transcription from an <dna>IgH promoter</dna> in conjunction with either <protein>Oct-1</protein> or <protein>Oct-2</protein> but shows no significant effect on the <dna>octamer</dna> / <dna>Oct</dna> -dependent transcription of the <dna>ubiquitously expressed histone H2B promoter</dna> and the transcription of <dna>USF- and Sp1-regulated promoters</dna> .


Taken together , our results suggest that OCA-B is a tissue- , promoter- , and factor-specific coactivator and that OCA-B may be a major determinant for B cell-specific activation of immunoglobulin promoters .

Taken together , our results suggest that <protein>OCA-B</protein> is a <protein>tissue- , promoter- , and factor-specific coactivator</protein> and that <protein>OCA-B</protein> may be a major determinant for B cell-specific activation of <dna>immunoglobulin promoters</dna> .


In light of the evidence showing physical and functional interactions between Oct factors and OCA-B , we propose a mechanism of action for OCA-B and discuss the implications of OCA-B for the transcriptional regulation of other tissue-specific promoters .

In light of the evidence showing physical and functional interactions between <protein>Oct factors</protein> and <protein>OCA-B</protein> , we propose a mechanism of action for <protein>OCA-B</protein> and discuss the implications of <protein>OCA-B</protein> for the transcriptional regulation of other <dna>tissue-specific promoters</dna> .


SCL and related hemopoietic helix-loop-helix transcription factors .

<protein>SCL</protein> and related <protein>hemopoietic helix-loop-helix transcription factors</protein> .


The helix-loop-helix ( HLH ) proteins are a family of transcription factors that include proteins critical to differentiation and development in species ranging from plants to mammals .

The <protein>helix-loop-helix ( HLH ) proteins</protein> are a family of <protein>transcription factors</protein> that include proteins critical to differentiation and development in species ranging from plants to mammals .


Five members of this family ( MYC , SCL , TAL-2 , LYL-1 and E2A ) are implicated in oncogenic events in human lymphoid tumors because of their consistent involvement in chromosomal translocations .

Five members of this family ( <protein>MYC</protein> , <protein>SCL</protein> , <protein>TAL-2</protein> , <protein>LYL-1</protein> and <protein>E2A</protein> ) are implicated in oncogenic events in human lymphoid tumors because of their consistent involvement in chromosomal translocations .


Although activated in T cell leukemias , expression of SCL and LYL-1 is low or undetectable in normal T cell populations .

Although activated in T cell leukemias , expression of <protein>SCL</protein> and <protein>LYL-1</protein> is low or undetectable in <cell_type>normal T cell populations</cell_type> .


SCL is expressed in erythroid , megakaryocyte and mast cell populations ( the same cell lineages as GATA-1 , a zinc-finger transcription factor ) .

<protein>SCL</protein> is expressed in <cell_type>erythroid , megakaryocyte and mast cell populations</cell_type> ( the same cell lineages as <protein>GATA-1</protein> , a <protein>zinc-finger transcription factor</protein> ) .


In addition , both SCL and GATA-1 undergo coordinate modulation during chemically induced erythroid differentiation of mouse erythroleukemia cells and are down-modulated during myeloid differentiation of human K562 cells , thus implying a role for SCL in erythroid differentiation events .

In addition , both <protein>SCL</protein> and <protein>GATA-1</protein> undergo coordinate modulation during chemically induced erythroid differentiation of <cell_type>mouse erythroleukemia cells</cell_type> and are down-modulated during myeloid differentiation of <cell_line>human K562 cells</cell_line> , thus implying a role for <protein>SCL</protein> in erythroid differentiation events .


However , in contrast to GATA-1 , SCL is expressed in the developing brain .

However , in contrast to <protein>GATA-1</protein> , <protein>SCL</protein> is expressed in the developing brain .


Studies of the function of SCL suggest it is also important in proliferation and self-renewal events in erythroid cells .

Studies of the function of <protein>SCL</protein> suggest it is also important in proliferation and self-renewal events in <cell_type>erythroid cells</cell_type> .


Induction of the POU domain transcription factor Oct-2 during T-cell activation by cognate antigen .

Induction of the <protein>POU domain transcription factor</protein> <protein>Oct-2</protein> during <cell_type>T-cell</cell_type> activation by cognate antigen .


Oct-2 is a transcription factor that binds specifically to octamer DNA motifs in the promoters of immunoglobulin and interleukin-2 genes .

<protein>Oct-2</protein> is a <protein>transcription factor</protein> that binds specifically to <dna>octamer DNA motifs</dna> in the <dna>promoters</dna> of <dna>immunoglobulin and interleukin-2 genes</dna> .


All tumor cell lines from the B-cell lineage and a few from the T-cell lineage express Oct-2 .

All <cell_line>tumor cell lines</cell_line> from the <cell_type>B-cell lineage</cell_type> and a few from the <cell_type>T-cell lineage</cell_type> express <protein>Oct-2</protein> .


To address the role of Oct-2 in the T-cell lineage , we studied the expression of Oct-2 mRNA and protein in nontransformed human and mouse T cells .

To address the role of <protein>Oct-2</protein> in the <cell_type>T-cell lineage</cell_type> , we studied the expression of <rna>Oct-2 mRNA</rna> and protein in <cell_line>nontransformed human and mouse T cells</cell_line> .


Oct-2 was found in CD4+ and CD8+ T cells prepared from human peripheral blood and in mouse lymph node T cells .

<protein>Oct-2</protein> was found in <cell_line>CD4+ and CD8+ T cells</cell_line> prepared from human peripheral blood and in <cell_type>mouse lymph node T cells</cell_type> .


In a T-cell clone specific for pigeon cytochrome c in the context of I-Ek , Oct-2 was induced by antigen stimulation , with the increase in Oct-2 protein seen first at 3 h after activation and continuing for at least 24 h .

In a <cell_line>T-cell clone</cell_line> specific for <protein>pigeon cytochrome c</protein> in the context of <protein>I-Ek</protein> , <protein>Oct-2</protein> was induced by antigen stimulation , with the increase in <protein>Oct-2 protein</protein> seen first at 3 h after activation and continuing for at least 24 h .


Oct-2 mRNA induction during antigen-driven T-cell activation was blocked by cyclosporin A , as well as by protein synthesis inhibitors .

<rna>Oct-2 mRNA</rna> induction during antigen-driven <cell_type>T-cell</cell_type> activation was blocked by cyclosporin A , as well as by protein synthesis inhibitors .


These results suggest that Oct-2 participates in transcriptional regulation during T-cell activation. The relatively delayed kinetics of Oct-2 induction suggests that Oct-2 mediates the changes in gene expression which occur many hours or days following antigen stimulation of T lymphocytes .

These results suggest that <protein>Oct-2</protein> participates in transcriptional regulation during <cell_type>T-cell</cell_type> activation. The relatively delayed kinetics of <protein>Oct-2</protein> induction suggests that <protein>Oct-2</protein> mediates the changes in gene expression which occur many hours or days following antigen stimulation of <cell_type>T lymphocytes</cell_type> .


Glucocorticoid receptor in patients with lupus nephritis : relationship between receptor levels in mononuclear leukocytes and effect of glucocorticoid therapy .

<protein>Glucocorticoid receptor</protein> in patients with lupus nephritis : relationship between receptor levels in <cell_type>mononuclear leukocytes</cell_type> and effect of glucocorticoid therapy .


We investigated the clinical significance of glucocorticoid receptor determination in 20 patients with systemic lupus erythematosus ( SLE ) who afterwards developed nephrotic syndrome .

We investigated the clinical significance of <protein>glucocorticoid receptor</protein> determination in 20 patients with systemic lupus erythematosus ( SLE ) who afterwards developed nephrotic syndrome .


Glucocorticoid receptor concentrations in mononuclear leukocytes ( MNL ) in these patients were comparable with those in both other patients with SLE and healthy persons .

<protein>Glucocorticoid receptor</protein> concentrations in <cell_type>mononuclear leukocytes</cell_type> ( <cell_type>MNL</cell_type> ) in these patients were comparable with those in both other patients with SLE and healthy persons .


Improvement in urinary protein excretion and in disease activity , which was scored according to the SLE Disease Activity Index system of the University of Toronto , closely related to the glucocorticoid receptor concentrations in MNL isolated from the corresponding patients .

Improvement in urinary protein excretion and in disease activity , which was scored according to the SLE Disease Activity Index system of the University of Toronto , closely related to the <protein>glucocorticoid receptor</protein> concentrations in <cell_type>MNL</cell_type> isolated from the corresponding patients .


In summary , glucocorticoid receptor determination in patients with lupus nephritis may be a predictive clue for assessing responsiveness to glucocorticoid therapy .

In summary , <protein>glucocorticoid receptor</protein> determination in patients with lupus nephritis may be a predictive clue for assessing responsiveness to glucocorticoid therapy .


[ Changes in plasma interleukin-1 and their possible relationship with the changes in glucocorticoid receptor in aged long-distance runner ]

[ Changes in <protein>plasma interleukin-1</protein> and their possible relationship with the changes in <protein>glucocorticoid receptor</protein> in aged long-distance runner ]


For the study of the changes in plasma interleukin-1 ( IL-1 ) and their possible relationship with the changes in glucocorticoid receptor ( GR ) , plasma IL-1 and GR in peripheral blood leukocytes in aged long-distance runner were measured simultaneously .

For the study of the changes in <protein>plasma interleukin-1</protein> ( <protein>IL-1</protein> ) and their possible relationship with the changes in <protein>glucocorticoid receptor</protein> ( <protein>GR</protein> ) , <protein>plasma IL-1</protein> and <protein>GR</protein> in <cell_type>peripheral blood leukocytes</cell_type> in aged long-distance runner were measured simultaneously .


The activity of IL-1 was expressed as its ability to stimulate 3H-TdR incorporation in the thymocytes of C57 mice .

The activity of <protein>IL-1</protein> was expressed as its ability to stimulate <protein>3H-TdR</protein> incorporation in the <cell_type>thymocytes</cell_type> of C57 mice .


GR was determined by whole cell assay with 3H-Dex .

<protein>GR</protein> was determined by whole cell assay with 3H-Dex .


The results showed that the activity of plasma IL-1 in aged long-distance runner was 209 % , 223 % and 145 % of the control at 14.7-18.7 , 3.8-7.0 and 1.5-2.6 KD fractions .

The results showed that the activity of plasma <protein>IL-1</protein> in aged long-distance runner was 209 % , 223 % and 145 % of the control at 14.7-18.7 , 3.8-7.0 and 1.5-2.6 KD fractions .


The GR in peripheral blood leukocytes in aged runner was 65 % of the control .

The <protein>GR</protein> in <cell_type>peripheral blood leukocytes</cell_type> in aged runner was 65 % of the control .


Possible relationship between the changes in IL-1 and GR in aged long-distance runner and its physiological significance are discussed .

Possible relationship between the changes in <protein>IL-1</protein> and <protein>GR</protein> in aged long-distance runner and its physiological significance are discussed .


Mineralocorticoid effector mechanism in preeclampsia .


Mineralocorticoid effector mechanisms were evaluated in 29 patients with preeclampsia and in 25 uncomplicated pregnancies by measurement of plasma aldosterone , levels of mineralocorticoid receptor ( MR ) in mononuclear leucocytes , and subtraction potential difference ( SPD ; rectal minus oral values ) .

Mineralocorticoid effector mechanisms were evaluated in 29 patients with preeclampsia and in 25 uncomplicated pregnancies by measurement of plasma aldosterone , levels of <protein>mineralocorticoid receptor</protein> ( <protein>MR</protein> ) in <cell_type>mononuclear leucocytes</cell_type> , and subtraction potential difference ( SPD ; rectal minus oral values ) .


Mean values for plasma aldosterone were not different between the two groups , but significant differences were observed for MR ( preeclampsia , 81 +/- 44 receptors/cell ; controls , 306 +/- 168 ) and SPD ( preeclampsia , 65 +/- 7 mV ; controls , 12 +/- 5 mV ) .

Mean values for plasma aldosterone were not different between the two groups , but significant differences were observed for <protein>MR</protein> ( preeclampsia , 81 +/- 44 receptors/cell ; controls , 306 +/- 168 ) and SPD ( preeclampsia , 65 +/- 7 mV ; controls , 12 +/- 5 mV ) .


In six cases we determined MR , plasma aldosterone , and SPD in patients with preeclampsia before and 3 months after delivery .

In six cases we determined <protein>MR</protein> , plasma aldosterone , and SPD in patients with preeclampsia before and 3 months after delivery .


MR were reduced before delivery ( 96 +/- 27 receptors/cell ) , and SPD increased ( 64 +/- 8 mV ) , with both parameters normalizing after delivery ( MR , 242 +/- 79 ; SPD , 14.0 +/- 4 mV ) .

<protein>MR</protein> were reduced before delivery ( 96 +/- 27 receptors/cell ) , and SPD increased ( 64 +/- 8 mV ) , with both parameters normalizing after delivery ( <protein>MR</protein> , 242 +/- 79 ; SPD , 14.0 +/- 4 mV ) .


Aldosterone levels returned to normal nonpregnant values after delivery .


These data suggest an important role for abnormalities in mineralocorticoid effector mechanisms in the etiology of preeclampsia and could be an useful marker for diagnosis .


Kinetics of nuclear translocation and turnover of the vitamin D receptor in human HL60 leukemia cells and peripheral blood lymphocytes -- coincident rise of DNA-relaxing activity in nuclear extracts .

Kinetics of nuclear translocation and turnover of the <protein>vitamin D receptor</protein> in <cell_line>human HL60 leukemia cells</cell_line> and <cell_type>peripheral blood lymphocytes</cell_type> -- coincident rise of DNA-relaxing activity in nuclear extracts .


High affinity receptors ( VDR ) for 1 , 25-dihydroxycholecalciferol ( calcitriol ) are expressed in HL60 human leukemia cells and in low numbers in peripheral blood lymphocytes ( PBL ) .

<protein>High affinity receptors</protein> ( <protein>VDR</protein> ) for 1 , 25-dihydroxycholecalciferol ( calcitriol ) are expressed in HL60 human leukemia cells and in low numbers in <cell_type>peripheral blood lymphocytes</cell_type> ( <cell_type>PBL</cell_type> ) .


HL60 cells , expressing some characteristics of promyelocytes , can be induced to monocytoid differentiation by calcitriol .

<cell_line>HL60 cells</cell_line> , expressing some characteristics of <cell_line>promyelocytes</cell_line> , can be induced to monocytoid differentiation by calcitriol .


Specific nuclear translocation of [ 3H ] calcitriol/VDR was examined after exposure of whole cells to 10 ( -9 ) M/l calcitriol in the presence and absence of a 500-fold excess of unlabeled ligand and subsequent isolation of nuclei .

Specific nuclear translocation of <protein>[ 3H ] calcitriol/VDR</protein> was examined after exposure of <cell_type>whole cells</cell_type> to 10 ( -9 ) M/l calcitriol in the presence and absence of a 500-fold excess of unlabeled ligand and subsequent isolation of nuclei .


Specific nuclear translocation of [ 3H ] calcitriol/VDR was found to be time dependent reaching a maximum of approximately 2100 binding sites/nucleus after 3 h of incubation in HL60 cells , whereas a maximum of approximately 310 binding sites/nucleus was found after 3 h in PBL .

Specific nuclear translocation of <protein>[ 3H ] calcitriol/VDR</protein> was found to be time dependent reaching a maximum of approximately 2100 binding sites/nucleus after 3 h of incubation in <cell_line>HL60 cells</cell_line> , whereas a maximum of approximately 310 binding sites/nucleus was found after 3 h in <cell_type>PBL</cell_type> .


Pulse exposure of HL60 to radiolabeled hormone for 3 h followed by culture in medium without serum and calcitriol lead to nuclear retention of approximately 1600 radiolabeled VDR by 8 h and approximately 1000 VDR by 24 h .

Pulse exposure of <cell_line>HL60</cell_line> to radiolabeled hormone for 3 h followed by culture in medium without serum and calcitriol lead to nuclear retention of approximately <protein>1600 radiolabeled VDR</protein> by 8 h and approximately 1000 <protein>VDR</protein> by 24 h .


Radiolabeled VDR disappeared from the nuclear compartment with a halflife of approximately 30 min if cells were cultured with identical concentrations of unlabeled hormone after the pulse ( pulse/chase-experiments ) .

<protein>Radiolabeled VDR</protein> disappeared from the nuclear compartment with a halflife of approximately 30 min if cells were cultured with identical concentrations of unlabeled hormone after the pulse ( pulse/chase-experiments ) .


No difference of VDR retention in pulse and pulse/chase-experiments was seen in PBL , where VDR halflife was approximately 30 min .

No difference of <protein>VDR</protein> retention in pulse and pulse/chase-experiments was seen in <cell_type>PBL</cell_type> , where <protein>VDR</protein> halflife was approximately 30 min .


No specific translocation into the nuclear compartment was seen when isolated nuclei were incubated in [ 3H ] calcitriol .


Radiolabeled hormone/receptor complexes of nuclei isolated from cells exposed for 3 h to radiolabeled hormone -- in contrast to identical experiments with intact cells -- did not disappear from the nuclear compartment upon incubation of nuclei with identical concentrations of the unlabeled compound .

<protein>Radiolabeled hormone/receptor complexes</protein> of nuclei isolated from cells exposed for 3 h to radiolabeled hormone -- in contrast to identical experiments with intact cells -- did not disappear from the nuclear compartment upon incubation of nuclei with identical concentrations of the unlabeled compound .


The activity of DNA relaxing enzymes ( e.g . topoisomerases I and II ) in nuclear extracts was measured using a PBR 322-relaxation-assay .

The activity of <protein>DNA relaxing enzymes</protein> ( e.g . <protein>topoisomerases I and II</protein> ) in nuclear extracts was measured using a PBR 322-relaxation-assay .


Enhanced overall enzyme activity was found in nuclear extracts by 1 h after incubation with calcitriol ( final ethanol concentration 0.0001 % v/v ) in HL60 and PBL .

Enhanced overall enzyme activity was found in nuclear extracts by 1 h after incubation with calcitriol ( final ethanol concentration 0.0001 % v/v ) in <cell_line>HL60</cell_line> and <cell_type>PBL</cell_type> .


The enhanced activity disappeared after 2 h in PBL , whereas it was still enhanced by 4 h in HL60 .

The enhanced activity disappeared after 2 h in <cell_type>PBL</cell_type> , whereas it was still enhanced by 4 h in <cell_line>HL60</cell_line> .


No effect was seen in ethanol treated controls .

No effect was seen in <cell_line>ethanol treated controls</cell_line> .


We conclude that a specific nuclear translocation mechanism exists for calcitriol in both cell types examined , most likely due to translocation of receptor proteins after hormone binding .

We conclude that a specific nuclear translocation mechanism exists for calcitriol in both cell types examined , most likely due to translocation of <protein>receptor proteins</protein> after hormone binding .


Translocated hormone/receptor complexes compete for a limited number of specific nuclear binding sites .

<protein>Translocated hormone/receptor complexes</protein> compete for a limited number of specific nuclear binding sites .


Enhanced activity of topoisomerases in nuclear extracts upon translocation of VDR might reflect interaction of both within the nuclear compartment , thus initiating DNA-unwinding , a prerequisite of transcription initiation .

Enhanced activity of <protein>topoisomerases</protein> in nuclear extracts upon translocation of <protein>VDR</protein> might reflect interaction of both within the nuclear compartment , thus initiating DNA-unwinding , a prerequisite of transcription initiation .


Influence of estradiol and tamoxifen on susceptibility of human breast cancer cell lines to lysis by lymphokine-activated killer cells .

Influence of estradiol and tamoxifen on susceptibility of <cell_line>human breast cancer cell lines</cell_line> to lysis by <cell_type>lymphokine-activated killer cells</cell_type> .


The design of combination hormonal and immunotherapeutic protocols for breast cancer patients may be facilitated by analysis of preclinical in vitro model systems .


Estrogen receptor positive ( ER+ : MCF-7 ) and negative ( ER- : MDA-MB-231 ) human breast cancer cell lines were utilized to evaluate the effects of tamoxifen ( TAM ) and estradiol ( E2 ) on modulation of breast cancer target susceptibility to lysis by lymphokine-activated killer ( LAK ) cells .

<cell_line>Estrogen receptor positive ( ER+ : MCF-7 ) and negative ( ER- : MDA-MB-231 ) human breast cancer cell lines</cell_line> were utilized to evaluate the effects of tamoxifen ( TAM ) and estradiol ( E2 ) on modulation of breast cancer target susceptibility to lysis by <cell_type>lymphokine-activated killer ( LAK ) cells</cell_type> .


E2-stimulated ER+ cells were more susceptible to lysis by LAK cells than corresponding TAM-treated or control cells , while treatment of ER- cells with either E2 or TAM alone did not alter from control their susceptibility to this immune-mediated lysis .

<cell_line>E2-stimulated ER+ cells</cell_line> were more susceptible to lysis by <cell_type>LAK cells</cell_type> than corresponding <cell_line>TAM-treated</cell_line> or <cell_type>control cells</cell_type> , while treatment of <cell_line>ER- cells</cell_line> with either E2 or TAM alone did not alter from control their susceptibility to this immune-mediated lysis .


All ER+ and ER- cells tested remained sensitive after treatment with TAM to lysis by LAK cells .

All <cell_line>ER+ and ER- cells</cell_line> tested remained sensitive after treatment with TAM to lysis by <cell_type>LAK cells</cell_type> .


In addition , an adenocarcinoma reactive human-mouse chimeric monoclonal antibody ( ING-1 ) was able to significantly boost in vivo generated LAK cell-mediated lysis of control , E2-treated , and TAM-treated ER+ and ER- cells .

In addition , an <protein>adenocarcinoma reactive human-mouse chimeric monoclonal antibody</protein> ( <protein>ING-1</protein> ) was able to significantly boost in vivo generated LAK cell-mediated lysis of <cell_line>control , E2-treated , and TAM-treated ER+ and ER- cells</cell_line> .


These in vitro results provide a preclinical rationale for in vivo testing of TAM , interleukin-2 ( IL-2 ) , and breast cancer reactive antibody-dependent cellular cytotoxicity facilitating antibody in patients with refractory or high risk breast cancer .

These in vitro results provide a preclinical rationale for in vivo testing of TAM , <protein>interleukin-2</protein> ( <protein>IL-2</protein> ) , and breast cancer reactive antibody-dependent cellular cytotoxicity facilitating antibody in patients with refractory or high risk breast cancer .


The cellular oncogene c-myb can interact synergistically with the Epstein-Barr virus BZLF1 transactivator in lymphoid cells .

The <dna>cellular oncogene</dna> <dna>c-myb</dna> can interact synergistically with the <protein>Epstein-Barr virus BZLF1 transactivator</protein> in <cell_type>lymphoid cells</cell_type> .


Regulation of replicative functions in the Epstein-Barr virus ( EBV ) genome is mediated through activation of a virally encoded transcription factor , Z ( BZLF1 ) .

Regulation of replicative functions in the <dna>Epstein-Barr virus ( EBV ) genome</dna> is mediated through activation of a <protein>virally encoded transcription factor</protein> , <protein>Z</protein> ( <protein>BZLF1</protein> ) .


We have shown that the Z gene product , which binds to AP-1 sites as a homodimer and has sequence similarity to c-Fos , can efficiently activate the EBV early promoter , BMRF1 , in certain cell types ( i.e. , HeLa cells ) but not others ( i.e. , Jurkat cells ) .

We have shown that the <protein>Z gene product</protein> , which binds to <dna>AP-1 sites</dna> as a homodimer and has sequence similarity to <dna>c-Fos</dna> , can efficiently activate the <dna>EBV early promoter</dna> , <dna>BMRF1</dna> , in certain cell types ( i.e. , <cell_line>HeLa cells</cell_line> ) but not others ( i.e. , <cell_line>Jurkat cells</cell_line> ) .


Here we demonstrate that the c-myb proto-oncogene product , which is itself a DNA-binding protein and transcriptional transactivator , can interact synergistically with Z in activating the BMRF1 promoter in Jurkat cells ( a T-cell line ) or Raji cells ( an EBV-positive B-cell ) , whereas the c-myb gene product by itself has little effect .

Here we demonstrate that the <protein>c-myb proto-oncogene product</protein> , which is itself a <protein>DNA-binding protein</protein> and <protein>transcriptional transactivator</protein> , can interact synergistically with <protein>Z</protein> in activating the <dna>BMRF1 promoter</dna> in <cell_line>Jurkat cells</cell_line> ( a <cell_line>T-cell line</cell_line> ) or <cell_line>Raji cells</cell_line> ( an <cell_line>EBV-positive B-cell</cell_line> ) , whereas the <protein>c-myb gene product</protein> by itself has little effect .


The simian virus 40 early promoter is also synergistically activated by the Z/c-myb combination .

The <dna>simian virus 40 early promoter</dna> is also synergistically activated by the <protein>Z/c-myb combination</protein> .


Synergistic transactivation of the BMRF1 promoter by the Z/c-myb combination appears to involve direct binding by the Z protein but not the c-myb protein .

Synergistic transactivation of the <dna>BMRF1 promoter</dna> by the <protein>Z/c-myb combination</protein> appears to involve direct binding by the <protein>Z protein</protein> but not the <protein>c-myb protein</protein> .


A 30-bp sequence in the BMRF1 promoter which contains a Z binding site ( a consensus AP-1 site ) is sufficient to transfer high-level lymphoid-specific responsiveness to the Z/c-myb combination to a heterologous promoter .

A <dna>30-bp sequence</dna> in the <dna>BMRF1 promoter</dna> which contains a <dna>Z binding site</dna> ( a <dna>consensus AP-1 site</dna> ) is sufficient to transfer high-level lymphoid-specific responsiveness to the <protein>Z/c-myb combination</protein> to a <dna>heterologous promoter</dna> .


That the c-myb oncogene product can interact synergistically with an EBV-encoded member of the leucine zipper protein family suggests c-myb is likely to engage in similar interactions with cellularly encoded transcription factors .

That the <protein>c-myb oncogene product</protein> can interact synergistically with an <protein>EBV-encoded member</protein> of the <protein>leucine zipper protein family</protein> suggests <dna>c-myb</dna> is likely to engage in similar interactions with <protein>cellularly encoded transcription factors</protein> .


Alpha-lipoic acid is a potent inhibitor of NF-kappa B activation in human T cells .

Alpha-lipoic acid is a potent inhibitor of <protein>NF-kappa B</protein> activation in <cell_type>human T cells</cell_type> .


Acquired immunodeficiency syndrome ( AIDS ) results from infection with a human immunodeficiency virus ( HIV ) .


The long terminal repeat ( LTR ) region of HIV proviral DNA contains binding sites for nuclear factor kappa B ( NF-kappa B ) , and this transcriptional activator appears to regulate HIV activation .

The <dna>long terminal repeat ( LTR ) region</dna> of <dna>HIV proviral DNA</dna> contains binding sites for <protein>nuclear factor kappa B</protein> ( <protein>NF-kappa B</protein> ) , and this <protein>transcriptional activator</protein> appears to regulate HIV activation .


Recent findings suggest an involvement of reactive oxygen species ( ROS ) in signal transduction pathways leading to NF-kappa B activation .

Recent findings suggest an involvement of reactive oxygen species ( ROS ) in signal transduction pathways leading to <protein>NF-kappa B</protein> activation .


The present study was based on reports that antioxidants which eliminate ROS should block the activation of NF-kappa B and subsequently HIV transcription , and thus antioxidants can be used as therapeutic agents for AIDS .

The present study was based on reports that antioxidants which eliminate ROS should block the activation of <protein>NF-kappa B</protein> and subsequently HIV transcription , and thus antioxidants can be used as therapeutic agents for AIDS .


Incubation of Jurkat T cells ( 1 x 10 ( 6 ) cells/ml ) with a natural thiol antioxidant , alpha-lipoic acid , prior to the stimulation of cells was found to inhibit NF-kappa B activation induced by tumor necrosis factor-alpha ( 25 ng/ml ) or by phorbol 12-myristate 13-acetate ( 50 ng/ml ) .

Incubation of <cell_line>Jurkat T cells</cell_line> ( 1 x 10 ( 6 ) cells/ml ) with a natural thiol antioxidant , alpha-lipoic acid , prior to the stimulation of cells was found to inhibit <protein>NF-kappa B</protein> activation induced by <protein>tumor necrosis factor-alpha</protein> ( 25 ng/ml ) or by phorbol 12-myristate 13-acetate ( 50 ng/ml ) .


The inhibitory action of alpha-lipoic acid was found to be very potent as only 4 mM was needed for a complete inhibition , whereas 20 mM was required for N-acetylcysteine .


These results indicate that alpha-lipoic acid may be effective in AIDS therapeutics .


Reticuloendotheliosis virus long terminal repeat elements are efficient promoters in cells of various species and tissue origin , including human lymphoid cells .

<dna>Reticuloendotheliosis virus long terminal repeat elements</dna> are efficient <dna>promoters</dna> in cells of various species and tissue origin , including <cell_type>human lymphoid cells</cell_type> .


Promiscuous transcriptional activity of the reticuloendotheliosis virus ( REV ) long terminal repeat ( LTR ) was detected in transient expression assays using LTR-chloramphenicol acetyltransferase-encoding gene chimeras , and cells of diverse species and tissue type ; levels of expression from two different REV LTRs correlate with reports of pathogenicity of the respective viruses in vivo .

Promiscuous transcriptional activity of the <dna>reticuloendotheliosis virus ( REV ) long terminal repeat</dna> ( <dna>LTR</dna> ) was detected in transient expression assays using <dna>LTR-chloramphenicol acetyltransferase-encoding gene chimeras</dna> , and cells of diverse species and tissue type ; levels of expression from two different <dna>REV LTRs</dna> correlate with reports of pathogenicity of the respective viruses in vivo .


REVs do not encode a transactivator targeted to the viral LTR , and cells infected with Marek 's disease virus , a herpesvirus with an overlapping host range , do not express factors that preferentially enhance expression from REV or avian sarcoma/leukemia virus LTRs .

REVs do not encode a transactivator targeted to the <dna>viral LTR</dna> , and cells infected with Marek 's disease virus , a herpesvirus with an overlapping host range , do not express factors that preferentially enhance expression from REV or <dna>avian sarcoma/leukemia virus LTRs</dna> .


REV LTRs work efficiently in human lymphoid cells , and are viable alternatives to promoters commonly used for expression of cloned genes .

<dna>REV LTRs</dna> work efficiently in <cell_type>human lymphoid cells</cell_type> , and are viable alternatives to <dna>promoters</dna> commonly used for expression of <dna>cloned genes</dna> .


They may also prove useful in the identification of new , ubiquitous cellular transcription factors .

They may also prove useful in the identification of new , <protein>ubiquitous cellular transcription factors</protein> .


A novel Ets-related transcription factor , Elf-1 , binds to human immunodeficiency virus type 2 regulatory elements that are required for inducible trans activation in T cells .

A novel <protein>Ets-related transcription factor</protein> , <protein>Elf-1</protein> , binds to <dna>human immunodeficiency virus type 2 regulatory elements</dna> that are required for inducible trans activation in <cell_type>T cells</cell_type> .


Human immunodeficiency virus type 1 ( HIV-1 ) and HIV-2 are structurally related retroviruses which both cause AIDS in humans .


Although both viruses establish latency in quiescent human-peripheral-blood T cells , the asymptomatic phase of HIV-2 infection may be more prolonged than that of HIV-1 .

Although both viruses establish latency in quiescent <cell_type>human-peripheral-blood T cells</cell_type> , the asymptomatic phase of HIV-2 infection may be more prolonged than that of HIV-1 .


The latent phases of both HIV-1 and HIV-2 infection have been shown to be disrupted by T-cell activation , a process that requires host cell transcription factors .


In the case of HIV-1 , the transcription factor NF-kappa B is sufficient for inducible transcriptional activation .

In the case of HIV-1 , the transcription factor <protein>NF-kappa B</protein> is sufficient for inducible transcriptional activation .


In contrast , factors in addition to NF-kappa B are required to activate HIV-2 transcription in infected T cells .

In contrast , factors in addition to <protein>NF-kappa B</protein> are required to activate HIV-2 transcription in <cell_type>infected T cells</cell_type> .


In this report , we demonstrate that a novel Ets-related transcription factor , Elf-1 , binds specifically to two purine-rich motifs in the HIV-2 enhancer .

In this report , we demonstrate that a novel <protein>Ets-related transcription factor</protein> , <protein>Elf-1</protein> , binds specifically to <dna>two purine-rich motifs</dna> in the <dna>HIV-2 enhancer</dna> .


Mutagenesis experiments demonstrated that these Elf-1 binding sites are required for induction of HIV-2 transcription following T-cell-receptor-mediated T-cell activation .

Mutagenesis experiments demonstrated that these <dna>Elf-1 binding sites</dna> are required for induction of HIV-2 transcription following T-cell-receptor-mediated T-cell activation .


Moreover , Elf-1 is the only factor present in activated T-cell nuclear extracts that binds to these sites in electrophoretic mobility shift assays .

Moreover , <protein>Elf-1</protein> is the only factor present in activated T-cell nuclear extracts that binds to these sites in electrophoretic mobility shift assays .


Thus , Elf-1 is a novel transcription factor that appears to be required for the T-cell-receptor-mediated trans activation of HIV-2 gene expression .

Thus , <protein>Elf-1</protein> is a <protein>novel transcription factor</protein> that appears to be required for the T-cell-receptor-mediated trans activation of HIV-2 gene expression .


These results may explain differences in the clinical spectra of diseases caused by HIV-1 and HIV-2 and may also have implications for the design of therapeutic approaches to HIV-2 infection .


Okadaic acid is a potent inducer of AP-1 , NF-kappa B , and tumor necrosis factor-alpha in human B lymphocytes .

Okadaic acid is a potent inducer of <protein>AP-1</protein> , <protein>NF-kappa B</protein> , and <protein>tumor necrosis factor-alpha</protein> in <cell_type>human B lymphocytes</cell_type> .


Treatment of human B lymphocytes with an optimal concentration of okadaic acid , an inhibitor of phosphatases 1 and 2A , resulted in the induction of the transcription factor , AP-1 and a marked increase in NF-kappa B levels .

Treatment of <cell_type>human B lymphocytes</cell_type> with an optimal concentration of okadaic acid , an inhibitor of <protein>phosphatases 1 and 2A</protein> , resulted in the induction of the <protein>transcription factor</protein> , <protein>AP-1</protein> and a marked increase in <protein>NF-kappa B</protein> levels .


In contrast , no effect on the levels of the octamer binding proteins , Oct-1 or Oct-2 , were found .

In contrast , no effect on the levels of the <protein>octamer binding proteins</protein> , <protein>Oct-1</protein> or <protein>Oct-2</protein> , were found .


Since both AP-1 and NF-kappa B have been reported to be important in the induction of the tumor necrosis factor-alpha ( TNF-alpha ) gene we examined the effects of okadaic acid on TNF-alpha mRNA levels .

Since both <protein>AP-1</protein> and <protein>NF-kappa B</protein> have been reported to be important in the induction of the <dna>tumor necrosis factor-alpha ( TNF-alpha ) gene</dna> we examined the effects of okadaic acid on <rna>TNF-alpha mRNA</rna> levels .


Treatment with okadaic acid resulted in a striking increase in TNF-alpha mRNA transcripts within 1 h of stimulation and large amounts of TNF-alpha were released into the culture media .

Treatment with okadaic acid resulted in a striking increase in <rna>TNF-alpha mRNA</rna> transcripts within 1 h of stimulation and large amounts of <protein>TNF-alpha</protein> were released into the culture media .


Although okadaic acid provides a potent inductive signal for AP-1 and NF-kappa B it did not induce either B cell proliferation or immunoglobulin secretion .

Although okadaic acid provides a potent inductive signal for <protein>AP-1</protein> and <protein>NF-kappa B</protein> it did not induce either B cell proliferation or <protein>immunoglobulin</protein> secretion .


Heterodimerization and transcriptional activation in vitro by NF-kappa B proteins .

Heterodimerization and transcriptional activation in vitro by <protein>NF-kappa B proteins</protein> .


The NF-kappa B family of transcription proteins represents multiple DNA binding , rel related polypeptides that contribute to regulation of genes involved in immune responsiveness and inflammation , as well as activation of the HIV long terminal repeat .

The <protein>NF-kappa B family</protein> of <protein>transcription proteins</protein> represents multiple DNA binding , <protein>rel related polypeptides</protein> that contribute to regulation of genes involved in immune responsiveness and inflammation , as well as activation of the <dna>HIV long terminal repeat</dna> .


In this study multiple NF-kappa B related polypeptides ranging from 85 to 45 kDa were examined for their capacity to interact with the PRDII regulatory element of interferon beta and were shown to possess distinct intrinsic DNA binding affinities for this NF-kappa B site and form multiple DNA binding homo- and heterodimer complexes in co-renaturation experiments .

In this study multiple <protein>NF-kappa B related polypeptides</protein> ranging from 85 to 45 kDa were examined for their capacity to interact with the <dna>PRDII regulatory element</dna> of <dna>interferon beta</dna> and were shown to possess distinct intrinsic DNA binding affinities for this <dna>NF-kappa B site</dna> and form <protein>multiple DNA binding homo- and heterodimer complexes</protein> in co-renaturation experiments .


Furthermore , using DNA templates containing two copies of the PRDII domain linked to the rabbit beta globin gene , the purified polypeptides specifically stimulated NF-kappa B dependent transcription in an in vitro reconstitution assay as heterodimers but not as p50 homodimers .

Furthermore , using <dna>DNA templates</dna> containing two copies of the <dna>PRDII domain</dna> linked to the <dna>rabbit beta globin gene</dna> , the purified polypeptides specifically stimulated <protein>NF-kappa B</protein> dependent transcription in an in vitro reconstitution assay as heterodimers but not as <protein>p50 homodimers</protein> .


These experiments emphasize the role of NF-kappa B dimerization as a distinct level of transcriptional control that may permit functional diversification of a limited number of regulatory proteins .

These experiments emphasize the role of <protein>NF-kappa B</protein> dimerization as a distinct level of transcriptional control that may permit functional diversification of a limited number of <protein>regulatory proteins</protein> .


c-myc mRNA expression in minor salivary glands of patients with Sjogren 's syndrome .

<rna>c-myc mRNA</rna> expression in minor salivary glands of patients with Sjogren 's syndrome .


c-myc protooncogene is implicated in the pathogenesis of B cell lymphoid malignancies and high levels of c-myc mRNA expression are observed in activated blood mononuclear cells .

<dna>c-myc protooncogene</dna> is implicated in the pathogenesis of B cell lymphoid malignancies and high levels of <rna>c-myc mRNA</rna> expression are observed in <cell_type>activated blood mononuclear cells</cell_type> .


Sjogren 's syndrome ( SS ) is characterized by lymphocytic infiltrates of exocrine glands , remarkable B cell hyperreactivity and a strong predisposition to B cell neoplasia .

Sjogren 's syndrome ( SS ) is characterized by <cell_type>lymphocytic infiltrates</cell_type> of exocrine glands , remarkable B cell hyperreactivity and a strong predisposition to B cell neoplasia .


In this study , c-myc protooncogene mRNA expression in 29 labial minor salivary gland biopsies from patients with primary SS and 15 controls was examined using in situ hybridization histochemistry .

In this study , <rna>c-myc protooncogene mRNA</rna> expression in 29 labial minor salivary gland biopsies from patients with primary SS and 15 controls was examined using in situ hybridization histochemistry .


Two 40mer oligonucleotides from the 1st and the 2nd exon of the c-myc gene , labeled with 35S , were used as probes .

Two 40mer oligonucleotides from the <dna>1st and the 2nd exon</dna> of the <dna>c-myc gene</dna> , labeled with 35S , were used as probes .


To detect the origin of the cell hybridized with a c-myc probe , a combined immunochemistry in situ hybridization histochemistry technique was used .

To detect the origin of the cell hybridized with a <dna>c-myc probe</dna> , a combined immunochemistry in situ hybridization histochemistry technique was used .


High c-myc mRNA expression was detected on acinar epithelial cells .

High <rna>c-myc mRNA</rna> expression was detected on <cell_type>acinar epithelial cells</cell_type> .


c-myc did not correlate with c-fos and c-jun protein expression .

<protein>c-myc</protein> did not correlate with <protein>c-fos</protein> and <protein>c-jun</protein> protein expression .


Stronger c-myc mRNA expression was detected in labial salivary glands of patients with longer disease duration ( p less than or equal to 0.002 ) and more intense T lymphocyte infiltrates ( p less than 0.05 ) although these patients revealed no hypergammaglobulinemia .

Stronger <rna>c-myc mRNA</rna> expression was detected in labial salivary glands of patients with longer disease duration ( p less than or equal to 0.002 ) and more intense <cell_type>T lymphocyte infiltrates</cell_type> ( p less than 0.05 ) although these patients revealed no hypergammaglobulinemia .


No correlation was observed between c-myc mRNA and B lymphocyte monoclonicity or lymphoma .

No correlation was observed between <rna>c-myc mRNA</rna> and B lymphocyte monoclonicity or lymphoma .


In conclusion , strong c-myc mRNA expression was observed on epithelial cells of labial salivary glands from patients with primary SS .

In conclusion , strong <rna>c-myc mRNA</rna> expression was observed on <cell_type>epithelial cells</cell_type> of labial salivary glands from patients with primary SS .


Our findings may indicate the presence of a reactivated virus hosted in these cells .


Corticosteroid receptors and lymphocyte subsets in mononuclear leukocytes in aging .

<protein>Corticosteroid receptors</protein> and <cell_type>lymphocyte subsets</cell_type> in <cell_type>mononuclear leukocytes</cell_type> in aging .


Plasma cortisol and aldosterone levels and number of related receptors in mononuclear leukocytes were measured in 49 healthy aged subjects ( 62-97 yr ) and in 21 adult controls ( 21-50 yr ) .

Plasma cortisol and aldosterone levels and number of related receptors in <cell_type>mononuclear leukocytes</cell_type> were measured in 49 healthy aged subjects ( 62-97 yr ) and in 21 adult controls ( 21-50 yr ) .


In all subjects , in addition , lymphocyte subsets were determined as an index of corticosteroid action .

In all subjects , in addition , <cell_type>lymphocyte subsets</cell_type> were determined as an index of corticosteroid action .


The mean number of type I and type II receptors was significantly lower in aged subjects than in controls ( respectively , 198 +/- 96 and 272 +/- 97 receptors /cell for type I , and 1 , 794 +/- 803 and 3 , 339 +/- 918 for type II receptors ) .

The mean number of <protein>type I and type II receptors</protein> was significantly lower in aged subjects than in controls ( respectively , 198 +/- 96 and 272 +/- 97 <protein>receptors</protein> /cell for <protein>type I</protein> , and 1 , 794 +/- 803 and 3 , 339 +/- 918 for type <protein>II receptors</protein> ) .


Plasma aldosterone and cortisol and lymphocyte subsets were not different in the two groups .

Plasma aldosterone and cortisol and <cell_type>lymphocyte subsets</cell_type> were not different in the two groups .


All of the parameters were also tested for correlation , and a significant inverse correlation was found between age and type I and type II receptors when all subjects were plotted and between aged and CD4 and age and CD4/CD8 in the aged group .

All of the parameters were also tested for correlation , and a significant inverse correlation was found between age and <protein>type I</protein> and <protein>type II receptors</protein> when all subjects were plotted and between aged and <cell_type>CD4</cell_type> and age and <cell_type>CD4/CD8</cell_type> in the aged group .


These data show that aged subjects have reductions of corticosteroid receptors that are not associated with increase of related steroids and that this situation probably represents a concomitant of the normal aging process .

These data show that aged subjects have reductions of <protein>corticosteroid receptors</protein> that are not associated with increase of related steroids and that this situation probably represents a concomitant of the normal aging process .


T cell-specific negative regulation of transcription of the human cytokine IL-4 .

T cell-specific negative regulation of transcription of the <protein>human cytokine IL-4</protein> .


IL-4 secreted by activated T cells is a pleiotropic cytokine affecting growth and differentiation of diverse cell types such as T cells , B cells , and mast cells .

<protein>IL-4</protein> secreted by <cell_type>activated T cells</cell_type> is a <protein>pleiotropic cytokine</protein> affecting growth and differentiation of diverse cell types such as <cell_type>T cells</cell_type> , <cell_type>B cells</cell_type> , and <cell_type>mast cells</cell_type> .


We investigated the upstream regulatory elements of the human IL-4 promoter .

We investigated the <dna>upstream regulatory elements</dna> of the <dna>human IL-4 promoter</dna> .


A novel T cell-specific negative regulatory element ( NRE ) composed of two protein-binding sites were mapped in the 5 ' flanking region of the IL-4 gene : -311CTCCCTTCT-303 ( NRE-I ) and -288CTTTTTGCTT-TGC-300 ( NRE-II ) .

A <dna>novel T cell-specific negative regulatory element</dna> ( <dna>NRE</dna> ) composed of two protein-binding sites were mapped in the 5 ' flanking region of the <dna>IL-4 gene</dna> : -311CTCCCTTCT-303 ( <dna>NRE-I</dna> ) and -288CTTTTTGCTT-TGC-300 ( <dna>NRE-II</dna> ) .


A T cell-specific protein Neg-1 and a ubiquitous protein Neg-2 binding to NRE-I and NRE-II , respectively , were identified .

A <protein>T cell-specific protein</protein> <protein>Neg-1</protein> and a <protein>ubiquitous protein</protein> <protein>Neg-2</protein> binding to <dna>NRE-I</dna> and <dna>NRE-II</dna> , respectively , were identified .


Furthermore , a positive regulatory element was found 45 bp downstream of the NRE .

Furthermore , a <dna>positive regulatory element</dna> was found <dna>45 bp downstream</dna> of the <dna>NRE</dna> .


The enhancer activity of the PRE was completely suppressed when the NRE was present .

The enhancer activity of the <dna>PRE</dna> was completely suppressed when the <dna>NRE</dna> was present .


These data suggest that IL-4 promoter activity is normally down-regulated by an NRE via repression of the enhancer positive regulatory element .

These data suggest that <dna>IL-4 promoter</dna> activity is normally down-regulated by an <dna>NRE</dna> via repression of the <dna>enhancer positive regulatory element</dna> .


These data may have implications for the stringent control of IL-4 expression in T cells .

These data may have implications for the stringent control of <protein>IL-4</protein> expression in <cell_type>T cells</cell_type> .


Interleukin 6-induced differentiation of a human B cell line into IgM-secreting plasma cells is mediated by c-fos .

Interleukin 6-induced differentiation of a <cell_line>human B cell line</cell_line> into <cell_type>IgM-secreting plasma cells</cell_type> is mediated by <dna>c-fos</dna> .


The role of the protooncogene c-fos in interleukin ( IL ) 6 -induced B cell differentiation was assessed .

The role of the <dna>protooncogene c-fos</dna> in <protein>interleukin ( IL ) 6</protein> -induced B cell differentiation was assessed .


Treatment of SKW 6.4 cells with IL 6 induced a transient and early stimulation of c-fos sense mRNA expression .

Treatment of SKW 6.4 cells with <protein>IL 6</protein> induced a transient and early stimulation of <rna>c-fos sense mRNA</rna> expression .


The effect appeared within 30 min and returned to basal levels after 2 h .


The addition of antisense oligonucleotides to c-fos significantly inhibited IL 6 -induced IgM production by SKW 6.4 cells ( p less than 0.001 ) , whereas control oligonucleotides had no inhibitory effect .

The addition of antisense oligonucleotides to <dna>c-fos</dna> significantly inhibited <protein>IL 6</protein> -induced <protein>IgM</protein> production by <cell_line>SKW 6.4 cells</cell_line> ( p less than 0.001 ) , whereas control oligonucleotides had no inhibitory effect .


These results indicate that activation of c-fos is involved in IL 6 -induced differentiation of SKW 6.4 cells into IgM-secreting cells .

These results indicate that activation of <dna>c-fos</dna> is involved in <protein>IL 6</protein> -induced differentiation of <cell_line>SKW 6.4 cells</cell_line> into <cell_line>IgM-secreting cells</cell_line> .


Transcriptional regulation during T-cell development : the alpha TCR gene as a molecular model .

Transcriptional regulation during <cell_type>T-cell</cell_type> development : the <dna>alpha TCR gene</dna> as a molecular model .


The regulation of gene expression during lymphocyte differentiation is a complex process involving interactions between multiple positive and negative transcriptional regulatory elements .

The regulation of gene expression during <cell_type>lymphocyte</cell_type> differentiation is a complex process involving interactions between <dna>multiple positive and negative transcriptional regulatory elements</dna> .


In this article , transcriptional regulation of the archetypal T-cell-specific gene , alpha TCR , is discussed .

In this article , transcriptional regulation of the <dna>archetypal T-cell-specific gene</dna> , <dna>alpha TCR</dna> , is discussed .


Major recent developments , including the identification of novel families of transcription factors that regulate multiple T-cell genes during thymocyte ontogeny and T-cell activation , are described .

Major recent developments , including the identification of novel families of <dna>transcription factors</dna> that regulate multiple <dna>T-cell genes</dna> during thymocyte ontogeny and <cell_type>T-cell</cell_type> activation , are described .


Photoaffinity labeling of plasma membrane receptors for aldosterone from human mononuclear leukocytes .

Photoaffinity labeling of <protein>plasma membrane receptors</protein> for aldosterone from <cell_type>human mononuclear leukocytes</cell_type> .


Non-genomic effects of aldosterone on the sodium-proton-antiport have been shown in human mononuclear leukocytes which could be related to a new aldosterone membrane receptor .

Non-genomic effects of aldosterone on the <protein>sodium-proton-antiport</protein> have been shown in <cell_type>human mononuclear leukocytes</cell_type> which could be related to a new <protein>aldosterone membrane receptor</protein> .


In the present paper plasma membranes from human mononuclear leukocytes were covalently photolabeled with a [ 125I ] -aldosterone derivative .

In the present paper plasma membranes from <cell_type>human mononuclear leukocytes</cell_type> were covalently photolabeled with a [ 125I ] -aldosterone derivative .


Sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed significant aldosterone binding at a molecular weight of approximately 50000 Dalton which was absent with 1 microM cold aldosterone , but not cortisol in the binding media .


The presence of the sulfhydryl agent dithiothreitol did not affect results suggesting the absence of disulfide bridges in the steroid binding domain of the receptor .

The presence of the sulfhydryl agent dithiothreitol did not affect results suggesting the absence of <protein>disulfide bridges</protein> in the <protein>steroid binding domain</protein> of the receptor .


These data are the first to define the molecular weight of the membrane receptor for aldosterone .

These data are the first to define the molecular weight of the <protein>membrane receptor</protein> for aldosterone .


Redox status of cells influences constitutive or induced NF-kappa B translocation and HIV long terminal repeat activity in human T and monocytic cell lines .

Redox status of cells influences constitutive or induced <protein>NF-kappa B</protein> translocation and <dna>HIV long terminal repeat</dna> activity in <cell_line>human T and monocytic cell lines</cell_line> .


We have tested the hypothesis that cellular activation events occurring in T lymphocytes and monocytes and mediated through translocation of the transcription factor NF-kappa B are dependent upon the constitutive redox status of these cells .

We have tested the hypothesis that cellular activation events occurring in <cell_type>T lymphocytes</cell_type> and <cell_type>monocytes</cell_type> and mediated through translocation of the <protein>transcription factor NF-kappa B</protein> are dependent upon the constitutive redox status of these cells .


We used phenolic , lipid-soluble , chain-breaking antioxidants ( butylated hydroxyanisole ( BHA ) , nordihydroquairetic acid , or alpha-tocopherol ( vitamin E ) to show that peroxyl radical scavenging in unstimulated and PMA- or TNF-stimulated cells blocks the functions depending on NF-kappa B activation .

We used phenolic , lipid-soluble , chain-breaking antioxidants ( butylated hydroxyanisole ( BHA ) , nordihydroquairetic acid , or alpha-tocopherol ( vitamin E ) to show that peroxyl radical scavenging in <cell_line>unstimulated and PMA- or TNF-stimulated cells</cell_line> blocks the functions depending on <protein>NF-kappa B</protein> activation .


BHA was found to suppress not only PMA- or TNF-induced , but also constitutive , HIV-enhancer activity concomitant to an inhibition of NF-kappa B binding activity in both lymphoblastoid T ( J.Jhan ) and monocytic ( U937 ) cell lines .

BHA was found to suppress not only PMA- or TNF-induced , but also constitutive , HIV-enhancer activity concomitant to an inhibition of <protein>NF-kappa B</protein> binding activity in both <cell_line>lymphoblastoid T</cell_line> ( <cell_line>J.Jhan</cell_line> ) and <cell_line>monocytic ( U937 ) cell lines</cell_line> .


This was also true for KBF ( p50 homodimer ) binding activity in U937 cells .

This was also true for KBF ( p50 homodimer ) binding activity in <cell_line>U937 cells</cell_line> .


Secretion of TNF , the product of another NF-kappa B-dependent gene , was abolished by BHA in PMA-stimulated U937 cells .

Secretion of <protein>TNF</protein> , the product of another <dna>NF-kappa B-dependent gene</dna> , was abolished by BHA in <cell_line>PMA-stimulated U937 cells</cell_line> .


The anti-oxidative effect of BHA was accompanied by an increase in thiol , but not glutathione , content in stimulated and unstimulated T cell , whereas TNF stimulation itself barely modified the cellular thiol level .

The anti-oxidative effect of BHA was accompanied by an increase in thiol , but not glutathione , content in <cell_line>stimulated and unstimulated T cell</cell_line> , whereas <protein>TNF</protein> stimulation itself barely modified the cellular thiol level .


Oxidative stress obtained by the addition of H2O2 to the culture medium of J.Jhan or U937 cells could not by itself induce NF-kappa B activation .

Oxidative stress obtained by the addition of H2O2 to the culture medium of <cell_line>J.Jhan</cell_line> or <cell_line>U937 cells</cell_line> could not by itself induce <protein>NF-kappa B</protein> activation .


These observations suggest that TNF and PMA do not lead to NF-kappa B activation through induction of changes in the cell redox status .

These observations suggest that <protein>TNF</protein> and <protein>PMA</protein> do not lead to <protein>NF-kappa B</protein> activation through induction of changes in the cell redox status .


Rather , TNF and PMA can exert their effect only if cells are in an appropriate redox status , because prior modification toward reduction with BHA treatment prevents this activation .

Rather , <protein>TNF</protein> and <protein>PMA</protein> can exert their effect only if cells are in an appropriate redox status , because prior modification toward reduction with BHA treatment prevents this activation .


It appears that a basal redox equilibrium tending toward oxidation is a prerequisite for full activation of transduction pathways regulating the activity of NF-kappa B-dependent genes .

It appears that a basal redox equilibrium tending toward oxidation is a prerequisite for full activation of transduction pathways regulating the activity of <dna>NF-kappa B-dependent genes</dna> .


Selection of optimal kappa B/Rel DNA-binding motifs : interaction of both subunits of NF-kappa B with DNA is required for transcriptional activation .

Selection of optimal kappa B/Rel DNA-binding motifs : interaction of both subunits of <protein>NF-kappa B</protein> with DNA is required for transcriptional activation .


Analysis of the p50 and p65 subunits of the NF-kappa B transcription factor complex has revealed that both proteins can interact with related DNA sequences through either homo- or heterodimer formation .

Analysis of the <protein>p50</protein> and <protein>p65 subunits</protein> of the <protein>NF-kappa B transcription factor complex</protein> has revealed that both proteins can interact with related DNA sequences through either homo- or heterodimer formation .


In addition , the product of the proto-oncogene c-rel can bind to similar DNA motifs by itself or as a heterodimer with p50 or p65 .

In addition , the product of the <dna>proto-oncogene c-rel</dna> can bind to similar DNA motifs by itself or as a heterodimer with <protein>p50</protein> or <protein>p65</protein> .


However , these studies have used a limited number of known kappa B DNA motifs , and the question of the optimal DNA sequences preferred by each homodimer has not been addressed .


Using purified recombinant p50 , p65 , and c-Rel proteins , optimal DNA-binding motifs were selected from a pool of random oligonucleotides .

Using purified recombinant <protein>p50</protein> , <protein>p65</protein> , and <protein>c-Rel proteins</protein> , optimal DNA-binding motifs were selected from a pool of random oligonucleotides .


Alignment of the selected sequences allowed us to predict a consensus sequence for binding of the individual homodimeric Rel-related proteins , and DNA-protein binding analysis of the selected DNA sequences revealed sequence specificity of the proteins .

Alignment of the selected sequences allowed us to predict a consensus sequence for binding of the individual <protein>homodimeric Rel-related proteins</protein> , and DNA-protein binding analysis of the selected DNA sequences revealed sequence specificity of the proteins .


Contrary to previous assumptions , we observed that p65 homodimers can interact with a subset of DNA sequences not recognized by p50 homodimers .

Contrary to previous assumptions , we observed that <protein>p65</protein> homodimers can interact with a subset of DNA sequences not recognized by <protein>p50 homodimers</protein> .


Differential binding affinities were also obtained with p50- and c-Rel-selected sequences .

Differential binding affinities were also obtained with <dna>p50- and c-Rel-selected sequences</dna> .


Using either a p50- or p65- selected kappa B motif , which displayed differential binding with respect to the other protein , little to no binding was observed with the heterodimeric NF-kappa B complex .

Using either a p50- or p65- selected kappa B motif , which displayed differential binding with respect to the other protein , little to no binding was observed with the <protein>heterodimeric NF-kappa B complex</protein> .


Similarly , in transfection experiments in which the selective kappa B binding sites were used to drive the expression of a chloramphenicol acetyltransferase reporter construct , the p65 -and p50-selected motifs were activated only in the presence of p65 and p50/65 ( a chimeric protein with the p50 DNA binding domain and p65 activation domain ) expression vectors , respectively , and neither demonstrated a significant response to stimuli that induce NF-kappa B activity .

Similarly , in transfection experiments in which the <dna>selective kappa B binding sites</dna> were used to drive the expression of a <dna>chloramphenicol acetyltransferase reporter construct</dna> , the <dna>p65 -and p50-selected motifs</dna> were activated only in the presence of <protein>p65</protein> and <protein>p50/65</protein> ( a <protein>chimeric protein</protein> with the <protein>p50 DNA binding domain</protein> and <protein>p65 activation domain</protein> ) expression vectors , respectively , and neither demonstrated a significant response to stimuli that induce <protein>NF-kappa B</protein> activity .


These findings demonstrate that interaction of both subunits of the heterodimeric NF-kappa B complex with DNA is required for DNA binding and transcriptional activation and suggest that transcriptional activation mediated by the individual rel-related proteins will differ dramatically , depending on the specific kappa B motifs present .

These findings demonstrate that interaction of both subunits of the <protein>heterodimeric NF-kappa B complex</protein> with DNA is required for DNA binding and transcriptional activation and suggest that transcriptional activation mediated by the individual <protein>rel-related proteins</protein> will differ dramatically , depending on the specific kappa B motifs present .


NF-kappa B -dependent induction of the NF-kappa B p50 subunit gene promoter underlies self-perpetuation of human immunodeficiency virus transcription in monocytic cells .

<protein>NF-kappa B</protein> -dependent induction of the <protein>NF-kappa B</protein> <dna>p50 subunit gene promoter</dna> underlies self-perpetuation of human immunodeficiency virus transcription in <cell_type>monocytic cells</cell_type> .