REGULATION OF GLUCOCORTICOID-INDUCIBLE HYDROXYSTEROID SULFOTRANSFERASE (SULT2A-40/41) GENE TRANSCRIPTION IN PRIMARY CULTURED RAT HEPATOCYTES: ROLE OF CCAAT/ENHANCER-BINDING PROTEIN LIVER-ENRICHED TRANSCRIPTION FACTORS

2004 ◽  
Vol 33 (1) ◽  
pp. 147-156 ◽  
Author(s):  
Hai-Lin Fang ◽  
Masumeh Abdolalipour ◽  
Zhengbo Duanmu ◽  
Jeffrey R. Smigelski ◽  
Amy Weckle ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Gene Transcription ◽  
Binding Protein ◽  
Rat Hepatocytes ◽  
Primary Cultured Rat Hepatocytes ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein ◽  
Cultured Rat Hepatocytes

Growth hormone induces CCAAT/enhancer binding protein α (C/EBPα) in cultured rat hepatocytes

2000 ◽  
Vol 32 (4) ◽  
pp. 618-626 ◽  
Author(s):  
Petra Strand ◽  
Linda Carlsson ◽  
Katarina Rask ◽  
Stanko Skrtic ◽  
Staffan Ekberg ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Binding Protein ◽  
Rat Hepatocytes ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein ◽  
Cultured Rat Hepatocytes

scholarly journals Cooperative Effects of STAT5 (Signal Transducer and Activator of Transcription 5) and C/EBP β (CCAAT/Enhancer-Binding Protein-β) onβ -Casein Gene Transcription Are Mediated by the Glucocorticoid Receptor

2001 ◽  
Vol 15 (2) ◽  
pp. 228-240 ◽  
Author(s):  
Shannon L. Wyszomierski ◽  
Jeffrey M. Rosen
Keyword(s):  
Transcription Factors ◽  
Glucocorticoid Receptor ◽  
Gene Transcription ◽  
Binding Protein ◽  
Transactivation Domain ◽  
Signal Transducer ◽  
Casein Gene ◽  
Amino Terminal ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein

Abstract β-Casein gene transcription is controlled primarily by a composite response element (CoRE) that integrates signaling from the lactogenic hormones, PRL, insulin, and hydrocortisone, in mammary epithelial cells. This CoRE contains binding sites for STAT5 (signal transducer and activator of transcription 5) and C/EBPβ (CCAAT/enhancer-binding protein-β) and several half-sites for glucocorticoid receptor (GR). To examine how interactions among these three transcription factors might regulateβ -casein gene transcription, a COS cell reconstitution system was employed. Cooperative transactivation was observed when all three factors were expressed, but unexpectedly was not seen between STAT5 and C/EBPβ in the absence of full-length, transcriptionally active GR. Cooperativity required the amino-terminal transactivation domain of C/EBPβ, and neither C/EBPα nor C/EBPδ was able to substitute for C/EBPβ when cotransfected with STAT5 and GR. Different GR determinants were needed for transcriptional cooperation between STAT5 and GR as compared with those required for all three transcription factors. These studies provide some new insights into the mechanisms responsible for high level, tissue-specific expression conferred by theβ -casein CoRE.

scholarly journals Glucocorticoids increase retinoid-X receptor alpha (RXRalpha) expression and enhance thyroid hormone action in primary cultured rat hepatocytes

1999 ◽  
Vol 22 (1) ◽  
pp. 81-90 ◽  
Author(s):  
S Yamaguchi ◽  
Y Murata ◽  
T Nagaya ◽  
Y Hayashi ◽  
S Ohmori ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Binding Protein ◽  
Rat Hepatocytes ◽  
Retinoid X Receptor ◽  
Type I ◽  
Receptor Alpha ◽  
Primary Cultured Rat Hepatocytes ◽  
Spot 14 ◽  
Cultured Rat Hepatocytes ◽  
Retinoid X Receptor Alpha

We have previously demonstrated that dexamethasone (DEX) enhances the T3-dependent increase in type I 5'-deiodinase (5'DI) mRNA in primary cultured rat hepatocytes grown as spheroids. Here we report that DEX-enhanced T3-responsiveness also occurs in two other T3-regulated hepatic genes, Spot 14 and malic enzyme. This enhancement was inhibited by pretreatment with cycloheximide and the stability of 5'DI and Spot 14 mRNAs was not affected by DEX. We thus hypothesized that a factor(s) that augments T3-responsiveness is induced by DEX. Among the possible candidates examined, retinoid-X receptor alpha (RXRalpha), which is a main heterodimer partner with T3 receptor, appeared to be involved. Whereas DEX increased the amount of RXRalpha mRNA, it did not affect the expression of other possible factors such as steroid receptor coactivator-1 and the binding protein of cAMP response element-binding protein. Northern and Western blot analysis, and electrophoretic mobility shift assay revealed that DEX increased RXRalpha expression at both the mRNA and protein levels. Maximal increase in RXRalpha protein was achieved with the addition of physiological concentrations of DEX (10(-8) M). To test whether the DEX-induced increase in RXRalpha affects ligand-dependent transcriptional activation through other receptors that form heterodimer with RXR, we examined its effect on the retinoic acid (RA)/RA receptor (RAR) system. Indeed, DEX also enhanced the RA-dependent increase in RARbeta mRNA in a cycloheximide-sensitive manner. Increase in the level of RXRalpha in hepatocytes by infection with the RXRalpha-expressing adenovirus resulted in enhancement of the T3-dependent increase in 5'DI mRNA. These results strongly suggest that the DEX-induced augmentation of T3-responsiveness in cultured hepatocytes is mediated, in part, by the increased expression of RXRalpha.

Role of transcription factor CCAAT/enhancer-binding protein alpha in human fetal liver cell typesin vitro

2014 ◽  
Vol 45 (8) ◽  
pp. 919-932 ◽  
Author(s):  
Jörg C. Gerlach ◽  
Patrick Over ◽  
Hubert G. Foka ◽  
Morris E. Turner ◽  
Robert L. Thompson ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Liver Cell ◽  
Fetal Liver ◽  
Binding Protein ◽  
Human Fetal Liver ◽  
Fetal Liver Cell ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein

scholarly journals Induction of Cytosolic Triiodo-L-Thyronine (T3) Binding Protein (CTBP) by T3 in Primary Cultured Rat Hepatocytes.

1993 ◽  
Vol 40 (4) ◽  
pp. 399-404 ◽  
Author(s):  
YUTAKA NISHII ◽  
KIYOSHI HASHIZUME ◽  
KAZUO ICHIKAWA ◽  
TEIJI TAKEDA ◽  
MUTSUHIRO KOBAYASHI ◽  
...  
Keyword(s):  
Binding Protein ◽  
Rat Hepatocytes ◽  
Primary Cultured Rat Hepatocytes ◽  
Cultured Rat Hepatocytes
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