pyruvate kinase C and glucose transporter GLUT-2 ( Valera et al. 1993 ), as well as the transcription factors c-fos and c-jun ( Gronowski & Rotwein 1995 ). More recent gene expression studies employing the microarray technology have identified many more
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Zhihao Liu, Fengrui Wu, Baowei Jiao, Xiuyue Zhang, Chongjiang Hu, Baofeng Huang, Linyan Zhou, Xigui Huang, Zhijian Wang, Yaoguang Zhang, Yoshitaka Nagahama, Christopher H K Cheng, and Deshou Wang
Introduction The doublesex and mab-3 (DM)-related transcription factor 1 ( Dmrt1 ) belongs to the DM domain gene family. Among the different phyla of the animal kingdom including vertebrates, it is the only gene found to be conserved
Kazunori Kageyama, Komaki Hanada, Yasumasa Iwasaki, Satoru Sakihara, Takeshi Nigawara, John Kasckow, and Toshihiro Suda
. Boutillier AL , Monnier D, Koch B & Loeffler JP 1994 Pituitary adenyl cyclase-activating peptide: a hypophysiotropic factor that stimulates proopiomelanocortin gene transcription, and proopiomelanocortin-derived peptide secretion in corticotropic cells
E N Fazio, M Everest, R Colman, R Wang, and C L Pin
pancreatic precursor cells into either acinar, islet or duct cells is apparent morphologically ( Slack 1995 ). The differentiation of these cells is regulated by the correct temporal and spatial expression of a series of transcription factors that direct
Marta Labeur, Damian Refojo, Barbara Wölfel, Johanna Stalla, Vivian Vargas, Marily Theodoropoulou, Michael Buchfelder, Marcelo Paez-Pereda, Eduardo Arzt, and Günter K Stalla
biosynthesis is coordinately controlled by different corticotrophin-releasing hormone (CRH)-triggered transcription factors at the level of the proopiomelanocortin ( Pomc ) promoter. Two Nur DNA-binding sites have been identified on the Pomc promoter. The
Mary Corless, Aoife Kiely, Neville H McClenaghan, Peter R Flatt, and Philip Newsholme
transcription factor, signal transduction, and metabolic enzyme gene expression. We have used 10 mM l -glutamine in the work reported in this paper, so as to saturate l -glutamine transport and allow comparison of our results with previously published studies
A Takenaka, K Komori, T Morishita, SI Takahashi, T Hidaka, and T Noguchi
To investigate the molecular mechanisms of increased transcription of the insulin-like growth factor-binding protein-1 (IGFBP-1) gene in dietary protein-deprived animals, the cis-acting sequence that is involved in this regulation was analyzed. We first showed that IGFBP-1 gene transcription was up-regulated by amino acid deprivation in cultured liver cell lines: H4IIE and HuH-7. Since HuH-7 cells showed a greater increase in IGFBP-1 mRNA in response to amino acid deprivation, this cell line was used in further experiments. Using a promoter function assay, we found that up-regulation of promoter activity responding to amino acid deprivation was abolished by deleting the region between -112 and -81 bp from the cap site from the gene construct. This cis-acting region includes the insulin-responsive element (IRE) and glucocorticoid responsive element (GRE) of IGFBP-1. In summary, the present observation suggests that the 32-bp (-112 to -81) in the IGFBP-1 gene 5' promoter region is involved in the induction of the IGFBP-1 gene in response to amino acid deprivation.
E Garcia, M Lacasa, B Agli, Y Giudicelli, and D Lacasa
Androgenic status affects rat preadipocyte adipose conversion from two deep intra-abdominal (epididymal and perirenal) fat depots differently. The aim of this study was to establish whether these site-specific alterations of adipogenesis are related to altered expressions of the transcriptional factors regulating proliferation and differentiation of preadipocytes, c-myc and CCAAT/enhancer binding proteins (C/EBPs: C/EBPalpha and beta). The increased proliferation of epididymal and perirenal preadipocytes from castrated rats was not linked to variations in c-myc mRNA and protein levels. The expression of the early marker of adipogenesis, lipoprotein lipase (LPL), was decreased by androgenic deprivation in epididymal cells but remained insensitive to the androgenic status in perirenal preadipocytes. In contrast, LPL expression increased in subcutaneous preadipocytes from castrated rats, an effect which was partly corrected by testosterone treatment. Expression of C/EBPbeta was unaffected by androgenic status whatever the anatomical origin of the preadipocytes. In contrast, the mRNA and protein levels of C/EBPalpha were greatly decreased by androgenic deprivation in epididymal cells, an alteration which could not be corrected by in vivo testosterone administration. Altogether these results demonstrated that in preadipocytes androgenic deprivation affects site-specifically the expression of LPL, an early marker of adipogenesis and of C/EBPalpha, a master regulator of adipogenesis. These observations contribute to an explanation of why castration induces defective adipose conversion in rat epididymal preadipocytes specifically.
Y Liu, P Cserjesi, A Nifuji, E N Olson, and M Noda
Abstract
Scleraxis is a recently identified transcription factor with a basic helix-loop-helix motif, which is expressed in sclerotome during embryonic development. We have examined the expression of scleraxis mRNA in rat osteoblastic cells and found that the scleraxis gene was expressed as a 1·2 kb mRNA species in osteoblastic osteosarcoma ROS 17/2·8 cells. The scleraxis mRNA expression was enhanced by type-β transforming growth factor (TGFβ) treatment. The TGFβ effect was observed in a dosedependent manner starting at 0·2 ng/ml and saturating at 2 ng/ml. The effect was time-dependent and was first observed within 12 h and peaked at 24 h. The TGFβ effect was blocked by cycloheximide, while no effect on scleraxis mRNA stability was observed. TGFβ treatment enhanced scleraxis-E box (Scx-E) binding activity in the nuclear extracts of ROS17/2·8 cells. Furthermore, TGFβ enhanced transcriptional activity of the CAT constructs which contain the Scx-E box sequence. TGFβ treatment also enhanced scleraxis gene expression in osteoblastenriched cells derived from primary rat calvaria. These findings indicated for the first time that the novel helixloop-helix type transcription factor (scleraxis) mRNA is expressed in osteoblasts and its expression is regulated by TGFβ.
Journal of Endocrinology (1996) 151, 491–499
B Lohrke, T Viergutz, SK Shahi, R Pohland, K Wollenhaupt, T Goldammer, H Walzel, and W Kanitz
A prominent functional change during differentiation of lutein cells from follicular thecal and granulosa cells is an enhanced production and secretion of progestins. The regulation of this process is not fully understood but may be associated with the expression of transcription factors which activate genes, products of which are involved in pathways of the cholesterol and lipid metabolism. As peroxisome proliferator-activated receptors (PPARs) play a role in both pathways, we were interested in the expression of PPARgamma, a PPAR form which is involved in adipogenic differentiation. First, we were able to show the expression of PPARgamma in bovine lutein cells (day 12 of the ovarian cycle) at the mRNA and protein level by imaging, flow cytometry and blot analysis, and secondly a role of PPARgamma in the secretion of progesterone. The cells (24 h culture) responded dose dependently by increasing progesterone secretion (up to 1.5-fold of the basal level) to an endogenous ligand of PPARgamma, 15-deoxy-delta12,14 prostaglandin J2 (15-dPGJ2) and to the thiazolidinedione ciglitizone. Aurintricarboxylic acid (ATA) was found to reduce the intracellular PPARgamma level and to promote cell cycle progress, indicating that ATA can be used as a tool for experimental changes of PPARgamma proteins in intact cells and for studying the physiological consequences. The ATA-mediated decrease of PPARgamma was accompanied by reduced progesterone production and a progression of the cell cycle, suggesting a function of PPARgamma in both processes. The response to ATA was abrogated by a high dose (>490 nM) of 15-dPGJ2, suggesting that 15-dPGJ2 exerts its effect on steroidogenic activity via PPARgamma and that the 15-dPGJ2-PPARgamma system plays a role in the maintenance of a differentiated quiescent stage in lutein cells.
