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Laboratory of Reproductive Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan
Department of Biochemistry and the Environmental Science Programme, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China
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Laboratory of Reproductive Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan
Department of Biochemistry and the Environmental Science Programme, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China
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Laboratory of Reproductive Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan
Department of Biochemistry and the Environmental Science Programme, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China
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Laboratory of Reproductive Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan
Department of Biochemistry and the Environmental Science Programme, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China
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Laboratory of Reproductive Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan
Department of Biochemistry and the Environmental Science Programme, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China
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Laboratory of Reproductive Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan
Department of Biochemistry and the Environmental Science Programme, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China
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Laboratory of Reproductive Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan
Department of Biochemistry and the Environmental Science Programme, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China
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Laboratory of Reproductive Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan
Department of Biochemistry and the Environmental Science Programme, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China
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Laboratory of Reproductive Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan
Department of Biochemistry and the Environmental Science Programme, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China
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Laboratory of Reproductive Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan
Department of Biochemistry and the Environmental Science Programme, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China
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Laboratory of Reproductive Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan
Department of Biochemistry and the Environmental Science Programme, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China
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Laboratory of Reproductive Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan
Department of Biochemistry and the Environmental Science Programme, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China
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Laboratory of Reproductive Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan
Department of Biochemistry and the Environmental Science Programme, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China
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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
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. 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
Physiology and Pharmacology and
Medicine, University of Western Ontario, Canada
Children’s Health Research Institute, London, Ontario, Canada
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Physiology and Pharmacology and
Medicine, University of Western Ontario, Canada
Children’s Health Research Institute, London, Ontario, Canada
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Physiology and Pharmacology and
Medicine, University of Western Ontario, Canada
Children’s Health Research Institute, London, Ontario, Canada
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Physiology and Pharmacology and
Medicine, University of Western Ontario, Canada
Children’s Health Research Institute, London, Ontario, Canada
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Physiology and Pharmacology and
Medicine, University of Western Ontario, Canada
Children’s Health Research Institute, London, Ontario, Canada
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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
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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
School of Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland, UK
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School of Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland, UK
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School of Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland, UK
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School of Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland, UK
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School of Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland, UK
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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
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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.
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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.
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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.
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Steroidogenic factor-1 (SF-1) is a key regulator of endocrine development, and mediates expression of gonadotrophin-specific genes in the pituitary. Basal and hormone stimulated transcription of the human glycoprotein hormone alpha-subunit gene (alphaGSU) in gonadotrophs involves SF-1 and its cognate binding site, the gonadotroph-specific element (GSE). In this study, we demonstrate that SF-1 significantly enhances basal and forskolin-stimulated transcription of the human alphaGSU promoter in GH(3) cells. Mutation of the GSE abolished the SF-1-mediated transactivation of basal alphaGSU promoter activity, and significantly attenuated the forskolin effect by 50%. Mutation of the Ser203 residue in SF-1 to Ala blocked basal transactivation of alphaGSU promoter activity, and halved the forskolin effect. These data collectively reveal a direct role for SF-1 and the GSE in mediating basal and forskolin-stimulated transcription of the human alphaGSU promoter in GH(3) cells. The phosphorylation site at Ser203 appears to be required for these effects.
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The transcription factor Pax8 plays an important role in the expression of the differentiated phenotype of thyroid follicular cells. It has recently been shown that Pax8 is necessary for thyroglobulin (Tg) gene expression in the fully differentiated rat thyroid cell line PC. We have used the PC model system to investigate the role of Pax8 as a mediator of TSH regulation of Tg gene expression. We have demonstrated that Pax8 expression, as well as Tg expression, is severely reduced in cells grown in the absence of hormones and serum. The re-addition of TSH or forskolin to the culture medium is able to restore to wild-type levels the expression of both Pax8 and Tg. We have determined that the action of TSH/forskolin on Pax8 is at the transcriptional level. However, the re-expression of Pax8 can be observed several hours before that of Tg, suggesting that either another factor is needed or that Pax8 itself must be post-translationally modified by a newly synthesized protein to become active. To distinguish between these two possibilities we have stably transfected into PC cells an exogenous Pax8 that is expressed independently of TSH. Our results indicate that in these cells the Tg promoter is still dependent on TSH despite the constitutive presence of Pax8. Furthermore, we also show that in this condition Tg gene transcription requires de novo protein synthesis. In conclusion, TSH regulates the expression of Pax8 at a transcriptional level and also regulates the activity of Pax8 by controlling the expression of one or more as yet unknown factors.
