HNF1b, HNF4a2 and HNF6 targets
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ABSTRACT:
PROVIDER: PRJNA99505 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series:; GSE1589: Targets of HNF1b, HNF4a2 and HNF6 in INS-1 cells; GSE1590: Targets of HNF1b mutants in INS-1; GSE1591: INS-1 cell lines (FLP-In T-REx) Experiment Overall Design: Refer to individual Series
2007-11-29 | E-GEOD-6428 | biostudies-arrayexpress
Project description:A rat insulinoma cell line (INS-1) was generated that contains a FRT site for FLP recombinase mediated site specific integration of specific genes. In addition, the line contains the tetracycline repressor allowing tetracycline (tet) induction of the introduced gene. By comparing the gene expression profiles of uninduced and tet-induced cells, target genes of introduced transcription factors HNF1b, HNF4a2, and HNF6 (onecut1) were identified. Two different clones containing the same transcription factor were analyzed in the non-induced and tet-induced (24 h) state. Keywords: ordered
2004-11-05 | GSE1589 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2006-12-03 | GSE6428 | GEO
Project description:∼40,000 HNF6 binding sites were identified in mouse liver chromatin, including several thousand sites showing significant differences in level of HNF6 binding between male and female mouse liver. These sex-biased HNF6 binding sites showed strong enrichment for sex-biased DNase hypersensitive sites and for proximity to genes showing local sex-biased chromatin marks and a corresponding sex-biased expression. ~90% of genome-wide CUX2 binding sites identified previously in female mouse liver (Conforto TL, Zhang Y, Sherman J, Waxman DJ., Mol Cell Biol. 2012;32(22):4611-4627) were also bound by HNF6, giving evidence for genome-wide competition between HNF6 and CUX2 for chromatin binding in female mouse liver. These HNF6/CUX2 common binding sites were enriched for genomic regions more accessible in male than in female mouse liver chromatin, and showed strongest enrichment for male-biased genes, suggesting HNF6 displacement by CUX2 as a mechanism to explain the observed CUX2 repression of male-biased genes in female liver. However, HNF6 binding was sex-independent at a majority of its binding sites, and peak regions of HNF6 binding were frequently associated with co-binding by multiple other liver transcription factors, consistent with HNF6 playing a global regulatory role in both male and female liver.
2015-07-28 | GSE60014 | GEO
Project description:A rat insulinoma cell line (INS-1) was generated that contains a FRT site for FLP recombinase mediated site specific integration of specific genes. In addition, the line contains the tetracycline repressor allowing tetracycline (tet) induction of the introduced gene. By comparing the gene expression profiles of uninduced and tet-induced cells, target genes of introduced transcription factors HNF1b and HNF1b mutants were identified. Two different clones containing the same transcription factor were analyzed in the non-induced and tet-induced (24 h) state. Keywords: ordered
2004-11-05 | GSE1590 | GEO
Project description:Animal models of parenchymal liver injury by bile duct ligation (BDL) and all forms of liver diseases including neonatal hepatitis and clinical obstructive cholangiopathies such as biliary atresia have the pathological features of cholestasis and liver dysfunction. Hepatocyte nuclear factors 6 (HNF6) is important to the transcriptional regulation, expression and function of essential hepatic genes involved in the differentiated as well as the adaptive response to liver injury. Using HNF6 conditional knock out mice where HNF6 is functionally deleted in the liver, we established that HNF6 is required for proper liver function of cholesterol clearance, improvement of cholestasis and hepatocyte regeneration. Enhancing HNF6 expression in wild type mice also diminished hepatic apoptosis and fibrosis. In this proposal, we propose to further characterize the biological function of HNF6 by testing the HYPOTHESIS that HNF6 direct transcriptional regulation of antiapoptotic and antifibrotic pathways contributes to hepatoprotection during bile duct injury. This hypothesis will be tested in two specific aims.
2016-10-06 | GSE80498 | GEO
Project description:∼40,000 HNF6 binding sites were identified in mouse liver chromatin, including several thousand sites showing significant differences in level of HNF6 binding between male and female mouse liver. These sex-biased HNF6 binding sites showed strong enrichment for sex-biased DNase hypersensitive sites and for proximity to genes showing local sex-biased chromatin marks and a corresponding sex-biased expression. ~90% of genome-wide CUX2 binding sites identified previously in female mouse liver (Conforto TL, Zhang Y, Sherman J, Waxman DJ., Mol Cell Biol. 2012;32(22):4611-4627) were also bound by HNF6, giving evidence for genome-wide competition between HNF6 and CUX2 for chromatin binding in female mouse liver. These HNF6/CUX2 common binding sites were enriched for genomic regions more accessible in male than in female mouse liver chromatin, and showed strongest enrichment for male-biased genes, suggesting HNF6 displacement by CUX2 as a mechanism to explain the observed CUX2 repression of male-biased genes in female liver. However, HNF6 binding was sex-independent at a majority of its binding sites, and peak regions of HNF6 binding were frequently associated with co-binding by multiple other liver transcription factors, consistent with HNF6 playing a global regulatory role in both male and female liver. Livers were excised from individual male and female mice, cross-linked and sonicated, then used to identify HNF6 binding sites by ChIP-Seq using antibody specific to HNF6 (sc-13050; Santa Cruz Biotechnology, Inc).
2015-07-28 | E-GEOD-60014 | biostudies-arrayexpress
Project description:The aim of this study was to test, in vivo, if Foxa2 inhibits HNF6-mediated transcription in the liver. We utilized hepatocyte-specific gene ablation of Foxa2 and the Mouse PromoterChip BCBC 3.0 and Mouse PancChip 5.0 cDNA microarrays to investigate HNF6 binding to its target promoters in vivo in the presence or absence of Foxa2. For the mouse promoter microarray analysis, chromatin immunoprecipitation using anti-HNF6 antibodies was performed on chromatin isolated from Foxa2loxP/loxP Alfp.Cre and control mouse livers. Along with sheared genomic DNA (common reference), the immunoprecipitated DNA was amplified, labeled and hybridized to the Mouse PromoterChip BCBC 3.0. For microarray analysis of gene expression, liver RNAs were isolated from three Foxa2loxP/loxP Alfp.Cre and three control mice. RNAs were reverse transcribed, labeled, and hybridized to the Mouse PancChip 5.0. Overall, our studies demonstrate that HNF6 binds to and regulates its target promoters in vivo in the presence and absence of Foxa2 and that the expression levels of HNF6 targets are not influenced by Foxa2.
2007-09-14 | E-CBIL-36 | biostudies-arrayexpress
Project description:We have identified HNF6 as an essential transcription factor for endocrine pancreatic development. HNF6 binds to and possibly regulates other isletogenesis transcription factors, driving endocrine differentiation. ATAC sequencing of control and HNF6-depleted hESC during in vitro pancreatic differentiation will help to understand the regulatory mechanisms during cell fate decisions.
2021-10-27 | GSE131816 | GEO
Project description:Targets of HNF1b, HNF4a2 and HNF6 in INS-1 cells
| PRJNA104741 | ENA