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Role of transcription factors ONECUT1 (HNF6), GATA6 and NKX6.1 during in vitro pancreatic differentiation of human pluripotent stem cells.

ABSTRACT: Role of transcription factors ONECUT1 (HNF6), GATA6 and NKX6.1 during in vitro pancreatic differentiation of human pluripotent stem cells.

PROVIDER: PRJNA545074 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15711671.fastq.gz	Fastqsanger.gz
	SRR15711672.fastq.gz	Fastqsanger.gz
	SRR9133810.fastq.gz	Fastqsanger.gz
	SRR9133811.fastq.gz	Fastqsanger.gz
	SRR9133812.fastq.gz	Fastqsanger.gz

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Role of transcription factors ONECUT1 (HNF6), GATA6 and NKX6.1 during in vitro pancreatic differentiation of human pluripotent stem cells.

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. ChIP sequencing of HNF6 as well as GATA6 and NKX6.1 during in vitro pancreatic differentiation will help to understand the regulatory mechanisms during cell fate decisions.

2021-10-27 | GSE131812 | GEO

Role of transcription factor ONECUT1 (HNF6) during in vitro pancreatic differentiation of human pluripotent stem cells [RNA-seq]

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. RNA 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 | GSE135416 | GEO

Role of transcription factor ONECUT1 (HNF6) during in vitro pancreatic differentiation of human pluripotent stem cells [ATAC-seq]

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

Mutations and variants of ONECUT1 in diabetes

Project description:Genes involved in distinct diabetes types suggest shared disease mechanisms. We show that rare ONECUT1 coding variants cause monogenic recessive diabetes (neonatal or very early-onset, syndromic) in two unrelated patients, and monogenic dominant diabetes (early adult-onset) in heterozygous relatives of these and 13 additional unrelated cases. Patients heterozygous for rare ONECUT1 coding variants define a subgroup of T2D with early-onset diabetes and other features. In addition, common regulatory ONECUT1 variants are associated with multifactorial T2D. Directed differentiation of human pluripotent stem cells to the pancreatic lineage revealed that loss of ONECUT1 impairs pancreatic progenitor formation and a subsequent endocrine program. We uncovered that ONECUT1 activates the pro-endocrine genes NKX6.1 and NKX2.2 through binding to their cis-regulatory elements. Globally, ONECUT1-directed gene transcription occurs in association with major islet transcription factors, at clusters of pancreas- and endocrine-specific enhancers within open chromatin. ONECUT1 regulates a transcriptional and epigenetic machinery critical for proper endocrine pancreatic development, involved in a spectrum of diabetes, monogenic recessive and dominant, and multifactorial.

2021-11-03 | PXD018887 | Pride

Role of transcription factor ONECUT1 (HNF6) during in vitro pancreatic differentiation of human pluripotent stem cells [ATAC-seq]

Project description:Role of transcription factor ONECUT1 (HNF6) during in vitro pancreatic differentiation of human pluripotent stem cells [ATAC-seq]

| PRJNA545075 | ENA

Role of transcription factor ONECUT1 (HNF6) during in vitro pancreatic differentiation of human pluripotent stem cells [RNA-seq]

Project description:Role of transcription factor ONECUT1 (HNF6) during in vitro pancreatic differentiation of human pluripotent stem cells [RNA-seq]

| PRJNA558795 | ENA

Targets of HNF1b, HNF4a2 and HNF6 in INS-1 cells

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

A CpG mutational hotspot in a ONECUT (HNF6) binding site accounts for the prevalent variant of Hemophilia B Leyden

Project description:Hemophilia B, or the 'Royal Disease', arises from mutations in the Coagulation Factor IX (F9) gene. Mutations within the F9 promoter are associated with a remarkable form of the disease, termed Hemophilia B Leyden, in which symptoms ameliorate after puberty. Mutations at the -5/-6 site account for the majority of Leyden cases, and have been postulated to disrupt the binding of a transcriptional activator, the identity of which has remained elusive for more than twenty years. Here we show that the ONECUT transcription factors (ONECUT1/HNF6 and ONECUT2/HNF6B) bind to the -5/-6 site. The various Hemophilia B Leyden mutations that have been reported in this site inhibit ONECUT binding to varying degrees that correlate well with their associated clinical severities. In addition, expression of F9 is crucially dependent on ONECUT factors in vivo and as such, mice that are deficient in either ONECUT1, ONECUT2 or both, exhibit depleted levels of F9. Taken together, our findings establish the ONECUT transcription factors as the missing regulators of Hemophilia B Leyden that operate through the -5/-6 site.

2013-03-06 | E-MTAB-890 | biostudies-arrayexpress

Identification of Hnf6 binding sites in male and female mouse liver

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

Pathophysiological role of hepatocyte nuclear factor 6 (HNF6) during cholestatic liver injury

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

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