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H19 regulates hepatic glucose production by epigenetic modification of Hnf4*

ABSTRACT: H19 regulates hepatic glucose production by epigenetic modification of Hnf4*

PROVIDER: PRJNA401336 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5985650_1.fastq.gz	Fastqsanger.gz
	SRR5985650_2.fastq.gz	Fastqsanger.gz
	SRR5985651_1.fastq.gz	Fastqsanger.gz
	SRR5985651_2.fastq.gz	Fastqsanger.gz
	SRR5985652_1.fastq.gz	Fastqsanger.gz

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H19 regulates hepatic glucose production by epigenetic modification of Hnf4*

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-08-30 | GSE103437 | GEO

Identification of genes regulated by Long noncoding RNA H19 in hepatic cells

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Drosophila HNF4 promotes glucose-stimulated insulin secretion and increased mitochondrial function in adults [ChIP-seq]

Project description:Although mutations in the nuclear receptor HNF4A were identified as the cause of Maturity Onset Diabetes of the Young 1 (MODY1) nearly two decades ago, the mechanisms by which HNF4A regulates glucose homeostasis remain unclear. Here we report that loss of Drosophila HNF4 recapitulates hallmark symptoms of MODY1, including adult-onset hyperglycemia, glucose intolerance and impaired glucose-stimulated insulin secretion (GSIS). These defects are linked to an unexpected role for dHNF4 within mitochondria to directly regulate mtDNA transcription, while also promoting the expression of nuclear genes involved in oxidative phosphorylation (OXPHOS) and Hex-C, a homolog of the MODY2 gene Glucokinase. dHNF4 is required in the fat body and insulin-producing cells to maintain glucose homeostasis by supporting a developmental switch toward OXPHOS and GSIS at the transition to adulthood. These findings establish an animal model for MODY1 and define a developmental reprogramming of metabolism to support the energetic needs of the mature animal.

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Drosophila HNF4 promotes glucose-stimulated insulin secretion and increased mitochondrial function in adults [RNA-seq]

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MicroRNA expression profiling of Igf2-p and H19-m mutant mouse embryos

Project description:Changes in microRNA expression in Igf2-p and H19-m mouse embryos (E9.5) were determined in order to assess whether perturbation of miR-483* and miR-675 in Igf2-p and H19-m mutants was likely to have contributed to a modification of tumour phenotype. The Igf2 gene contains miR-483* but the targeted deletion of Igf2-p in these mice spares the region encoding this microRNA. The H19 gene contains miR-675 and its expression was mono-allelelic in heterozygous H19-m mice as evidenced by a significant reduction in miR-675 in these mice relative to WT.

2011-12-01 | E-MTAB-873 | biostudies-arrayexpress

Drosophila HNF4 promotes glucose-stimulated insulin secretion and increased mitochondrial function in adults

Project description:Drosophila HNF4 promotes glucose-stimulated insulin secretion and increased mitochondrial function in adults

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Identification of genes regulated by long noncoding RNA H19 in skeletal muscle

Project description:Soleus muscle has the most abundant H19 expression compared to other skeletal muscle tissues. In order to identify genes regulated by long noncoding RNA H19 in skeletal muscle, we performed RNA-Seq with dissected WT and H19KO soleus muscles from 21 week old mice. Among the differentially expressed genes, we found skeletal muscle - overexpressed gene DUSP27, which potentially plays an important role in regulating skeletal muscle glucose metabolisim by regulating the activitiy of AMPK, might be a target of H19 mediated regulation.

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Transcription profiling of mouse HNF4 null mutant colon vs. control colons

Project description:Background and Aims: HNF4? is a nuclear hormone receptor transcription factor that has been shown to be required for hepatocyte differentiation and development of the liver. It has also been implicated in regulating expression of genes that act in the epithelium of the lower gastrointestinal tract. This implied that HNF4? might be required for development of the gut. Methods: We generated mouse embryos in which Hnf4? was ablated in the epithelial cells of the fetal colon using Cre-loxP technology. Embryos were examined using a combination of histology, immunohistochemistry, gene array and RT-PCR, and chromatin immunoprecipitation analyses to define the consequence of loss of HNF4? on colon development. Results: Embryos could be generated until E18.5 that lacked HNF4? in their colon. Although, early stages of colonic development occurred, HNF4? null colons failed to form normal crypts. In addition, goblet cell maturation was perturbed and expression of an array of genes that encode proteins with diverse roles in colon function was disrupted. Several genes whose expression in the colon was dependent on HNF4? contained HNF4?âbinding sites sequences within putative transcriptional regulatory regions and a subset of these sites were occupied by HNF4? in vivo. Conclusion: HNF4? is a transcription factor that is essential for development of the mammalian colon, regulates goblet cell maturation and is required for expression of genes that control normal colon function and epithelial cell differentiation. Experiment Overall Design: COMPARISON OF 3 MUTANT TO 2 CONTROL COLONS.

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Accessible chromatin profiles of intestinal epithelial cells upon HNF4 loss in embryos by ATAC-seq

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2019-07-29 | GSE128674 | GEO

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