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Insulin receptor associates with promoters genome-wide and regulates gene expression [RNA-seq]

ABSTRACT: RNA-seq analysis identifies transcripts regulated by insulin treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE107334 | GEO | 2019/04/04

REPOSITORIES: GEO

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Insulin receptor associates with promoters genome-wide and regulates gene expression [RNA-seq 2]

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Insulin Receptor Associates with Promoters Genome-wide and Regulates Gene Expression.

Project description:Insulin receptor (IR) signaling is central to normal metabolic control and dysregulated in prevalent chronic diseases. IR binds insulin at the cell surface and transduces rapid signaling via cytoplasmic kinases. However, mechanisms mediating long-term effects of insulin remain unclear. Here, we show that IR associates with RNA polymerase II in the nucleus, with striking enrichment at promoters genome-wide. The target genes were highly enriched for insulin-related functions including lipid metabolism and protein synthesis and diseases including diabetes, neurodegeneration, and cancer. IR chromatin binding was increased by insulin and impaired in an insulin-resistant disease model. Promoter binding by IR was mediated by coregulator host cell factor-1 (HCF-1) and transcription factors, revealing an HCF-1-dependent pathway for gene regulation by insulin. These results show that IR interacts with transcriptional machinery at promoters and identify a pathway regulating genes linked to insulin's effects in physiology and disease.

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Insulin receptor associates with promoters genome-wide and regulates gene expression [ChIP-seq]

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Insulin receptor associates with promoters genome-wide and regulates gene expression

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Insulin receptor associates with promoters genome-wide and regulates gene expression

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

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Insulin receptor associates with promoters genome-wide and regulates gene expression [RNA-seq]

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Insulin receptor associates with promoters genome-wide and regulates gene expression [ChIP-seq]

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Insulin receptor signaling in osteoblasts regulates postnatal bone acquisition and body composition

Project description:Global energy balance in mammals is controlled by the actions of circulating hormones that coordinate fuel production and utilization in metabolically active tissues. Bone-derived osteocalcin, in its undercarboxylated, hormonal form, regulates fat deposition and is a potent insulin secretagogue. Here, we show that insulin receptor (IR) signaling in osteoblasts controls osteoblast development and osteocalcin expression by suppressing the Runx2 inhibitor Twist-2. Mice lacking IR in osteoblasts have low circulating undercarboxylated osteocalcin and reduced bone acquisition due to decreased bone formation and deficient numbers of osteoblasts. With age, these mice develop marked peripheral adiposity and hyperglycemia accompanied by severe glucose intolerance and insulin resistance. The metabolic abnormalities in these mice are improved by infusion of exogenous under-carboxylated osteocalcin. These results indicate the existence of a bone-pancreas endocrine loop through which insulin signaling in the osteoblast ensures osteoblast differentiation and stimulates osteocalcin production, which in turn regulates insulin sensitivity and pancreatic insulin secretion to control glucose homeostasis. We used microarrays to detail the global gene expression changes in response to insulin acting through insulin receptor in osteoblasts and identified distinct genes specifically involved in bone remodeling process. 4 groups and 3 time points (0h as a control, 6h, 12h, and 24h)

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