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A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism: Liver RNA profiles of mice treated with adenoviruses expressing either Mafg cDNA or empty vector.

ABSTRACT: A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism: Liver RNA profiles of mice treated with adenoviruses expressing either Mafg cDNA or empty vector.

PROVIDER: PRJNA497096 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8064890_1.fastq.gz	Fastqsanger.gz
	SRR8064890_2.fastq.gz	Fastqsanger.gz
	SRR8064891_1.fastq.gz	Fastqsanger.gz
	SRR8064891_2.fastq.gz	Fastqsanger.gz
	SRR8064892_1.fastq.gz	Fastqsanger.gz

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A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism: Liver RNA profiles of mice treated with adenoviruses expressing either Mafg cDNA or empty vector.

Project description:Obesity and type 2 diabetes mellitus are global emergencies and long noncoding RNAs (lncRNAs) are regulatory transcrips with elusive functions in metabolism. Here we report that an unexpectedly high fraction of lncRNAs, but not protein-coding mRNAs, is repressed during diet-induced obesity (DIO) and refeeding, whilst nutrient deprivation specifically induced lncRNAs in mouse liver. Similarly, lncRNAs were lost in diabetic humans. LncRNA promoter analyses, global cistrome and gain-of-function analyses confirmed that increased MAFG signaling during DIO curbs lncRNA expression. Silencing Mafg in primary hepatocytes and in vivo elicited a fasting-like expression profile, improved glucose metabolism, derepressed lncRNAs and prevented mammalian target of rapamycin (mTOR)-driven protein translation. We found that obesity-repressed lincIRS2 is controlled by MAFG and observed that genetic and RNAi-mediated lincIRS2 loss causes hyperglycemia, insulin resistance and aberrant glucose output in lean mice. Taken together, we identify a novel MAFG-lncRNA axis controlling hepatic glucose metabolism in health and metabolic disease.

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Genome wide RNA-sequencing of human pluripotent stem-cell derived endothelial cells 48h after transduction with adenoviruses expressing either empty vector or single transcription factor

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A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism: Liver RNA profiles of mice injected with control, Mafg and LncIRS2 LNA.

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Genome wide RNA-sequencing of human pluripotent stem-cell derived endothelial cells 48h after transduction with adenoviruses expressing either empty vector of different combination of transcription factors

Project description:To induce barrier of stem-cell derived endothelial cells in vitro cells have been transduced with a mixture of adenovirus overexpressing transcription factors with potential role in endothelial cell barrier stabilization. Adenoviruses overexpressing ETS1, SOX18 and SOX7 have been part of both transcription factor mixtures. As fourth transcription factor in the mixture included TAL1 while the other mixture included LEF1. Each transcription factor was used at 20 MOI. As control adenovirus overexpressing empty vectors has been used (80 MOI).

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Comparison of gene expression profiles of MafF-/-: MafG-/-: MafK-/- embryos and MafF-/-: MafG+/+: MafK-/- embyos

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A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism: Liver RNA profiles of obese and lean mice.

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