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RNA sequencing of SHP -/- knockout mouse transcriptome

ABSTRACT: Goal of this study is to identify annotated and non-annotated genes transcriptionally regulated by small heterodime partner (SHP, Nrob2) expression. Liver 5' capped RNA samples from three SHP -/- and three wild type mice were sequenced with Illumina GAII sequencer.

ORGANISM(S): Mus musculus

SUBMITTER: Don Delker

PROVIDER: E-GEOD-43893 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide transcriptome analysis identifies novel gene signatures implicated in human chronic liver disease.

Smalling Rana V RV Delker Don A DA Zhang Yuxia Y Nieto Natalia N McGuiness Michael S MS Liu Shuanghu S Friedman Scott L SL Hagedorn Curt H CH Wang Li L

American journal of physiology. Gastrointestinal and liver physiology 20130627 5

The molecular mechanisms behind human liver disease progression to cirrhosis remain elusive. Nuclear receptor small heterodimer partner (SHP/Nr0b2) is a hepatic tumor suppressor and a critical regulator of liver function. SHP expression is diminished in human cirrhotic livers, suggesting a regulatory role in human liver diseases. The goal of this study was to identify novel SHP-regulated genes that are involved in the development and progression of chronic liver disease. To achieve this, we cond ...[more]

PMID: 23812039

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RNA sequencing of SHP -/- knockout mouse transcriptome

Project description:Goal of this study is to identify annotated and non-annotated genes transcriptionally regulated by small heterodime partner (SHP, Nrob2) expression.

2013-10-22 | GSE43893 | GEO

Concomitant deletion of Shp-1 and Shp-2 in T cells fails to improve anticancer responses

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2022-09-29 | PXD034897 | Pride

Gene expression analysis of FXR null, SHP null, and double FXR/SHP null mice

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SHP-1 regulates transcription of PCK1 to control gluconeogenesis

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Gene expression analysis of FXR null, SHP null, and double FXR/SHP null mice

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A Themis:SHP complex promotes T cell survival

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2015-01-07 | PXD001410 | Pride

Feeding activates FGF15-SHP-TFEB-mediated lipophagy in the gut

Project description:Lysosome-mediated macroautophagy, including lipophagy, is activated under nutrient deprivation but is repressed after feeding. We show that feeding unexpectedly activates intestinal lipophagy in a manner dependent on both the orphan nuclear receptor, small heterodimer partner (SHP/NR0B2), and the late fed-state gut hormone, fibroblast growth factor-15/19 (FGF15/19). Postprandial intestinal triglycerides (TGs) and apolipoprotein-B48 (ApoB48), the TG-rich chylomicron marker, were elevated in SHP-knockout and FGF15-knockout mice. Genomic analyses in mouse intestine revealed that SHP partners with the key lysosomal activator, transcription factor-EB (TFEB), upregulating autophagy/lipolysis network genes after feeding. In HT29 intestinal cells, FGF19 treatment activated lipophagy in a manner dependent on both SHP and TFEB, reducing TG and ApoB48 levels. Mechanistically, feeding-induced FGF15/19 signaling increases nuclear localization of TFEB and SHP via PKCβ/ζ-mediated phosphorylation, leading to transcriptional induction of Ulk1 and Atgl. Collectively, these results demonstrate that after feeding, FGF15/19-activated SHP and TFEB paradoxically activate gut lipophagy, limiting postprandial TG levels. As excess lipids cause dyslipidemia and obesity, the FGF15/19-SHP-TFEB axis that reduces intestinal TGs via lipophagic activation provides promising therapeutic targets for obesity-associated metabolic disease.

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