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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Microarray analysis of genes regulated by SHP in wild-type and ob/ob mice.

ABSTRACT: Liver gene expression was compared in wild type, SHP knockout, ob/ob, and ob/ob SHP double mutant mice. A total of eight samples were analyzed using Affymetrix arrays. Each of the four genotypes studied were assayed in duplicate.

ORGANISM(S): Mus musculus

SUBMITTER: Scott Ochsner

PROVIDER: E-GEOD-40775 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Microarray analysis of genes regulated by SHP in wild-type and ob/ob mice.

Project description:Liver gene expression was compared in wild type, SHP knockout, ob/ob, and ob/ob SHP double mutant mice.

2012-09-12 | GSE40775 | GEO

Gene expression in the GWAT of ob/ob and ob/ob/Fsp27-/- mice

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Gene expression in the GWAT of ob/ob and ob/ob/Fsp27-/- mice

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Gene Expression in the BAT and WAT of ob/ob and ob/ob/Cidea-/-/Cidec-/- mice

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Whole-genome hypothalamic transcriptome data collected from wild-type and ob/ob Pdyn-eGFP-RPL10a mice using BAC TRAP procedure

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SHP-1 regulates transcription of PCK1 to control gluconeogenesis

Project description:The protein-tyrosine phosphatase SHP-1 (PTPN6) is an important glucose homeostasis modulator. Besides negatively regulating insulin signaling, the specific role of SHP-1 in metabolic control remains poorly understood. We show that SHP-1 acts as a co-activator for transcription of the phosphoenolpyruvate carboxykinase 1 (PCK1) gene, thereby modulating basal gluconeogenesis in hepatocytes. SHP-1 interacts with RNA polymerase II-subunits and signal transducer and activator of transcription 5 (STAT5), and localizes to the nucleus, where a sub-fraction of SHP-1 associates with chromatin. While SHP-1 binds to the PCK1-promoter, its loss affects RNA polymerase II-recruitment to this and other promoters of genes enriched for glucose metabolism-related functions. SHP-1-downregulation, and similarly STAT5 pharmacological inhibition reduce PCK1-transcript levels correlating with blunted gluconeogenesis. Overall, we identified a novel molecular SHP-1-function, that of a regulator of PCK1-transcription and subsequently hepatic gluconeogenesis, through physical interaction with the transcription machinery, mediated by an Akt-independent mechanism, but independent of STAT5 tyrosine-phosphorylation status.

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