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ChREBP is activated by reductive stress and mediates GCKR-associated metabolic traits

ABSTRACT: We investigate the transcriptional effect of alcohol gavages on wildtype versus ChREBP KO mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE227057 | GEO | 2024/01/02

REPOSITORIES: GEO

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ChREBP is activated by reductive stress and mediates GCKR-associated metabolic traits

Project description:We investigate the transcriptional effect of alcohol gavages on wildtype versus ChREBP KO mice.

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ChREBP is activated by reductive stress and mediates GCKR-associated metabolic traits

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Proline hydroxylation of ChREBP

Project description:This project investigated proline hydroxylation of ChREBP. Proline hydroxylation was investigated in flag-IP enriched protein extracts from ChREBP-flag overexpressing HEK293 cells (A) and in ChREBP-IP enriched mouse liver protein (male, C57BL6/J) (B).

2020-10-19 | PXD019137 | Pride

Gene expression altered by high-fructose diet feeding and Chrebp deficiency

Project description:Epidemiologic and animal studies implicate overconsumption of fructose in the development of non-alcoholic fatty liver disease, but the molecular mechanisms underlying fructose-induced chronic liver diseases remains largely unknown. We present evidence supporting the essential function of the lipogenic transcription factor ChREBP in mediating adaptation response to fructose and protecting against fructose-induced hepatotoxicity. High-fructose diet (HFrD) activates hepatic lipogenesis via a ChREBP-dependent manner in wildtype mice, while inducing steatohepatitis in Chrebp-KO mice. In Chrebp-KO mouse livers, HFrD reduces levels of molecular chaperones and activates the CHOP-dependent unfolded protein response, whereas administration of chemical chaperone or Chop shRNA rescues liver injury. Gene expression profiling revealed elevated expression of cholesterol biosynthesis genes in Chrebp-KO livers after HFrD, in parallel with increased abundance of nuclear SREBP2. genes expression were compared between livers of wildtype mice fed 70%-fructose-diet v.s. regular chow, and between livers of Chrebp-/- mice v.s. wildtype mice fed 70%-fructose-diet.

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Cooperative Regulation of Normal and Neoplastic Hepatocyte Proliferation by Myc and ChREBP

Project description:By analogy to the c-Myc (Myc)/Max family of transcription factors, there also exists a “parallel” network of structurally and functionally related bHLH-ZIP proteins with certain Myc-like functions. Two closely related “Myc-like” paralogs termed Mondo A and MondoB/ChREBP (ChREBP) positively regulate gene expression in heterodimeric association with the Max-like factor Mlx. Myc is necessary to support liver cancer cell growth but not for normal hepatocyte proliferation. Here, we investigated the role for ChREBP and its relationship to Myc in these processes. Unlike Myc, ChREBP loss conferred a marked proliferative disadvantage to normal hepatocytes as did the loss of both ChREBP and Myc. In addition, hepatoblastomas (HBs) originating in myc-/-, chrebp-/- or myc-/-/chrebp-/- backgrounds grew significantly more slowly. Metabolic studies performed on livers and HBs arising in all three backgrounds showed marked differences in oxidative phosphorylation, fatty acid -oxidation (FAO) and the activity of pyruvate dehydrogenase. RNAseq of livers and HBs indicated seven distinct forms of target transcript regulation. Gene ontology analysis indicated that many transcripts de-regulated in the chrebp-/- background encode enzymes functioning in glycolysis, the TCA cycle and - and-FAO whereas those in myc-/- background encode enzymes for glycolysis, glutaminolysis and sterol biosynthesis. Transcript de-regulation in the double knockout group was similar but also included those involved in peroxisomal - and -FAO. Finally, we identified cooperative positive regulation by Myc and ChREBP of virtually all ribosomal protein genes. Our findings define the global proliferative, metabolic and transcriptional roles for the more general “Extended Myc Network” under both normal and neoplastic conditions.

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