Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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JNK-mediated control of gene expression in liver


ABSTRACT: RNAseq analysis of gene expression in Liver of Control and JNK deficient mice fed a control or a High fat diet Contro(Albcre+)l and mice with liver-specific defiency of JNK (Alb Cre+ Jnk1flox/flox, Jnk2flox/flox or Jnk1flox/floxJnk2flox/flox) were fed a control or a high fat diet for 16 weeks. Gene expression analysis in liver was analyzed by RNAseq

ORGANISM(S): Mus musculus

SUBMITTER: Roger Davis 

PROVIDER: E-GEOD-55190 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

The PPARα-FGF21 hormone axis contributes to metabolic regulation by the hepatic JNK signaling pathway.

Vernia Santiago S   Cavanagh-Kyros Julie J   Garcia-Haro Luisa L   Sabio Guadalupe G   Barrett Tamera T   Jung Dae Young DY   Kim Jason K JK   Xu Jia J   Shulha Hennady P HP   Garber Manuel M   Gao Guangping G   Davis Roger J RJ  

Cell metabolism 20140717 3


The cJun NH2-terminal kinase (JNK) stress signaling pathway is implicated in the metabolic response to the consumption of a high-fat diet, including the development of obesity and insulin resistance. These metabolic adaptations involve altered liver function. Here, we demonstrate that hepatic JNK potently represses the nuclear hormone receptor peroxisome proliferator-activated receptor α (PPARα). Therefore, JNK causes decreased expression of PPARα target genes that increase fatty acid oxidation  ...[more]

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