A glucose-responsive transcription factor that regulates carbohydrate metabolism in the liver
By H. Yamashita, M. Takenoshita, M. Sakurai, R. Bruick, W. Henzel, W. Shillinglaw, D. Arnot, K. Uyeda. Proceedings of the National Academy of Sciences of the United States of America, 2001
681 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/2d107b092ac477a446c9fb194de7a9bce2e3f4a1
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Citations in the corpus
- Thioredoxin-interacting protein mediates ER stress-induced β cell death through initiation of the inflammasome (2012, background): “ChREBP is a transcription factor that binds to the carbohydrate response element of the LPK gene (Yamashita et al., 2001) and has been shown to be involved in TXNIP upregulation by chronic hyperglycemia in INS-1 cells (Minn et al., 2005).”
- Molecular mediators of hepatic steatosis and liver injury. (2004, neutral): “Carbohydrate (glucose)-mediated stimulation of lipogenesis is transcriptionally mediated by a second bHLH-Zip transcription factor, designated carbohydrate response element binding protein (ChREBP) (36).”
- Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease (2018, background): “ChREBP mediates carbohydrate, but not fat-induced DNL as high fat diets do not activate ChREBP and may even decrease ChREBP activity [43, 47].”
- Energy Metabolism in the Liver (2014, neutral): “ChREBP binds to the E-box motifs in the L-PK promoter and activates L-PK expression in hepatocytes (290).”
- Insulin resistance drives hepatic de novo lipogenesis in nonalcoholic fatty liver disease. (2019, background): “Data from studies conducted in cell systems and rodent models have shown insulin and glucose independently regulate hepatic DNL by activating SREBP-1c and ChREBP, respectively (25, 27-30, 39), which in turn activate nearly all the genes involved in hepatic DNL.”
- Mouse models in non‐alcoholic fatty liver disease and steatohepatitis research (2006, background): “Targeted disruption of the ChREBP gene in a mouse model has been shown to produce a 50% reduction in the expression of key enzymes that mediate lipogenesis (Iizuka et al. 2004).”