ArticleMolecular endocrinology (Baltimore, Md.)2010
c-Myc is required for the CHREBP-dependent activation of glucose-responsive genes.
Article in Molecular endocrinology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 54 citations in OpenAlex.
- The Use of Patient-Derived Organoids in the Study of Molecular Metabolic Adaptation in Breast Cancer.International journal of molecular sciences · 2024Review
- Body-Wide Inactivation of the Myc-Like Mlx Transcription Factor Network Accelerates Aging and Increases the Lifetime Cancer Incidence.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Liver ChREBP deficiency inhibits fructose-induced insulin resistance in pregnant mice and female offspring.EMBO reports · 2024Article
- MYC: there is more to it than cancer.Frontiers in cell and developmental biology · 2024Review
- The Myc-Like Mlx Network Impacts Aging and Metabolism.bioRxiv : the preprint server for biology · 2023Article
- Article
- Regulation of Normal and Neoplastic Proliferation and Metabolism by the Extended Myc Network.Cells · 2022Review
- Maladaptive positive feedback production of ChREBPβ underlies glucotoxic β-cell failure.Nature communications · 2022Article
- Review
- Coordinated Cross-Talk Between the Myc and Mlx Networks in Liver Regeneration and Neoplasia.Cellular and molecular gastroenterology and hepatology · 2022Article
- A lack of ChREBP inhibits mitochondrial cristae formation in brown adipose tissue.Molecular and cellular biochemistry · 2021Article
- Myc Is Required for Adaptive β-Cell Replication in Young Mice but Is Not Sufficient in One-Year-Old Mice Fed With a High-Fat Diet.Diabetes · 2019Article
- The MYC Oncogene Cooperates with Sterol-Regulated Element-Binding Protein to Regulate Lipogenesis Essential for Neoplastic Growth.Cell metabolism · 2019Article
- Article
- Myc and ChREBP transcription factors cooperatively regulate normal and neoplastic hepatocyte proliferation in mice.The Journal of biological chemistry · 2018Article
- Activation of Nrf2 Is Required for Normal and ChREBPα-Augmented Glucose-Stimulated β-Cell Proliferation.Diabetes · 2018Article
- DNA methylation alters transcriptional rates of differentially expressed genes and contributes to pathophysiology in mice fed a high fat diet.Molecular metabolism · 2017Article
- Review
- Glucose regulates the intrinsic inflammatory response of the heart to surgically induced hypothermic ischemic arrest and reperfusion.Physiological genomics · 2017Article
- Immune surveillance of liver cancer in non-alcoholic fatty liver disease: excess lipids cause CD4 T-cells loss and promote hepatocellular carcinoma development.Hepatobiliary surgery and nutrition · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Glucose regulates programs of gene expression that orchestrate changes in cellular phenotype in several metabolically active tissues. Carbohydrate response element-binding protein (ChREBP) and its binding partner, Mlx, mediate glucose-regulated gene expression by binding to carbohydrate response elements on target genes, such as the prototypical glucose-responsive gene, liver-type pyruvate kinase (Pklr). c-Myc is also required for the glucose response of the Pklr gene, although the relationship between c-Myc and ChREBP has not been defined. Here we describe the molecular events of the glucose-mediated activation of Pklr and determine the effects of decreasing the activity or abundance of c-Myc on this process. Time-course chromatin immunoprecipitation revealed a set of transcription factors [hepatocyte nuclear factor (HNF)1alpha, HNF4alpha, and RNA polymerase II (Pol II)] constitutively resident on the Pklr promoter, with a relative enrichment of acetylated histones 3 and 4 in the same region of the gene. Glucose did not affect HNF1alpha binding or the acetylation of histones H3 or H4. By contrast, glucose promoted the recruitment of ChREBP and c-Myc and increased the occupancy of HNF4alpha and RNA Pol II, which were coincident with the glucose-mediated increase in transcription as determined by a nuclear run-on assay. Depletion of c-Myc activity using a small molecule inhibitor (10058-F4/1RH) abolished the glucose-mediated recruitment of HNF4alpha, ChREBP, and RNA Pol II, without affecting basal gene expression, histone acetylation, and HNF1alpha or basal HNF4alpha occupancy. The activation and recruitment of ChREBP to several glucose-responsive genes were blocked by 1RH, indicating a general necessity for c-Myc in this process.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.