ArticleDiabetes2012
Glucose-induced nuclear shuttling of ChREBP is mediated by sorcin and Ca(2+) ions in pancreatic β-cells.
Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 53 citations in OpenAlex.
- ChREBPα: a central metabolic sensor driving lipid droplet renewal in preimplantation mouse embryos.Frontiers in cell and developmental biology · 2026Article
- Molecular glues of the regulatory ChREBP/14-3-3 complex protect beta cells from glucolipotoxicity.Nature communications · 2025Article
- Molecular glues of the regulatory ChREBP/14-3-3 complex protect beta cells from glucolipotoxicity.bioRxiv : the preprint server for biology · 2024Article
- Review
- The downregulation of SCGN induced by lipotoxicity promotes NLRP3-mediated β-cell pyroptosis.Cell death discovery · 2024Article
- Maladaptive positive feedback production of ChREBPβ underlies glucotoxic β-cell failure.Nature communications · 2022Article
- The polyol pathway is an evolutionarily conserved system for sensing glucose uptake.PLoS biology · 2022Article
- Roles of Sorcin in Drug Resistance in Cancer: One Protein, Many Mechanisms, for a Novel Potential Anticancer Drug Target.Cancers · 2020Review
- Article
- Calcium Signaling in ß-cell Physiology and Pathology: A Revisit.International journal of molecular sciences · 2019Review
- Short-term high glucose culture potentiates pancreatic beta cell function.Scientific reports · 2018Article
- Article
- Nutrient regulation of pancreatic β-cell proliferation.Biochimie · 2017Review
- Negative Regulation of Hepatic Inflammation by the Soluble Resistance-Related Calcium-Binding ProteinFrontiers in immunology · 2017Article
- Islet ChREBP-β is increased in diabetes and controls ChREBP-α and glucose-induced gene expression via a negative feedback loop.Molecular metabolism · 2016Article
- Multifaceted Roles of ALG-2 in Ca(2+)-Regulated Membrane Trafficking.International journal of molecular sciences · 2016Review
- Article
- Induction of the ChREBPβ Isoform Is Essential for Glucose-Stimulated β-Cell Proliferation.Diabetes · 2015Article
- Genome-Wide Analysis of ChREBP Binding Sites on Male Mouse Liver and White Adipose Chromatin.Endocrinology · 2015Article
- Fractalkine (CX3CL1), a new factor protecting β-cells against TNFα.Molecular metabolism · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Carbohydrate-responsive element-binding protein (ChREBP) is a regulator of pancreatic β-cell gene expression and an important mediator of glucotoxicity. Glucose increases the activity and nuclear localization of ChREBP by still ill-defined mechanisms. Here we reveal, using both MIN6 and primary mouse β-cells, a unique mechanism behind ChREBP nuclear translocation. At low glucose concentrations, ChREBP interacts with sorcin, a penta EF hand Ca(2+) binding protein, and is sequestered in the cytosol. Sorcin overexpression inhibits ChREBP nuclear accumulation at high glucose and reduced the activity of L-type pyruvate kinase (L-PK) and TxNIP promoters, two well-characterized ChREBP target genes. Sorcin inactivation by RNA interference increases ChREBP nuclear localization and in vivo binding to the L-PK promoter at low glucose concentrations. Ca(2+) influx was essential for this process since Ca(2+) chelation with EGTA, or pharmacological inhibition with diazoxide and nifedipine, blocked the effects of glucose. Conversely, mobilization of intracellular Ca(2+) with ATP caused the nuclear accumulation of ChREBP. Finally, sorcin silencing inhibited ATP-induced increases in intracellular Ca(2+) and glucose-stimulated insulin secretion. We therefore conclude that sorcin retains ChREBP in the cytosol at low glucose concentrations and may act as a Ca(2+) sensor for glucose-induced nuclear translocation and the activation of ChREBP-dependent genes.
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What OpenQuestion holds
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.