ArticleNature structural & molecular biology2014
A phospho-BAD BH3 helix activates glucokinase by a mechanism distinct from that of allosteric activators.
Article in Nature structural & molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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Who cites it
26 citing papers in PubMed, 54 citations in OpenAlex.
- Cornea Arcus and Dyslipidemia in Unrelated Adults With Monoallelic Germline Variants in theClinical medicine insights. Endocrinology and diabetes · 2026Article
- Renalase inhibition defends against acute and chronic β cell stress by regulating cell metabolism.Molecular metabolism · 2025Article
- Exploring the Chemical Features and Biomedical Relevance of Cell-Penetrating Peptides.International journal of molecular sciences · 2024Review
- Site-Specifically Modified Peptide Inhibitors of Protein Tyrosine Phosphatase 1B and T-Cell Protein Tyrosine Phosphatase with Enhanced Stability and Improved In Vivo Long-Acting Activity.ACS pharmacology & translational science · 2024Article
- Identification of Metastasis-Associated Genes in Cutaneous Squamous Cell Carcinoma Based on Bioinformatics Analysis and Experimental Validation.Advances in therapy · 2022Article
- Glucose metabolism and pyruvate carboxylase enhance glutathione synthesis and restrict oxidative stress in pancreatic islets.Cell reports · 2021Article
- Discovery of Novel PTP1B Inhibitors Derived from the BH3 Domain of Proapoptotic Bcl-2 Proteins with Antidiabetic Potency.ACS medicinal chemistry letters · 2021Article
- The chaperone Hsp70 is a BH3 receptor activated by the pro-apoptotic Bim to stabilize anti-apoptotic clients.The Journal of biological chemistry · 2020Article
- Publisher Correction: A BAD portion of glucose can be good for inflamed beta cells.Nature metabolism · 2020Article
- Hydrocarbon-Stitched Peptide Agonists of Glucagon-Like Peptide-1 Receptor.ACS chemical biology · 2020Article
- Glucose-dependent partitioning of arginine to the urea cycle protects β-cells from inflammation.Nature metabolism · 2020Article
- BCL-2 family protein BOK is a positive regulator of uridine metabolism in mammals.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- HCF-1 Regulates De Novo Lipogenesis through a Nutrient-Sensitive Complex with ChREBP.Molecular cell · 2019Article
- Molecular and cellular regulation of human glucokinase.Archives of biochemistry and biophysics · 2019Review
- BEZ235 enhances chemosensitivity of paclitaxel in hepatocellular carcinoma through inhibiting the PI3K/Akt/mTOR pathway.American journal of translational research · 2019Article
- Biochemical and biophysical investigations of the interaction between human glucokinase and pro-apoptotic BAD.PloS one · 2017Article
- Small-Molecule and Peptide Inhibitors of the Pro-Survival Protein Mcl-1.ChemMedChem · 2016Review
- Metabolic Regulation of Apoptosis in Cancer.International review of cell and molecular biology · 2016Review
- Redefining the BH3 Death Domain as a 'Short Linear Motif'.Trends in biochemical sciences · 2015Review
- Cellular Uptake and Ultrastructural Localization Underlie the Pro-apoptotic Activity of a Hydrocarbon-stapled BIM BH3 Peptide.ACS chemical biology · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Glucokinase (GK) is a glucose-phosphorylating enzyme that regulates insulin release and hepatic metabolism, and its loss of function is implicated in diabetes pathogenesis. GK activators (GKAs) are attractive therapeutics in diabetes; however, clinical data indicate that their benefits can be offset by hypoglycemia, owing to marked allosteric enhancement of the enzyme's glucose affinity. We show that a phosphomimetic of the BCL-2 homology 3 (BH3) α-helix derived from human BAD, a GK-binding partner, increases the enzyme catalytic rate without dramatically changing glucose affinity, thus providing a new mechanism for pharmacologic activation of GK. Remarkably, BAD BH3 phosphomimetic mediates these effects by engaging a new region near the enzyme's active site. This interaction increases insulin secretion in human islets and restores the function of naturally occurring human GK mutants at the active site. Thus, BAD phosphomimetics may serve as a new class of GKAs.
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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 Socratic graph.