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Mitochondrial dysfunction: Glucokinase downregulation lowers interaction of glucokinase with mitochondria, resulting in apoptosis of pancreatic β-cells

https://doi.org/10.1016/j.cellsig.2008.09.015

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What this work says

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On the Role of VDAC in Apoptosis: Fact and Fiction

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Glucokinase regulatory protein is associated with mitochondria in hepatocytes

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Mitochondria-to-nucleus stress signaling in mammalian cells: Nature of nuclear gene targets, transcription regulation, and induced resistance to apoptosis

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Bcl-2 Regulation of Mitochondrial Energetics

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Metabolism meets death

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Mitochondrial hexokinases, novel mediators of the antiapoptotic effects of growth factors and Akt

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Ethidium Bromide-induced Inhibition of Mitochondrial Gene Transcription Suppresses Glucose-stimulated Insulin Release in the Mouse Pancreatic β-Cell Line βHC9

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Depletion of Mitochondrial DNA Causes Impaired Glucose Utilization and Insulin Resistance in L6 GLUT4myc Myocytes

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Progressive Accumulation of Mitochondrial DNA Mutations and Decline in Mitochondrial Function Lead to β-Cell Failure

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Oxidative Stress and Pancreatic β-Cell Dysfunction

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Mitochondrial Dysfunction in the Elderly: Possible Role in Insulin Resistance

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The Homeodomain of PDX-1 Mediates Multiple Protein-Protein Interactions in the Formation of a Transcriptional Activation Complex on the Insulin Promoter

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Hexokinase II: The Integration of Energy Metabolism and Control of Apoptosis

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Alterations of Mitochondrial DNA in Common Diseases and Disease States: Aging, Neurodegeneration, Heart Failure, Diabetes and Cancer

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Creation and characterization of a mitochondrial DNA-depleted pancreatic beta-cell line: impaired insulin secretion induced by glucose, leucine, and sulfonylureas.

inferredcites →https://doi.org/10.2337/diabetes.54.9.2602openalex-snapshot

Exposure to Chronic High Glucose Induces β-Cell Apoptosis Through Decreased Interaction of Glucokinase With Mitochondria

What points at this work

Incoming claims: where this work appears in other papers’ reference lists and arguments.

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Treatment with glucokinase activator, YH-GKA, increases cell proliferation and decreases glucotoxic apoptosis in INS-1 cells

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