ArticleProceedings of the National Academy of Sciences of the United States of America2007
Beta cell-specific deficiency of the stimulatory G protein alpha-subunit Gsalpha leads to reduced beta cell mass and insulin-deficient diabetes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 64 citations in OpenAlex.
- Design of a metabolically-stable peptide therapeutic with triple-hormone-receptor agonist activity.Journal of computer-aided molecular design · 2026Article
- Beta-Cell Tipe1 Orchestrates Insulin Secretion and Cell Proliferation by Promoting Gαs/cAMP Signaling via USP5.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The Potential Role of R4 Regulators of G Protein Signaling (RGS) Proteins in Type 2 Diabetes Mellitus.Cells · 2022Review
- Integrated proteogenomic characterization across major histological types of pituitary neuroendocrine tumors.Cell research · 2022Article
- A recurrent somatic missense mutation in GNAS gene identified in familial thyroid follicular cell carcinomas in German longhaired pointer dogs.BMC genomics · 2022Article
- The therapeutic potential of GLP-1 receptor biased agonism.British journal of pharmacology · 2022 · on this mapReview
- Therapeutic potentials of agonist and antagonist of adenosine receptors in type 2 diabetes.Reviews in endocrine & metabolic disorders · 2021Review
- Gsα-dependent signaling is required for postnatal establishment of a functional β-cell mass.Molecular metabolism · 2021Article
- Chemogenetic approaches to identify metabolically important GPCR signaling pathways: Therapeutic implications.Journal of neurochemistry · 2021Review
- Review
- Pancreatic Islets Exhibit Dysregulated Adaptation of Insulin Secretion after Chronic Epinephrine Exposure.Current issues in molecular biology · 2021Article
- Detour Ahead: Incretin Hormone Signaling Alters Its Intracellular Path as β-Cell Failure Progresses During Diabetes.Frontiers in endocrinology · 2021Article
- TBK1 regulates regeneration of pancreatic β-cells.Scientific reports · 2020Article
- Role of Phosphodiesterase in the Biology and Pathology of Diabetes.International journal of molecular sciences · 2020Review
- Essential Roles for the Non-Canonical IκB Kinases in Linking Inflammation to Cancer, Obesity, and Diabetes.Cells · 2019Review
- Inhibition of TBK1/IKKε Promotes Regeneration of Pancreatic β-cells.Scientific reports · 2018Article
- Phytonutrient genistein is a survival factor for pancreatic β-cells via GPR30-mediated mechanism.The Journal of nutritional biochemistry · 2018Article
- GLP-1 signalling compensates for impaired insulin signalling in regulating beta cell proliferation in βIRKO mice.Diabetologia · 2017Article
- Incretin-Based Therapies: Revisiting Their Mode of Action.Endocrinology · 2017Article
- Regulator of G protein signaling 2 is a key regulator of pancreatic β-cell mass and function.Cell death & disease · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The G protein alpha-subunit G(s)alpha is required for hormone-stimulated cAMP generation. In pancreatic beta cells, G(s)alpha mediates the signaling of glucagon-like peptide 1 and other incretin hormones, which are implicated as important regulators of beta cell survival and insulin release. Studies have suggested that G(s)alpha/cAMP mediates these actions by stimulating insulin receptor substrate 2 (IRS2) expression. Mice with beta cell-specific G(s)alpha deficiency (betaGsKO) were generated by mating G(s)alpha-floxed mice to rat insulin II promoter-cre recombinase mice. betaGsKO mice had poor survival and postnatal growth with low serum insulin-like growth factor 1 levels. betaGsKO mice also developed severe hyperglycemia and glucose intolerance with severe hypoinsulinemia and reduced islet insulin content and glucose-stimulated insulin release. betaGsKO mice had markedly reduced average islet size and beta cell mass, which was partially explained by reduced beta cell size. In addition, betaGsKO mice had significantly reduced beta cell proliferation and increased beta cell apoptosis and markedly reduced expression of the cell cycle protein cyclin D2. The effects on beta cell mass and proliferation, but not apoptosis, were present from birth. Unexpectedly expression of Irs2 and the downstream gene Pdx1 were unaffected. These results show that G(s)alpha/cAMP pathways are critical regulators of beta cell function and proliferation that can work through IRS2-independent mechanisms.
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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.