ArticleProceedings of the National Academy of Sciences of the United States of America2013
SAD-A kinase controls islet β-cell size and function as a mediator of mTORC1 signaling.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 41 citations in OpenAlex.
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- Upregulation of α-ENaC induces pancreatic β-cell dysfunction, ER stress, and SIRT2 degradation.Journal of biomedical research · 2024Article
- Islet-resident macrophage-derived miR-155 promotes β cell decompensation via targeting PDX1.iScience · 2024Article
- Regulation of autophagy by perilysosomal calcium: a new player in β-cell lipotoxicity.Experimental & molecular medicine · 2024Review
- BRSK2 in pancreatic β cells promotes hyperinsulinemia-coupled insulin resistance and its genetic variants are associated with human type 2 diabetes.Journal of molecular cell biology · 2023Article
- Review
- Deleterious Variation in BR Serine/Threonine Kinase 2 Classified a Subtype of Autism.Frontiers in molecular neuroscience · 2022Article
- Protocol for in vivo and ex vivo assessments of glucose-stimulated insulin secretion in mouse islet β cells.STAR protocols · 2021Article
- M1 macrophage-derived exosomes impair beta cell insulin secretion via miR-212-5p by targeting SIRT2 and inhibiting Akt/GSK-3β/β-catenin pathway in mice.Diabetologia · 2021Article
- Article
- SAD-A Promotes Glucose-Stimulated Insulin Secretion Through Phosphorylation and Inhibition of GDIα in Male Islet β Cells.Endocrinology · 2018Article
- Article
- Real-Time Monitoring of Insulin Using a Graphene Field-Effect Transistor Aptameric Nanosensor.ACS applied materials & interfaces · 2017Article
- The Molecular Mechanism of Glucagon-Like Peptide-1 Therapy in Alzheimer's Disease, Based on a Mechanistic Target of Rapamycin Pathway.CNS drugs · 2017Article
- GLP-1 receptor signalling promotes β-cell glucose metabolism via mTOR-dependent HIF-1α activation.Scientific reports · 2017Article
- Mild hyperglycemia triggered islet function recovery in streptozotocin-induced insulin-deficient diabetic rats.Journal of diabetes investigation · 2017Article
- NT-3 promotes proprioceptive axon regeneration when combined with activation of the mTor intrinsic growth pathway but not with reduction of myelin extrinsic inhibitors.Experimental neurology · 2016Article
- Structural insight into the mechanism of synergistic autoinhibition of SAD kinases.Nature communications · 2015Article
- Loss of Liver Kinase B1 (LKB1) in Beta Cells Enhances Glucose-stimulated Insulin Secretion Despite Profound Mitochondrial Defects.The Journal of biological chemistry · 2015Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
The mammalian target of rapamycin (mTOR) plays an important role in controlling islet β-cell function. However, the underlying molecular mechanisms remain poorly elucidated. Synapses of amphids defective kinase-A (SAD-A) is a 5' adenosine monophosphate-activated protein kinase-related protein kinase that is exclusively expressed in pancreas and brain. In this study, we investigated a role of the kinase in regulating pancreatic β-cell morphology and function as a mediator of mTOR complex 1 (mTORC1) signaling. We show that global SAD-A deletion leads to defective glucose-stimulated insulin secretion and petite islets, which are reminiscent of the defects in mice with global deletion of ribosomal protein S6 kinase 1, a downstream target of mTORC1. Consistent with these findings, selective deletion of SAD-A in pancreas decreased islet β-cell size, whereas SAD-A overexpression significantly increased the size of mouse insulinomas cell lines β-cells. In direct support of SAD-A as a unique mediator of mTORC1 signaling in islet β-cells, we demonstrate that glucose dramatically stimulated SAD-A protein translation in isolated mouse islets, which was potently inhibited by rapamycin, an inhibitor of mTORC1. Moreover, the 5'-untranslated region of SAD-A mRNA is highly structured and requires mTORC1 signaling for its translation initiation. Together, these findings identified SAD-A as a unique pancreas-specific effector protein of mTORC1 signaling.
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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.