ArticleCellular and molecular life sciences : CMLS2015
CaV1.2 and CaV1.3 channel hyperactivation in mouse islet β cells exposed to type 1 diabetic serum.
Article in Cellular and molecular life sciences : CMLS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- CircRbfox1 Contributes to Colonic Hypersensitivity in Rats With Diabetes by Altering HuC Subcellular Localization to Regulate RBFOX1 Expression.CNS neuroscience & therapeutics · 2026Article
- Article
- In Vivo CaBiomedicines · 2023Article
- The adipocyte-enriched secretory protein tetranectin exacerbates type 2 diabetes by inhibiting insulin secretion from β cells.Science advances · 2022Article
- Inositol hexakisphosphate primes syndapin I/PACSIN 1 activation in endocytosis.Cellular and molecular life sciences : CMLS · 2022Article
- Role of High Voltage-Gated CaCells · 2021Review
- Apolipoprotein CIII Is an Important Piece in the Type-1 Diabetes Jigsaw Puzzle.International journal of molecular sciences · 2021Review
- The eye as a novel imaging site in diabetes research.Pharmacology & therapeutics · 2019Review
- A Selectivity Filter Gate Controls Voltage-Gated Calcium Channel Calcium-Dependent Inactivation.Neuron · 2019Article
- Regulation of L-type CaCell calcium · 2017Article
- Regulation of L-type Ca2+ Channel Activity and Insulin Secretion by Huntingtin-associated Protein 1.The Journal of biological chemistry · 2016Article
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Authors and funding
11 authors at 4 institutions in 4 countries.
Funding
Abstract
The voltage-gated Ca(2+) (CaV) channel acts as a key player in β cell physiology and pathophysiology. β cell CaV channels undergo hyperactivation subsequent to exposure to type 1 diabetic (T1D) serum resulting in increased cytosolic free Ca(2+) concentration and thereby Ca(2+)-triggered β cell apoptosis. The present study was aimed at revealing the subtypes of CaV1 channels hyperactivated by T1D serum as well as the biophysical mechanisms responsible for T1D serum-induced hyperactivation of β cell CaV1 channels. Patch-clamp recordings and single-cell RT-PCR analysis were performed in pancreatic β cells from CaV1 channel knockout and corresponding control mice. We now show that functional CaV1.3 channels are expressed in a subgroup of islet β cells from CaV1.2 knockout mice (CaV1.2(-/-)). T1D serum enhanced whole-cell CaV currents in islet β cells from CaV1.3 knockout mice (CaV1.3(-/-)). T1D serum increased the open probability and number of functional unitary CaV1 channels in CaV1.2(-/-) and CaV1.3(-/-) β cells. These data demonstrate that T1D serum hyperactivates both CaV1.2 and CaV1.3 channels by increasing their conductivity and number. These findings suggest CaV1.2 and CaV1.3 channels as potential targets for anti-diabetes therapy.
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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 OpenQuestion graph.