Journal
DIABETES
Volume 51, Issue -, Pages S183-S189Publisher
AMER DIABETES ASSOC
DOI: 10.2337/diabetes.51.2007.S183
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Funding
- NIDDK NIH HHS [R01 DK 48494] Funding Source: Medline
- PHS HHS [NIH P01 544681] Funding Source: Medline
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Nonselective cation channels may play a role in insulin secretion by regulating pancreatic beta-cell plasma membrane potential, Ca2+ homeostasis, and thereby glucose signaling. Transient receptor potential channel (TRPC)-related genes encode nonselective cation channels, some of which are similar to those described for beta-cells. Some TRPC-like channels are activated via G. protein-coupled mechanisms, some have been reported to be calcium-store-operated channels (SOC), and others are activated by novel signaling molecules or are sensitive to pressure and osmotic strength. Here we report the cloning and expression of mSTRPC4 from a mouse insulinoma cDNA library. mSTRPC4 encoded a protein of 97 kd, expressed in both endocrine cells and the brain. Stable cell lines expressing mSTRPC4 showed abundant mSTRPC4 protein, but no reproducible currents could be detected. mSTRPC4 therefore probably functions as a heteromultimer. We also report that LTRPC2, a G-protein and adenosine 5'-diphosphoribose (ADPR)-activated nonselective cation channel, is also expressed in human islets. TRPC-like channels may provide a pathway for depolarization or Ca2+ entry in beta-cells and may be interesting targets for manipulating beta-cell function. Diabetes 51 (Suppl. 1):S183-S189,2002.
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