期刊
JOURNAL OF CELL BIOLOGY
卷 166, 期 4, 页码 537-548出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200404079
关键词
calcium homeostasis; IP3R; calcium entry channel; calcium binding protein; ER
类别
资金
- NCI NIH HHS [F32 CA103374] Funding Source: Medline
- NIAMS NIH HHS [P01 AR144650] Funding Source: Medline
- NINDS NIH HHS [R01 NS42183, R01 NS042183] Funding Source: Medline
In many cell types agonist-receptor activation leads to a rapid and transient release of Ca2+ from intracellular stores via activation of inositol 1,4,5 trisphosphate (InsP(3)) receptors (InsP(3)Rs). Stimulated cells activate store- or receptor-ope rated calcium channels localized in the plasma membrane, allowing entry of extracellular calcium into the cytoplasm, and thus replenishment of intracellular calcium stores. Calcium entry must be finely regulated in order to prevent an excessive intracellular calcium increase. junctate, an integral calcium binding protein of endo(sarco)plasmic reticulum membrane, (a) induces and/or stabilizes peripheral couplings between the ER and the plasma membrane, and (b) forms a supramolecular complex with the InsP(3)R and the canonical transient receptor potential protein (TRPC) 3 calcium entry channel. The full-length protein modulates both agonist-induced and store depletion-induced calcium entry, whereas its NH2 terminus affects receptor-activated calcium entry. RNA interference to deplete cells of endogenous junctate, knocked down both agonist-activated calcium release from intracellular stores and calcium entry via TRPC3. These results demonstrate that junctate is a new protein involved in calcium homeostasis in eukaryotic cells.
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