Junctate is a key element in calcium entry induced by activation of InsP3 receptors and/or calcium store depletion

Susan Treves, Clara Franzini-Armstrong, Luca Moccagatta, Christophe Arnoult, Cristiano Grasso, Adam Schrum, Sylvie Ducreux, Michael X. Zhu, Katsuhiko Mikoshiba, Thierry Girard, Sophia Smida-Rezgui, Michel Ronjat, Francesco Zorzato

Research output: Contribution to journalArticlepeer-review

97 Scopus citations


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 (InsP3) receptors (InsP3Rs). Stimulated cells activate store- or receptor-operated 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 InsP3R 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.

Original languageEnglish (US)
Pages (from-to)537-548
Number of pages12
JournalJournal of Cell Biology
Issue number4
StatePublished - Aug 16 2004


  • Calcium binding protein
  • Calcium entry channel
  • Calcium homeostasis
  • ER
  • IPR

ASJC Scopus subject areas

  • Cell Biology


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