Transient receptor potential 1 regulates capacitative Ca2+ entry and Ca2+ release from endoplasmic reticulum in B lymphocytes

Yasuo Mori, Minoru Wakamori, Tomoya Miyakawa, Meredith Hermosura, Yuji Hara, Motohiro Nishida, Kenzo Hirose, Akiko Mizushima, Mari Kurosaki, Emiko Mori, Kumiko Gotoh, Takaharu Okada, Andrea Fleig, Reinhold Penner, Masamitsu Iino, Tomohiro Kurosaki

Research output: Contribution to journalArticle

170 Citations (Scopus)

Abstract

Capacitative Ca2+ entry (CCE) activated by release/depletion of Ca2+ from internal stores represents a major Ca2+ influx mechanism in lymphocytes and other nonexcitable cells. Despite the importance of CCE in antigen-mediated lymphocyte activation, molecular components constituting this mechanism remain elusive. Here we demonstrate that genetic disruption of transient receptor potential (TRP)1 significantly attenuates both Ca2+ release-activated Ca2+ currents and inositol 1,4,5-trisphosphate (IP3)-mediated Ca2+ release from endoplasmic reticulum (ER) in DT40 B cells. As a consequence, B cell antigen receptor-mediated Ca2+ oscillations and NF-AT activation are reduced in TRP1-deficient cells. Thus, our results suggest that CCE channels, whose formation involves TRP1 as an important component, modulate IP3 receptor function, thereby enhancing functional coupling between the ER and plasma membrane in transduction of intracellular Ca2+ signaling in B lymphocytes.

Original languageEnglish
Pages (from-to)673-681
Number of pages9
JournalJournal of Experimental Medicine
Volume195
Issue number6
DOIs
Publication statusPublished - Mar 18 2002
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Fingerprint Dive into the research topics of 'Transient receptor potential 1 regulates capacitative Ca<sup>2+</sup> entry and Ca<sup>2+</sup> release from endoplasmic reticulum in B lymphocytes'. Together they form a unique fingerprint.

Cite this