Transient Receptor Potential 1 Regulates Capacitative Ca2+ Entry and Ca2+ Release from Endoplasmic Reticulum in B Lymphocytes 〉
Autor: | Yuji Hara, Reinhold Penner, Andrea Fleig, Yasuo Mori, Mari Kurosaki, Kumiko Gotoh, Tomoya Miyakawa, Tomohiro Kurosaki, Emiko Mori, Takaharu Okada, Akiko Mizushima, Masamitsu Iino, Motohiro Nishida, Meredith C. Hermosura, Kenzo Hirose, Minoru Wakamori |
---|---|
Jazyk: | angličtina |
Rok vydání: | 2002 |
Předmět: |
Immunology
B-cell receptor store-operated Ca2+ channel Biology Endoplasmic Reticulum TRP Cell Line Transient receptor potential channel Ca2+ release Immunology and Allergy Animals Humans Calcium Signaling Calcium signaling TRPC Cation Channels SOC channels B-Lymphocytes Voltage-dependent calcium channel B cell receptor Endoplasmic reticulum Inositol trisphosphate receptor Cell biology capacitative Ca2+ entry Original Article Calcium Calcium Channels Chickens Intracellular Gene Deletion |
Zdroj: | The Journal of Experimental Medicine |
ISSN: | 1540-9538 0022-1007 |
Popis: | Capacitative Ca(2+) entry (CCE) activated by release/depletion of Ca(2+) from internal stores represents a major Ca(2+) 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 Ca(2+) release-activated Ca(2+) currents and inositol 1,4,5-trisphosphate (IP(3))-mediated Ca(2+) release from endoplasmic reticulum (ER) in DT40 B cells. As a consequence, B cell antigen receptor-mediated Ca(2+) 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 IP(3) receptor function, thereby enhancing functional coupling between the ER and plasma membrane in transduction of intracellular Ca(2+) signaling in B lymphocytes. |
Databáze: | OpenAIRE |
Externí odkaz: |