Transient Receptor Potential 1 Regulates Capacitative Ca2+ Entry and Ca2+ Release from Endoplasmic Reticulum in B Lymphocytes

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  • Yasuo Mori
    1Center for Integrative Bioscience and Department of Information Physiology, National Institute for Physiological Sciences, Okazaki 444-8585, Japan
  • Minoru Wakamori
    1Center for Integrative Bioscience and Department of Information Physiology, National Institute for Physiological Sciences, Okazaki 444-8585, Japan
  • Tomoya Miyakawa
    2Department of Pharmacology, Graduate School of Medicine, The University of Tokyo, CREST, Japan Science and Technology Corporation, Tokyo 113-0033, Japan
  • Meredith Hermosura
    3Laboratory of Cell and Molecular Signaling, Center for Biomedical Research at The Queen's Medical Center, and John A. Burns School of Medicine at the University of Hawaii, Honolulu, HI 96813
  • Yuji Hara
    1Center for Integrative Bioscience and Department of Information Physiology, National Institute for Physiological Sciences, Okazaki 444-8585, Japan
  • Motohiro Nishida
    1Center for Integrative Bioscience and Department of Information Physiology, National Institute for Physiological Sciences, Okazaki 444-8585, Japan
  • Kenzo Hirose
    2Department of Pharmacology, Graduate School of Medicine, The University of Tokyo, CREST, Japan Science and Technology Corporation, Tokyo 113-0033, Japan
  • Akiko Mizushima
    2Department of Pharmacology, Graduate School of Medicine, The University of Tokyo, CREST, Japan Science and Technology Corporation, Tokyo 113-0033, Japan
  • Mari Kurosaki
    4Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, and Laboratory for Lymphocyte Differentiation, RIKEN Research Center for Allergy and Immunology, Moriguchi 570-8506, Japan
  • Emiko Mori
    1Center for Integrative Bioscience and Department of Information Physiology, National Institute for Physiological Sciences, Okazaki 444-8585, Japan
  • Kumiko Gotoh
    4Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, and Laboratory for Lymphocyte Differentiation, RIKEN Research Center for Allergy and Immunology, Moriguchi 570-8506, Japan
  • Takaharu Okada
    1Center for Integrative Bioscience and Department of Information Physiology, National Institute for Physiological Sciences, Okazaki 444-8585, Japan
  • Andrea Fleig
    3Laboratory of Cell and Molecular Signaling, Center for Biomedical Research at The Queen's Medical Center, and John A. Burns School of Medicine at the University of Hawaii, Honolulu, HI 96813
  • Reinhold Penner
    3Laboratory of Cell and Molecular Signaling, Center for Biomedical Research at The Queen's Medical Center, and John A. Burns School of Medicine at the University of Hawaii, Honolulu, HI 96813
  • Masamitsu Iino
    2Department of Pharmacology, Graduate School of Medicine, The University of Tokyo, CREST, Japan Science and Technology Corporation, Tokyo 113-0033, Japan
  • Tomohiro Kurosaki
    4Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, and Laboratory for Lymphocyte Differentiation, RIKEN Research Center for Allergy and Immunology, Moriguchi 570-8506, Japan

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<jats:p>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.</jats:p>

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