Functional role of NO-induced Ca2+ release in skeletal muscle

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460303
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General physiology
• Research Institution: Jikei University School of Medicine
• Principal Investigator: Yamazawa Toshiko 東京慈恵会医科大学, 医学部, 講師 (00282616)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 一酸化窒素 / カルシウム / リアノジン受容体

Outline of Final Research Achievements

We found that nitric oxide (NO) -induced Ca2+ release (NICR), and that NICR is involved in NO-induced neuronal cell death. We investigated properties of the RyR1 channels carrying disease-associated mutations at the N-terminal region. HEK293 cells expressing the mutant RyR1 channels exhibited alterations in Ca2+ homeostasis, i.e., enhanced CICR and NICR sensitivity, decrease of ER Ca2+ contents, increases in resting cytoplasmic Ca2+ concentration, changes in pattern of electrostatic interaction. We investigated characterization of RyR1C3636A channels in skeletal muscle.

Free Research Field

医歯薬学