2012 Fiscal Year Final Research Report
Endocytosis of human K channel by receptor activation and its intracellular mechanisms
| Project/Area Number |
22590235
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Yamagata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YAMAZAKI Yoshihiko 山形大学, 医学部, 准教授 (10361247)
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| Project Period (FY) |
2010 – 2012
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| Keywords | 電位依存性 Kチャネル / エンドサイトーシス |
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| Research Abstract |
The slowly activating delayed rectifier K^+ channel (IKs channel) is composed of KCNQ1 and KCNE1 subunits. The present study was designed to investigate whether activation of Gq protein-coupled receptor (GqPCR) caused endocytosis of the I_<Ks> channel.
1. Effects of GqPCR activation on localization of the pore-forming subunit KCNQ1 were investigated by confocal laser scanning microscopy. It was suggested that AT_1R activation resulted in endocytosis of KCNQ1.
2. AT_1R-induced endocytosis of KCNQ1 was clathrin-dependent, where PKC activation was involved. Ubiquitination of KCNQ1 seemed to have nothing to do with the endocytosis.
3. Activation of α_<1A> and α_<1B> receptor obviously caused endocytosis of KCNQ1. Although AR_<α1>-induced endocytosis of KCNQ1 was clathrin-dependent, it did not require PKC activation in contrast to AT_1R. Involvement of ubiquitination of KCNQ1 was suggested.
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[Journal Article] NMDA receptor-mediated Ca^<2+> influx triggers nucleocytoplasmic translocation of diacylglycerol kinase ζ un -der oxygen-glucose deprivation conditions, an in vitro model of ischemia, in rat hippocampal slices2012
Author(s)
Suzuki Y, Yamazaki Y, Hozumi Y, Okada M, Tanaka T, Iseki K, Ohta N, Aoyagi M, Fujii S, Goto K.
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Journal Title
Histochem Cell Biol
Volume: 137
Pages: 499-511
DOI
Peer Reviewed
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