| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10954065 | Journal of Molecular and Cellular Cardiology | 2011 | 8 Pages |
Abstract
⺠LPC-16) concentration-dependently and reversibly increased IKs in atrial cells. ⺠Inhibitions of G protein, PKC and Rho pathways reduced LPC-16 action on IKs. ⺠G2A immunofluorescence was distributed in the plasma membrane of atrial myocytes.
Keywords
SPCRho-kinaseGDPβSLPCIKSG2ApKaNCDCPLCAPD90IKrPKCAPDPTXguanosine 5′-O-(2-thiodiphosphate)ICa,LSphingosylphosphorylcholinebisindolylmaleimide IG proteinpertussis toxinphosphatidylcholinephospholipase CLysophosphatidylcholineAction potential durationaction potential duration at 90% repolarizationprotein kinase AProtein kinase CL-type Ca2+ channels
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Authors
Wei-Guang Ding, Futoshi Toyoda, Hisao Ueyama, Hiroshi Matsuura,