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G protein‐activated K + channels: a reporter for rapid activation of G proteins by lysophosphatidic acid in Xenopus oocytes
Author(s) -
Itzhaki Van-Ham Irit,
Peleg Sagit,
Dascal Nathan,
Shapira Hagit,
Oron Yoram
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(04)00334-5
Subject(s) - lysophosphatidic acid , pertussis toxin , g protein coupled inwardly rectifying potassium channel , xenopus , g protein , desensitization (medicine) , chemistry , chloride channel , agonist , microbiology and biotechnology , biology , biophysics , biochemistry , receptor , gene
Threshold concentrations of lysophosphatidic acid (LPA) or acetylcholine (ACh) induce pertussis toxin (PTX)‐sensitive rapid desensitization of responses to LPA in Xenopus oocytes. To demonstrate that threshold [LPA] rapidly activates Gi/o proteins, we used the G protein‐activated K + channel (GIRK) as a reporter. Low [LPA] induced I K + in <3 s of the agonist addition with little or no activation of chloride current. Depletion of Gαo/Gαo1 each decreased the LPA‐induced I K + by approximately 40–50%, while PTX completely abolished it. This is the first direct evidence showing the activation of GIRK by LPA, and the involvement of G proteins of the Go family in rapid desensitization of LPA responses.