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The question is how these might act to reinforce normal heart rhythm or act as substrates for cardiac arrhythmia. We have specific interests in a range of potassium channels and heterotrimeric G-protein signalling in the heart and blood vessels. Technically we are using unique strains of genetically modified mice and we combine this with murine phenotyping capabilities including single-cell electrophysiology and imaging of cardiac myocytes (ventricular, atrial and SA nodal), telemetry and electrophysiology studies. In addition, we also have an established track record in molecular and cellular studies in these areas and are still performing such work. I have several very distinctive research strands being pursued in my laboratory with a focus on ATP-sensitive K+ channels, G-protein gated inwardly rectifying K+ channels.
He C, Yan X, Zhang H, Mirshahi T, Jin T, Huang A, Logothetis DE (February 2002). "Identification of critical residues controlling G protein-gated inwardly rectifying K(+) channel activity through interactions with the beta gamma subunits of G proteins". J. Biol. Chem. 277 (8): 6088–96. doi:10.
Jelacic TM, Kennedy ME, Wickman K, Clapham DE (November 2000). "Functional and biochemical evidence for G-protein-gated inwardly rectifying K+ (GIRK) channels composed of GIRK2 and GIRK3". J. Biol. Chem. 275 (46): 36211–6. doi:10.