GAP domains responsible for ras p21-dependent inhibition of muscarinic atrial K+ channel currents.
GAP domains responsible for ras p21-dependent inhibition of muscarinic atrial K+ channel currents.
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GAP 结构域负责 ras p21 依赖性毒蕈碱性心房 K 通道电流的抑制。
DOI：
10.1126/science.1553544
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
McCormick,F
中科院分区：
文献类型：
--
作者：
Martin,GA;Yatani,A;Clark,R;Conroy,L;Polakis,P;Brown,AM;McCormick,F
低分子量G蛋白ras p21与鸟苷三磷酸酶激活蛋白（GAP）之间的相互作用使异三聚体G蛋白（Gk）与毒菌碱受体分离。通过使用分离的心房细胞膜和基因工程的GAP缺失突变体，GAP氨基末端的src同源区域（SH2-SH3）已被确定为负责这种效应的结构域。在该系统中，刺激ras p21鸟苷三磷酸酶活性所需结构域的缺失减轻了对ras p21的需求。一个模型表明ras p21诱导GAP的构象变化，使GAP的SH2-SH3区域发挥作用。
The interaction between the low molecular weight G protein ras p21 and a guanosine triphosphatase activating protein (GAP) uncouples a heterotrimeric G protein (Gk) from muscarinic receptors. Through the use of isolated atrial cell membranes and genetically engineered GAP deletion mutants, the src homology regions (SH2-SH3) at the amino terminus of GAP have been identified as the domains responsible for this effect. Deletion of the domain required to stimulate the guanosine triphosphatase activity of ras p21 relieves the requirement for ras p21 in this system. A model is presented that suggests that ras p21 induces a conformational change in GAP, which allows the SH2-SH3 regions of GAP to function.