Duprat F, Lesage F, Guillemare E, Fink M, Hugnot J P, Bigay J, Lazdunski M, Romey G, Barhanin J
Institut de Pharmacologie Moléculaire et Cellulaire, Valbonne, France.
Biochem Biophys Res Commun. 1995 Jul 17;212(2):657-63. doi: 10.1006/bbrc.1995.2019.
The family of G-protein-activated inward-rectifiers K+ channels presently comprise at least 3 cloned members called GIRK1, GIRK2 and GIRK3. A close structural parent of GIRK channels has recently been described as being an ATP-sensitive K+ channel. This paper shows that Xenopus expression of this new channel that we call GIRK4 does not produce an ATP-inhibitable activity with a pharmacological activation by pinacidil as previously described but instead a G-protein activated inward-rectifier. While oocyte expression of single subunits is infrequent and relatively modest in intensity, expression of GIRK1,2, GIRK1,4 and GIRK2,4 mixtures leads to routine and robust expression of K+ channels indicating that heterologous subunit assembly is necessary for activity. Activity of GIRK1,2, GIRK1,4 and GIRK2,4 channels required the presence of ATP acting as an activator at the cytoplasmic face and is further activated by the beta gamma subunits.
G蛋白激活的内向整流钾通道家族目前至少包括3个克隆成员，分别称为GIRK1、GIRK2和GIRK3。GIRK通道的一个结构紧密的亲本最近被描述为一种ATP敏感性钾通道。本文表明，我们称为GIRK4的这种新通道在非洲爪蟾中的表达，并未产生如先前所述的通过吡那地尔进行药理学激活的ATP抑制活性，而是产生了一种G蛋白激活的内向整流器。虽然单个亚基在卵母细胞中的表达很少见且强度相对适中，但GIRK1,2、GIRK1,4和GIRK2,4混合物的表达会导致钾通道的常规且强劲的表达，这表明异源亚基组装对于活性是必要的。GIRK1,2、GIRK1,4和GIRK2,4通道的活性需要ATP作为细胞质面的激活剂存在，并且会被βγ亚基进一步激活。
