Resolution of the identity of the Ca2(+)-antagonist receptor in skeletal muscle.
Resolution of the identity of the Ca2(+)-antagonist receptor in skeletal muscle.
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骨骼肌中 Ca2( ) 拮抗剂受体身份的解析。
DOI：
10.1016/0165-6147(88)90066-1
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发表时间：
1988
影响因子：
13.8
通讯作者：
Schwartz,A
中科院分区：
文献类型：
--
作者：
Vaghy,PL;McKenna,E;Itagaki,K;Schwartz,A
本文对Cazi-ckunne ~ i~ kj~ i受体的鉴定作一综述。在过去的两年里没有改变。Preutous s&die= MIfl IvI（LcLI=（L. - I u; h.. bn.- l-11~ a ~ 2 + _，&，ye~ C，l.. P.，抑制剂药物受体与由两个（140 kDa和30 kDa）二硫键连接的组分组成的单个170 kDa多肽结合。然而，如Arnold Schwartz和同事在此所综述的，最近的研究表明，2，4-d-kydropyrdines和PkenylkyZ-mines结合到不含锌的、未被识别的、最高的165 kDzz型pept-de上，其在二硫键还原时不影响电泳迁移率。该受体的一级结构与其他电压依赖性阳离子通道具有同源性。这一结果以及从纯化的受体制剂中重建的Ca ~（2+）通道活性表明，Ca ~（2+）拮抗剂受体（afone）或与其它亚单位的玉米黄酮（corbiffufio ~ z）形成了T型电压依赖性的CR ~（2+）~（3+）~（3+）。最具选择性作用的药物属于三种化学基团之一：1，2-二氢吡啶类（DE-P）、苯丙氨酸内斯和苯并硫氮杂卓类。这些药物仅抑制L型CaZ+通道，
Tke view on tke jdenfify of receptors for Cazi-ckunne~ i~ kj~ ifor drugs has... t chunged durtng rne zast two years. Preutous s&die= MIfl IvI (LcLI=(L...-I u; h.. bn.-l-11~ a2+ _, &,,, ye~ C, l.. P., inhibitor drug receptors to a single 170 kDa polypcptide consisting of two (140kDa and 30 kDa) disulfide-linked components. However, as reviewed here by Arnold Schwartz and colleagues, more recent studies show that 2, 4-d~ kydropyr~ dines and Pkeny~~ lkyZ~ mines bind to~ not~ zer, pr~ v~ ousiy unreco~-nized, upproximately 165 kDzz oiypept~ de which does not ifzangtl ifs clectrophoretic mobility upon disulfide reduction. The primary structure of the receptor exhibits homolog with other voltage-dependent cation chunnels. This, and reconstitution of Ca X-channel activity from purified receptor preparations: suggests that the Ca2’antagonist receptor, afone or in cornbiffufio~ z with otker subunits, forms the t-type voltage-dependent CR’+ c~ zann~ r.Ca*+ antagonists have been successfully used for the treatment of several cardiovascular disorders such as coronary heart disease, supraventricular arrhythmias and hypertension. The most selectively acting drugs belong to one of three chemical groups: l,+ dihydropyridines (DE-P), phenyla~ kylam~ nes and benzothiazepines. These drugs inhibit only the L-type CaZ+ chan-