Nakamura S, Nonomura Y
J Biochem. 1986 May;99(5):1359-69. doi: 10.1093/oxfordjournals.jbchem.a135604.
Cross-linked complex of gizzard myosin light chain kinase (MLCK) and calmodulin (CM) was produced by glutaraldehyde treatment of a mixture of these proteins in a high Ca2+ (0.1 mM) solution. Although the specific activity was reduced, this complex showed MLCK activity in a Ca2+-independent manner, different from the original MLCK whose activity was Ca2+-dependent. Chlorpromazine, one of the CM antagonists, was no longer able to inhibit the MLCK activity of this complex. These observations support the previously proposed hypothesis on the regulatory mechanism of MLCK activity via Ca2+. This complex could be regarded as another kind of Ca2+-independent MLCK different from that obtained by chymotryptic digestion of MLCK (Walsh, M.P., Dabrowska, R., Hinkins, S., & Hartshorne, D.J. (1982) Biochemistry 21, 1919-1925). This complex caused superprecipitation of gizzard actomyosin and enhanced actin-activated ATPase of myosin Ca2+-independently.
通过在高钙(0.1 mM)溶液中用戊二醛处理肌胃肌球蛋白轻链激酶(MLCK)和钙调蛋白(CM)的混合物,产生了它们的交联复合物。尽管比活性降低了,但该复合物以不依赖于钙的方式表现出MLCK活性,这与活性依赖于钙的原始MLCK不同。CM拮抗剂之一氯丙嗪不再能够抑制该复合物的MLCK活性。这些观察结果支持了先前提出的关于通过钙调节MLCK活性的机制的假设。该复合物可被视为另一种不依赖于钙的MLCK,不同于通过胰凝乳蛋白酶消化MLCK获得的那种(Walsh, M.P., Dabrowska, R., Hinkins, S., & Hartshorne, D.J. (1982) Biochemistry 21, 1919 - 1925)。该复合物导致肌胃肌动球蛋白超沉淀,并独立于钙增强肌球蛋白的肌动蛋白激活的ATP酶活性。