Brain fodrin: substrate for calpain I, an endogenous calcium-activated protease.
Brain fodrin: substrate for calpain I, an endogenous calcium-activated protease.
复制标题
脑蛋白:钙蛋白酶 I(一种内源性钙激活蛋白酶)的底物。
DOI:
10.1073/pnas.81.11.3572
复制
发表时间:
1984
影响因子:
11.1
通讯作者:
Lynch,G
中科院分区:
文献类型:
--
作者:
Siman,R;Baudry,M;Lynch,G
The calcium-activated thiol-protease calpain I, which is present in cytosolic and membrane preparations from rat brain, was tested for its capacity to degrade the neuronal spectrin-like protein fodrin. In the presence of micromolar calcium concentrations purified calpain I degraded both purified fodrin and the fodrin present in hippocampal and cerebellar membranes. Fodrin was identified as a high molecular weight protein present in brain membranes by the following criteria: (i) comigration on NaDodSO4/polyacrylamide gels with purified fodrin, (ii) reactivity with antibodies to purified fodrin, and (iii) a proteolytic map following calpain activation comparable to that found after calpain-mediated degradation of purified fodrin. The fodrin breakdown was selective in that calpain I did not affect at least 15 other membrane-associated polypeptides. Fodrin degradation by the protease was rapid and was accompanied by the appearance of a lower molecular weight breakdown product. Calpain I had a high affinity for fodrin, with a Km for degradation of about 50 nM. Purified calpain I also degraded purified spectrin and the spectrin present in erythrocyte membranes. Calpain I-mediated degradation of spectrin-like proteins could provide a mechanism by which brief increases in intracellular free calcium levels modify the structure of the submembraneous cytoskeleton and the distribution of cell surface receptors and alter cell shape.
登录
查看更多内容
影响因子:
64.5
作者:
J. Glenney;P. Glenney;M. Osborn;K. Weber
通讯作者:
K. Weber
影响因子:
56.9
作者:
E. Lazarides;W. Nelson
通讯作者:
W. Nelson
影响因子:
56.9
作者:
BAUDRY, M;BUNDMAN, MC;LYNCH, GS
通讯作者:
LYNCH, GS
影响因子:
--
作者:
K. Burridge
通讯作者:
K. Burridge
DOI:
--
发表时间:
1983
影响因子:
11.1
作者:
J. Levine;M. Willard
通讯作者:
M. Willard