Calcium and calmodulin-dependent protein phosphorylation in rabbit ileum.
Calcium and calmodulin-dependent protein phosphorylation in rabbit ileum.
复制标题
兔回肠中钙和钙调蛋白依赖性蛋白磷酸化。
DOI:
10.1016/0014-5793(81)80395-x
复制
发表时间:
1981
期刊:
影响因子:
3.5
通讯作者:
Sharp,GW
中科院分区:
文献类型:
--
作者:
Taylor,L;Guerina,VJ;Donowitz,M;Cohen,M;Sharp,GW
Evidence is accumulating to suggest that calcium is a physiological regulator of intestinal electrolyte transport [1-3]. Conditions which increase intracellular calcium such as the use of the calcium ionophore A23187 [1, 2] or exposure to neurohumoral substances such as serotonin [4] or carbachol [1] cause stimulation of intestinal chloride secretion and/or inhibition ofNa÷ and C1-absorption. To the contrary, conditions which decrease intracellular calcium, such as exposure to the calcium channel blocker verapamil, stimulate Na÷ and C1-absorption [3]. Calmodulin may be involved in these effects since the anti-psychotic drug trifluoperazine (an inhibitor of the calcium-calmodulin complex) inhibited intestinal secretion caused by the calcium ionophore A23187 [5, 6]. The intracellular mechanisms by which calcium and calmodulin affect intestinal ion transport are not known. However, as calcium and calmodulin affect phosphorylation and function of specific proteins in several other systems [7, 8], phosphorylation is a potential control mechanism for ileal electrolyte transport. These studies are the first demonstration that calcium and calmodulin can cause phosphorylation of intestinal peptides.