Modulation of cofactor requirement for the activation of protein kinase C by heparin. Possible effect at the regulatory domain.
Modulation of cofactor requirement for the activation of protein kinase C by heparin. Possible effect at the regulatory domain.
复制标题
肝素调节蛋白激酶 C 激活的辅因子需求。
DOI：
10.1016/0014-5793(91)80533-9
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发表时间：
1991
期刊：
影响因子：
3.5
通讯作者：
Ahmed,K
中科院分区：
文献类型：
--
作者：
Goueli,SA;Hanten,JA;Ahmed,K
研究发现，肝素可以刺激Ca 2 +/磷脂依赖性蛋白激酶（蛋白激酶C或PKC）催化的组蛋白H1磷酸化，但不能刺激硫酸鱼精蛋白磷酸化。肝素对组蛋白H1磷酸化的影响似乎是由于在肝素存在下磷脂酰丝氨酸对PKC活化的亲和力增加。当胰蛋白酶化的、不依赖于辅因子的PKC被用于磷酸化组蛋白H1时，肝素的这种作用被消除。这些研究表明，肝素作用于PKC的调节域，并强调负电荷在影响底物对PKC作用的可及性方面的重要性
Heparin was found to stimulate the phosphorylation of histone H1 but not protamine sulfate catalyzed by Ca2+/phospholipid‐dependent protein kinase (protein kinase C or PKC). The effect of heparin on histone H1 phosphorylation appeared to be due to an increase in phosphatidylserine affinity for PKC activation in the presence of heparin. This effect of heparin was abolisched when trypsinized, cofactor‐independent, PKC was employed to phosphorylate histone H1. These studies suggest that heparin acts at the regulatory domain of PKC, and emphasize the importance of the negative charge in influencing the accessibility of the substrate to PKC action