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神经生长因子通过降低PC12细胞中肌球蛋白轻链的磷酸化水平来诱导神经突生长。

NGF induces neurite outgrowth via a decrease in phosphorylation of myosin light chain in PC12 cells.

作者信息

Fujita A, Hattori Y, Takeuchi T, Kamata Y, Hata F

机构信息

Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, Osaka Prefecture University, 1-1 Gakuencho, Sakai, Osaka 599-8531, Japan.

出版信息

Neuroreport. 2001 Nov 16;12(16):3599-602. doi: 10.1097/00001756-200111160-00045.

Abstract

The relationship between phosphorylation of myosin light chain (MLC) and neurite outgrowth induced by nerve growth factor (NGF) was studied in PC12 cells. Inhibitors of Rho kinase, HA-1077 or Y-27632 also induced neurite outgrowth. As already reported botulinum exoenzyme C3 which inactivates Rho protein also induced neurite outgrowth. Calyeulin A, an inhibitor of phosphatase counteracted both NGF- and C3- induced neurite outgrowth. Treatments of both NGF and C3 resulted in significant and transient decrease in phosphorylated MLC. These results suggest that NGF induces neurite outgrowth of PC12 by a transient decrease in phosphorylated MLC which is brought about by activation of MLC phosphatase via inhibition of Rho-Rho kinase pathway.

摘要

在PC12细胞中研究了肌球蛋白轻链(MLC)磷酸化与神经生长因子(NGF)诱导的神经突生长之间的关系。Rho激酶抑制剂HA-1077或Y-27632也可诱导神经突生长。如先前报道的那样,使Rho蛋白失活的肉毒杆菌外毒素C3也可诱导神经突生长。磷酸酶抑制剂Calyeulin A可抵消NGF和C3诱导的神经突生长。NGF和C3处理均导致磷酸化MLC显著且短暂地减少。这些结果表明,NGF通过磷酸化MLC的短暂减少诱导PC12细胞的神经突生长,而这种减少是通过抑制Rho-Rho激酶途径激活MLC磷酸酶实现的。

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