期刊
FASEB JOURNAL
卷 19, 期 13, 页码 109-+出版社
FEDERATION AMER SOC EXP BIOL
DOI: 10.1096/fj.05-4826fje
关键词
hippocampus; CaMK; NeuroD
Excitatory stimuli are known to be a potent regulator for induction of neuronal differentiation. Calbindin-D-28K buffers intracellular Ca2+ and modifies synaptic functions in neurons. However, the effects of calbindin-D-28K on the regulation of activity-induced neuronal differentiation and related biochemical modifications remain unsolved. In the present study, by a gain-of-function study with retroviral vector system and dicer-generated small interfering RNA (d-siRNA) to effectively knock down the expression of calbindin-D-28K, we demonstrated that calbindin-D-28K at a physiologically relevant level promoted neuronal differentiation and neurite outgrowth. Increase of neuronal differentiation by calbindin-D-28K overexpression was concurrent with the expression of basic helix-loop-helix ( bHLH) transcriptional factors, phosphorylation of calcium and calmodulin-dependent protein kinase II (CaMKII) and NeuroD at Ser(336). KN-62, a highly specific CaMKII inhibitor, blocked the up-regulation of proneural bHLH genes, p-CaMKII, and pSer(336)NeuroD. Calbindin-D-28K appeared to facilitate neuronal differentiation of both fetal and adult hippocampal progenitor cells. Together, these findings establish the novel calbindin-regulated function of CaMKII and NeuroD in control of neuronal differentiation and neurite outgrowth.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据