钙离子/ CREB/ CBP依赖性基因调控：一种在长期突触可塑性和神经元存活中起关键作用的共同机制。

Ca(2+)/CREB/CBP-dependent gene regulation: a shared mechanism critical in long-term synaptic plasticity and neuronal survival.

作者信息

Bito Haruhiko, Takemoto-Kimura Sayaka

机构信息

Department of Neurochemistry, University of Tokyo Graduate School of Medicine, Bunkyo-ku, 113-0033 Tokyo, Japan.

出版信息

Cell Calcium. 2003 Oct-Nov;34(4-5):425-30. doi: 10.1016/s0143-4160(03)00140-4.

DOI:10.1016/s0143-4160(03)00140-4

PMID:12909086

Abstract

CREB is a transcription factor critical for long-term synaptic plasticity. Intriguingly, recent work has elucidated a role for CREB, as well as upstream CREB kinases, in the control of activity-dependent neuronal survival. Additionally, analysis of the molecular pathology of polyglutamine-repeat diseases suggest that alteration of pCREB-CBP function may underlie, at least in part, the neurodegenerative process. Taken together, these new findings support the idea that Ca(2+)/CREB/CBP-dependent gene regulation might be a shared mechanism critical in both long-term synaptic plasticity and neuronal survival.

摘要

CREB是一种对长期突触可塑性至关重要的转录因子。有趣的是，最近的研究阐明了CREB以及上游CREB激酶在活性依赖的神经元存活控制中的作用。此外，对多聚谷氨酰胺重复疾病分子病理学的分析表明，pCREB-CBP功能的改变可能至少部分地是神经退行性过程的基础。综上所述，这些新发现支持了这样一种观点，即Ca(2+)/CREB/CBP依赖的基因调控可能是长期突触可塑性和神经元存活中共同的关键机制。