γCaMKII将Ca2+/CaM运送到核中,从而触发CREB酸化和基因表达
Huan Ma1, Rachel D Groth2, Samuel M Cohen1
1Department of Neuroscience and Physiology, Neuroscience Institute, NYU Langone Medical Center, New York, NY 10016, USA.
Cell
|October 11, 2014
概括
研究人员发现了一种用于长距离神经元通信的新型细胞通路. 一种穿蛋白将信号运送到细胞核,这对神经元可塑性至关重要,并与神经精神疾病有关.
科学领域:
- 神经科学是一个神经科学.
- 分子生物学分子生物学
- 细胞信号传递 细胞信号传递
背景情况:
- 活动依赖的CREB酸化对长期的神经元可塑性至关重要.
- 在CaV1通道的局部信号引发了这些事件,但核传输机制尚不清楚.
研究的目的:
- 阐明神经元可塑性的长距离细胞内通信机制.
- 为了确定负责将Ca2+/calmodulin (CaM) 运送到细胞核的穿蛋白.
主要方法:
- 通过生物化学测试和细胞成像,研究了Ca2+/CaM运输.
- 研究了玛-CaMKII (γCaMKII),β-CaMKII (βCaMKII) 和素素 (CaN) 在信号通路中的作用.
主要成果:
- 确定了γCaMKII作为从细胞表面到细胞核的Ca2+/CaM的穿蛋白.
- 证明βCaMKII可酸化γCaMKII,保护Ca2+/CaM信号,而CaN会触发其核转位.
- 表明核Ca(2+) /CaM激活了CaMKK和CaMKIV,导致了CREB酸化.
结论:
- 一个涉及γCaMKII作为Ca(2+) /CaM穿的新机制解决了向核的信号通路.
- 这一途径对神经元可塑性至关重要,其失调与神经精神疾病有关.
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