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轴突-体通讯在神经元损伤中的作用。

Axon-soma communication in neuronal injury.

机构信息

Department of Biological Chemistry, Weizmann Institute of Science, 76100 Rehovot, Israel.

出版信息

Nat Rev Neurosci. 2014 Jan;15(1):32-42. doi: 10.1038/nrn3609. Epub 2013 Dec 11.

Abstract

The extensive lengths of neuronal processes necessitate efficient mechanisms for communication with the cell body. Neuronal regeneration after nerve injury requires new transcription; thus, long-distance retrograde signalling from axonal lesion sites to the soma and nucleus is required. In recent years, considerable progress has been made in elucidating the mechanistic basis of this system. This has included the discovery of a priming role for early calcium waves; confirmation of central roles for mitogen-activated protein kinase signalling effectors, the importin family of nucleocytoplasmic transport factors and molecular motors such as dynein; and demonstration of the importance of local translation as a key regulatory mechanism. These recent findings provide a coherent mechanistic framework for axon-soma communication in the injured nerve and shed light on the integration of cytoplasmic and nuclear transport in all eukaryotic cells.

摘要

神经元突起的长度很长,这就需要有高效的机制来与细胞体进行通讯。神经损伤后的神经元再生需要新的转录;因此,需要从轴突损伤部位向胞体和核进行长距离逆行信号传递。近年来,人们在阐明这个系统的机制基础方面取得了相当大的进展。这包括发现早期钙波的启动作用;确认丝裂原活化蛋白激酶信号效应物、核质运输因子导入蛋白家族和分子马达(如动力蛋白)在中枢的作用;并证明局部翻译作为关键调节机制的重要性。这些最近的发现为损伤神经中的轴突-胞体通讯提供了一个连贯的机制框架,并揭示了细胞质和核质运输在所有真核细胞中的整合。

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