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驱动“汽车(运转)”——控制活细胞中货物运输的新方式。

Drive the Car(go)s-New Modalities to Control Cargo Trafficking in Live Cells.

作者信息

Mondal Payel, Khamo John S, Krishnamurthy Vishnu V, Cai Qi, Zhang Kai

机构信息

Department of Biochemistry, University of Illinois at Urbana-Champaign Urbana, IL, USA.

Department of Biochemistry, University of Illinois at Urbana-ChampaignUrbana, IL, USA; Neuroscience Program, University of Illinois at Urbana-ChampaignUrbana, IL, USA; Center for Biophysics and Quantitative Biology, University of Illinois at Urbana-ChampaignUrbana, IL, USA.

出版信息

Front Mol Neurosci. 2017 Jan 20;10:4. doi: 10.3389/fnmol.2017.00004. eCollection 2017.

DOI:10.3389/fnmol.2017.00004
PMID:28163671
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5247435/
Abstract

Synaptic transmission is a fundamental molecular process underlying learning and memory. Successful synaptic transmission involves coupled interaction between electrical signals (action potentials) and chemical signals (neurotransmitters). Defective synaptic transmission has been reported in a variety of neurological disorders such as Autism and Alzheimer's disease. A large variety of macromolecules and organelles are enriched near functional synapses. Although a portion of macromolecules can be produced locally at the synapse, a large number of synaptic components especially the membrane-bound receptors and peptide neurotransmitters require active transport machinery to reach their sites of action. This spatial relocation is mediated by energy-consuming, motor protein-driven cargo trafficking. Properly regulated cargo trafficking is of fundamental importance to neuronal functions, including synaptic transmission. In this review, we discuss the molecular machinery of cargo trafficking with emphasis on new experimental strategies that enable direct modulation of cargo trafficking in live cells. These strategies promise to provide insights into a quantitative understanding of cargo trafficking, which could lead to new intervention strategies for the treatment of neurological diseases.

摘要

突触传递是学习和记忆背后的一个基本分子过程。成功的突触传递涉及电信号(动作电位)和化学信号(神经递质)之间的耦合相互作用。在多种神经疾病如自闭症和阿尔茨海默病中,已报道存在有缺陷的突触传递。大量的大分子和细胞器富集在功能性突触附近。尽管一部分大分子可以在突触局部产生,但大量的突触成分,尤其是膜结合受体和肽类神经递质,需要主动运输机制才能到达它们的作用位点。这种空间重定位是由消耗能量、由运动蛋白驱动的货物运输介导的。货物运输的适当调节对于包括突触传递在内的神经元功能至关重要。在这篇综述中,我们讨论货物运输的分子机制,重点是能够直接调节活细胞中货物运输的新实验策略。这些策略有望为定量理解货物运输提供见解,这可能会带来治疗神经疾病的新干预策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3370/5247435/e4dc80a5972f/fnmol-10-00004-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3370/5247435/e4dc80a5972f/fnmol-10-00004-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3370/5247435/e4dc80a5972f/fnmol-10-00004-g0001.jpg

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