Tsc1-Tsc2复合物通过调节TORC1活性和SAD水平影响神经元极性。
The Tsc1-Tsc2 complex influences neuronal polarity by modulating TORC1 activity and SAD levels.
作者信息
Wildonger Jill, Jan Lily Yeh, Jan Yuh Nung
机构信息
Department of Physiology and Department of Biochemistry, Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, California 94143, USA.
出版信息
Genes Dev. 2008 Sep 15;22(18):2447-53. doi: 10.1101/gad.1724108.
Abstract
Neuronal function depends on the specification of neuronal processes as axons or dendrites. In this issue of Genes & Development Choi and colleagues (2485-2495) show that without Tuberous Sclerosis Complex 1 (Tsc1) or Tsc2, molecules linked to the autosomal dominant disease tuberous sclerosis, an increase in the activity of the translational regulator Target of Rapamycin 1 (TORC1) causes neurons to have multiple axons and the translation of SAD kinase increases as well. Thus, in addition to the kinase LKB1, the Tsc1-Tsc2 complex, acting through TORC1, also modulates SAD to regulate axon formation.
摘要
神经元的功能取决于神经元突起分化为轴突或树突。在本期《基因与发育》中，崔及其同事（第2485 - 2495页）表明，在缺乏与常染色体显性疾病结节性硬化症相关的分子结节性硬化复合物1（Tsc1）或结节性硬化复合物2（Tsc2）的情况下，翻译调节因子雷帕霉素靶蛋白1（TORC1）活性的增加会导致神经元产生多个轴突，同时SAD激酶的翻译也会增加。因此，除了激酶LKB1外，通过TORC1发挥作用的Tsc1 - Tsc2复合物也会调节SAD以调控轴突形成。
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