Requirement of the transmembrane semaphorin Sema4C for myogenic differentiation
Requirement of the transmembrane semaphorin Sema4C for myogenic differentiation
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DOI：
10.1016/j.febslet.2005.03.022
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发表时间：
2005-04-11
期刊：
影响因子：
3.5
通讯作者：
Inui, M
中科院分区：
文献类型：
--
作者：
Ko, JA;Gondo, T;Inui, M
脑信号蛋白构成了一个大家族的信号蛋白，有助于轴突的指导。在这里，我们表明，跨膜信号蛋白Sema4C上调C2C12小鼠骨骼肌成肌细胞分化成肌管的早期阶段，在体内损伤诱导的肌肉再生。C2C12细胞中Sema4C的耗尽导致肌管形成的显著衰减。含有细胞外Sema结构域和对应于Sema4C的细胞内COOH末端区域的肽的融合蛋白各自抑制C2C12细胞的分化。这些发现表明，Sema4C介导的成肌细胞之间的相互作用在终末肌源性分化中起着重要作用。(c)2005年欧洲生物化学学会联合会。Elsevier B.V.出版，保留所有权利。
Semaphorins constitute a large family of signaling proteins that contribute to axonal guidance. Here we demonstrate that the transmembrane semaphorin Sema4C is up-regulated both in the early stage of differentiation of C2C12 mouse skeletal myoblasts into myotubes and during injury-induced muscle regeneration in vivo. Depletion of Sema4C in C2C12 cells resulted in marked attenuation of myotube formation. A fusion protein containing the extracellular Sema domain and a peptide corresponding to the intracellular COOH-terminal region of Sema4C each inhibited the differentiation of C2C12 cells. These findings indicate that Sema4C-mediated interaction among myoblasts plays an important role in terminal myogenic differentiation. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.