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肌肉特异性微管相关蛋白4在肌发生早期表达,且不足以诱导微管重组。

Muscle-specific microtubule-associated protein 4 is expressed early in myogenesis and is not sufficient to induce microtubule reorganization.

作者信息

Casey Liam M, Lyon Hiram D, Olmsted Joanna B

机构信息

Department of Biology, University of Rochester, Rochester, New York 14627, USA.

出版信息

Cell Motil Cytoskeleton. 2003 Apr;54(4):317-36. doi: 10.1002/cm.10105.

Abstract

The expression of a muscle-specific variant of microtubule-associated protein 4 (mMAP4) has been analyzed during myogenesis of C(2)C(12) cells using an isoform-specific antibody. MMAP4 localizes to microtubules (MTs) and is expressed prior to a very early morphogenetic event, the formation of mononucleate spindle-shaped cells. MMAP4 protein appears at about the same time as titin and coincident with Golgi reorganization, but antedates myosin expression. Misexpression of EGFP-mMAP4 in non-muscle and proliferating C(2)C(12) cells does not induce dramatic changes in MT organization or stability, nor in Golgi organization. Expression of full-length mMAP4 or of a truncated form lacking the MT-binding domain does not disrupt myotube formation or myofibrillogenesis. While previous antisense studies indicated that mMAP4 is necessary for normal myotube formation [Mangan and Olmsted, 1996: Development 122:771-781], these data indicate mMAP4 is not sufficient to induce the reorganization of MTs or the Golgi into patterns typical of muscle cells. Thus, with respect to MT organizing properties, this tissue-specific variant differs from related neuronal MAPs, MAP2, and tau, which induce neural-like changes in MT organization.

摘要

利用一种亚型特异性抗体,在C2C12细胞的成肌过程中分析了微管相关蛋白4(mMAP4)的肌肉特异性变体的表达情况。MMP4定位于微管(MTs),且在一个非常早期的形态发生事件——单核纺锤形细胞形成之前就已表达。MMP4蛋白与肌联蛋白大约同时出现,并与高尔基体重组同时发生,但早于肌球蛋白的表达。在非肌肉和增殖性C2C12细胞中过表达EGFP - mMMP4,不会引起MT组织或稳定性以及高尔基体组织的显著变化。全长mMAP4或缺乏MT结合结构域的截短形式的表达,不会破坏肌管形成或肌原纤维生成。虽然先前的反义研究表明mMAP4是正常肌管形成所必需的[Mangan和Olmsted,1996:发育122:771 - 781],但这些数据表明mMAP4不足以诱导MTs或高尔基体重组成肌肉细胞典型的模式。因此,就MT组织特性而言,这种组织特异性变体不同于相关的神经元微管相关蛋白(MAPs)、MAP2和tau,它们会诱导MT组织发生类神经变化。

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