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β-连环蛋白募集到钙黏蛋白介导的细胞间黏附中参与了成肌诱导。

Recruitment of beta-catenin to cadherin-mediated intercellular adhesions is involved in myogenic induction.

作者信息

Goichberg P, Shtutman M, Ben-Ze'ev A, Geiger B

机构信息

Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel.

出版信息

J Cell Sci. 2001 Apr;114(Pt 7):1309-19. doi: 10.1242/jcs.114.7.1309.

Abstract

Cadherin-mediated cell adhesion is involved in muscle differentiation from early stages of myogenic induction to late stages of myoblast interaction and fusion. beta-Catenin is a major constituent of cadherin-based adherens junctions and also serves as a signal transduction molecule that regulates gene expression during development. In this study, we explored the involvement of beta-catenin in myogenic differentiation. We show here that shortly after a switch from growth to differentiation medium, beta-catenin translocates to cell-cell junctions and its levels increase. We further show that elevation of beta-catenin levels, induced either by inhibition of its breakdown, using LiCl, or by its overexpression, suppresses the formation of adherens junctions, resulting in a sharp decline in myogenin expression and an arrest of myogenic progression. Recruitment of beta-catenin to adherens junctions after transfection with N-cadherin restores myogenin expression in the transfected cells. These results suggest that increased cadherin-mediated adhesion and translocation of beta-catenin to adherens junctions are involved in activating the early steps of myogenic differentiation.

摘要

钙黏蛋白介导的细胞黏附参与了从成肌诱导早期到成肌细胞相互作用与融合后期的肌肉分化过程。β-连环蛋白是基于钙黏蛋白的黏附连接的主要成分,并且还作为一种信号转导分子,在发育过程中调节基因表达。在本研究中,我们探讨了β-连环蛋白在成肌分化中的作用。我们在此表明,在从生长培养基转换为分化培养基后不久,β-连环蛋白易位至细胞间连接且其水平升高。我们进一步表明,通过使用氯化锂抑制其降解或通过其过表达诱导的β-连环蛋白水平升高,会抑制黏附连接的形成,导致肌细胞生成素表达急剧下降并使成肌进程停滞。用N-钙黏蛋白转染后将β-连环蛋白招募至黏附连接可恢复转染细胞中的肌细胞生成素表达。这些结果表明,增加的钙黏蛋白介导的黏附以及β-连环蛋白向黏附连接的易位参与激活成肌分化的早期步骤。

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