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Necdin 通过促进凋亡介质 CCAR1/CARP1 的降解来增强成肌细胞的存活。

Necdin enhances myoblasts survival by facilitating the degradation of the mediator of apoptosis CCAR1/CARP1.

机构信息

Department of Experimental Medicine, University of Milano-Bicocca, Monza, Italy.

出版信息

PLoS One. 2012;7(8):e43335. doi: 10.1371/journal.pone.0043335. Epub 2012 Aug 14.

DOI:10.1371/journal.pone.0043335
PMID:22905258
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3419192/
Abstract

Regeneration of muscle fibers, lost during pathological muscle degeneration or after injuries, is sustained by the production of new myofibers by means of the satellite cells. Survival of the satellite cells is a critical requirement for efficient muscle reconstitution. Necdin, a member of the MAGE proteins family, is expressed in satellite cell-derived myogenic precursors during perinatal growth and in the adult upon activation during muscle regeneration, where it plays an important role both in myoblast differentiation and survival. We show here that necdin exerts its pro-survival activity by counteracting the action of the pro-apoptotic protein Cell Cycle Apoptosis Regulatory Protein (CCAR1/CARP1) that we have identified as a new molecular interactor of necdin by two-hybrid screening. Necdin is responsible for the maintenance of CCAR1 protein levels, by implementing its ubiquitination and degradation through the proteasome. Taken together, these data shed new light on the molecular mechanism of necdin anti-apoptotic activity in myogenesis.

摘要

肌肉纤维在病理性肌肉退化或受伤后会丢失，卫星细胞通过产生新的肌纤维来维持肌肉纤维的再生。卫星细胞的存活是肌肉有效重建的关键要求。在围产期生长过程中，神经细胞黏附分子（Necdin）作为 MAGE 蛋白家族的一员，在卫星细胞衍生的成肌前体细胞中表达，在成年后肌肉再生时被激活，在成肌细胞分化和存活中发挥重要作用。我们在这里表明，Necdin 通过抵消凋亡蛋白细胞周期凋亡调控蛋白（CCAR1/CARP1）的作用发挥其促生存活性，我们通过双杂交筛选将其鉴定为 Necdin 的一个新的分子相互作用蛋白。Necdin 通过蛋白酶体实施其泛素化和降解，从而负责维持 CCAR1 蛋白水平。总之，这些数据为 Necdin 在成肌细胞中的抗凋亡活性的分子机制提供了新的认识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99e2/3419192/1795a1125410/pone.0043335.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99e2/3419192/99d033554344/pone.0043335.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99e2/3419192/ae7f7eff79a4/pone.0043335.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99e2/3419192/7cbeba3732c0/pone.0043335.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99e2/3419192/1795a1125410/pone.0043335.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99e2/3419192/99d033554344/pone.0043335.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99e2/3419192/ae7f7eff79a4/pone.0043335.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99e2/3419192/7cbeba3732c0/pone.0043335.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99e2/3419192/1795a1125410/pone.0043335.g004.jpg

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