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首页> 外文期刊>Journal of Cellular Physiology >Stem cell antigen-1 localizes to lipid microdomains and associates with insulin degrading enzyme in skeletal myoblasts.
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Stem cell antigen-1 localizes to lipid microdomains and associates with insulin degrading enzyme in skeletal myoblasts.

机译：脂质干细胞antigen-1本地化microdomains与胰岛素和同事骨胳肌母细胞降解酶。

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摘要

Stem cell antigen-1 (Sca-1, Ly6A/E) is a glycosylphosphotidylinositol-anchored protein that identifies many tissue progenitor cells. We originally identified Sca-1 as a marker of myogenic precursor cells and subsequently demonstrated that Sca-1 regulates proliferation of activated myoblasts, suggesting an important role for Sca-1 in skeletal muscle homeostasis. Beyond its functional role in regulating proliferation, however, little is known about the mechanism(s) that drive Sca-1-mediated events. We now report that lipid microdomain organization is essential for normal myogenic differentiation, and that Sca-1 constitutively localizes to these domains during myoblast proliferation and differentiation. We also demonstrate that Sca-1 associates with insulin degrading enzyme (IDE), a catalytic protein responsible for the cleavage of mitogenic peptides, in differentiating myoblasts. We show that chemical inhibition of IDE as well as RNAi knockdown of IDE mRNA recapitulates the phenotype of Sca-1 interference, that is, sustained myoblast proliferation and delayed myogenic differentiation. These findings identify the first signaling protein that physically and functionally associates with Sca-1 in myogenic precursor cells, and suggest a potential pathway for Sca-1-mediated signaling. Future efforts to manipulate this pathway may lead to new strategies for augmenting the myogenic proliferative response, and ultimately muscle repair.
机译：干细胞antigen-1(本来Ly6A / E)glycosylphosphotidylinositol-anchored蛋白质许多组织祖细胞识别。最初发现本来的标志肌原性的前体细胞,随后证明了本来就调节扩散激活的成肌细胞,表明一个重要角色本来就在骨骼肌内稳态。超出其在调节功能的作用然而,扩散是知之甚少机制(s)驱动Sca-1-mediated事件。现在报告,脂质microdomain组织对于正常的肌原性的分化,,本来这些既定的本地化在成肌细胞增殖和域分化。同事与胰岛素降解酶(IDE)催化蛋白质的乳沟负责促有丝分裂的多肽,在区分成肌细胞。我们也表明,化学抑制的IDE作为IDE mRNA概括的RNAi击倒表型的本来就干扰,持续的成肌细胞增殖和延迟肌原性的分化。第一个信号蛋白质,身体和功能的同事,本来就在肌原性的前体细胞,并建议潜在的途径Sca-1-mediated信号。操纵这个途径可能导致新的为增加肌原性的策略增生性反应,最终肌肉修复。

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