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Changes in Nup62 content affect contact-induced differentiation of cultured myoblasts

机译:NUP62含量的变化会影响培养肌细胞的接触诱导分化

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Differentiation of cultured skeletal myoblasts is induced by extrinsic signals that include reduction in ambient mitogen concentration and increased cell density. Using an established murine myoblast cell line (C2C12), we have found that experimental reduction of the nucleoporin p62 (Nup62) content of myoblasts enhances differentiation in high-mitogen medium, while forced expression of Nup62 inhibits density-induced differentiation. In contrast, differentiation of myoblasts induced by low-mitogen medium was unaffected by ectopic Nup62 expression. Further analyses suggested that Nup62 content affects density-induced myoblast differentiation through a mechanism involving activation of p38 MAP kinase. Nuclear pore complex (NPC) composition, in particular changes in NUP62 content, may be altered during viral infection, differentiation, and in neoplastic growth. The results support a functional role for changes in Nup62 composition in NPCs and density-induced myogenic differentiation, and suggest a link between loss of Nup62 content and induction of an intracellular stress signaling pathways.
机译:体外培养的骨骼肌成肌细胞的分化是由外部信号诱导的,这些信号包括周围有丝分裂原浓度的降低和细胞密度的增加。利用已建立的小鼠成肌细胞系(C2C12),我们发现实验性降低成肌细胞的核孔蛋白p62(Nup62)含量可增强高有丝分裂原培养基中的分化,而强制表达Nup62可抑制密度诱导的分化。相反,低有丝分裂原培养基诱导的成肌细胞分化不受异位Nup62表达的影响。进一步的分析表明,Nup62含量通过激活p38 MAP激酶的机制影响密度诱导的成肌细胞分化。在病毒感染、分化和肿瘤生长过程中,核孔复合体(NPC)的组成,尤其是NUP62含量的变化,可能会发生改变。研究结果支持NPC中Nup62组成的变化和密度诱导的肌源性分化的功能作用,并表明Nup62含量的丧失与细胞内应激信号通路的诱导之间存在联系。

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