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5-氮杂胞苷在一个分化缺陷细胞系中诱导了肌生成。

5-Azacytidine induced myogenesis in a differentiation defective cell line.

作者信息

Walker C, Shay J W

出版信息

Differentiation. 1984;25(3):259-63. doi: 10.1111/j.1432-0436.1984.tb01364.x.

Abstract

A differentiation defective cell line variant, the T984-15, has lost the capacity to differentiate myogenically. Following treatment with the hypomethylating agent 5-azacytidine, T984-15 cells were induced to differentiate into myogenic colonies containing fused myotubes. Myogenic colonies when cloned, maintained their ability to differentiate after prolonged culture in the absence of further 5-azacytidine treatment. These results indicate that 5-azacytidine treatment resulted in a stable alteration in the capacity of T984-15 cells to differentiate and suggests that the loss of myogenic potential may have occurred as a result of an epigenetic phenomenon rather than a somatic mutational event.

摘要

一种分化缺陷的细胞系变体T984-15已丧失了肌源性分化能力。在用低甲基化剂5-氮杂胞苷处理后,T984-15细胞被诱导分化为含有融合肌管的肌源性集落。克隆后的肌源性集落在不进行进一步5-氮杂胞苷处理的情况下长期培养后仍保持其分化能力。这些结果表明,5-氮杂胞苷处理导致T984-15细胞分化能力发生稳定改变,并提示肌源性潜能的丧失可能是表观遗传现象而非体细胞突变事件所致。

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