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[对MyoD调控的新见解:参与横纹肌肉瘤途径?]

[New insight into MyoD regulation: involvement in rhabdomyosarcoma pathway?].

作者信息

Tintignac L A, Leibovitch M P, Leibovitch S A

机构信息

Laboratoire de génétique oncologique, UMR 1599 CNRS, Institut Gustave-Roussy, 94805 Villejuif.

出版信息

Bull Cancer. 2001 Jun;88(6):545-8.

Abstract

The transcription factor MyoD, member of the myogenic regulators family, induces differentiation in precursor cells by its ability to arrest cell proliferation and to activate muscle specific genes. MyoD plays a key role in the antagonism between proliferation and differentiation. The withdrawal from the cell cycle and the activation of muscle differentiation are related to the level of MyoD protein. The cyclin E-cdk2 complex, one of the key regulators of the G1/S transition is directly implicated in the degradation of MyoD by the ubiquitin-proteasome pathway, leading the myoblasts to proliferate. The display of this control in normal myoblasts suggests that its deficiency in the muscle stem cells could lead to the formation of rhabdomyosarcomas which have lost both the control of cell proliferation and the transcriptional activity of MyoD.

摘要

转录因子MyoD是生肌调节因子家族的成员,它通过抑制细胞增殖和激活肌肉特异性基因的能力,诱导前体细胞分化。MyoD在增殖与分化的拮抗作用中起关键作用。退出细胞周期和肌肉分化的激活与MyoD蛋白水平有关。细胞周期蛋白E-cdk2复合物是G1/S期转换的关键调节因子之一,直接参与泛素-蛋白酶体途径介导的MyoD降解,导致成肌细胞增殖。在正常成肌细胞中这种调控的表现表明,其在肌肉干细胞中的缺陷可能导致横纹肌肉瘤的形成,横纹肌肉瘤同时失去了对细胞增殖的控制和MyoD的转录活性。

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