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CNS翻译练习：Myc-nick: 一种Myc在细胞质中的剪切产物，能促进alpha-微管蛋白乙酰化和细胞分化
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Myc-nick: 一种Myc在细胞质中的剪切产物，能促进alpha-微管蛋白乙酰化和细胞分化。
Cell. 2010 Aug 6;142(3):480-93.
Myc-nick: a cytoplasmic cleavage product of Myc that promotes alpha-tubulin acetylation and cell differentiation.
Conacci-Sorrell M, Ngouenet C, Eisenman RN.
Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
Abstract
The Myc oncoprotein family comprises transcription factors that control multiple cellular functions and are widely involved in oncogenesis. Here we report the identification of Myc-nick, a cytoplasmic form of Myc generated by calpain-dependent proteolysis at lysine 298 of full-length Myc. Myc-nick retains conserved Myc box regions but lacks nuclear localization signals and the bHLHZ domain essential for heterodimerization with Max and DNA binding. Myc-nick induces alpha-tubulin acetylation and altered cell morphology by recruiting histone acetyltransferase GCN5 to microtubules. During muscle differentiation, while the levels of full-length Myc diminish, Myc-nick and acetylated alpha-tubulin levels are increased. Ectopic expression of Myc-nick accelerates myoblast fusion, triggers the expression of myogenic markers, and permits Myc-deficient fibroblasts to transdifferentiate in response to MyoD. We propose that the cleavage of Myc by calpain abrogates the transcriptional inhibition of differentiation by full-length Myc and generates Myc-nick, a driver of cytoplasmic reorganization and differentiation.
Myc-nick: 一种Myc在细胞质中的剪切产物，能促进alpha-微管蛋白乙酰化和细胞分化。
Abstract
Myc癌蛋白家族包括一些控制多种细胞功能的转录因子，它们广泛参与肿瘤发生。这里我们报道了Myc-nick的确认，一种由钙蛋白酶依赖的在Myc全长第298位氨基酸裂解的Myc细胞质形式。 Myc-nick 保留了Myc盒区域但是缺少核定位信号和与Max形成异源二聚体以及和DNA结合的必须的bHLHZ域。Myc-nick引导alpha-微管蛋白乙酰化并通过募集组蛋白乙酰转移酶GCN5到微管上改变细胞形态。肌肉分化的过程中，当全长Myc消失时，Myc-nick和乙酰化的alpha-微管蛋白水平提高了。 Myc-nick的异位表达加速了成肌蛋白的融合，引发了生肌信号的表达，并允许Myc缺陷的纤维母细胞对MyoD应答以转移分化。我们认为钙蛋白酶对Myc的剪切消除了全长Myc的对分化的转录抑制作用，其产物Myc-nick是细胞质重组和分化的驱动器。
https://blog.sciencenet.cn/blog-464637-356657.html
上一篇：西行漫记03--迷路
下一篇：CNS翻译练习：深海喷油丰富了周围的石油降解细菌
Cell. 2010 Aug 6;142(3):480-93.
Myc-nick: a cytoplasmic cleavage product of Myc that promotes alpha-tubulin acetylation and cell differentiation.
Conacci-Sorrell M, Ngouenet C, Eisenman RN.
Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
Abstract
The Myc oncoprotein family comprises transcription factors that control multiple cellular functions and are widely involved in oncogenesis. Here we report the identification of Myc-nick, a cytoplasmic form of Myc generated by calpain-dependent proteolysis at lysine 298 of full-length Myc. Myc-nick retains conserved Myc box regions but lacks nuclear localization signals and the bHLHZ domain essential for heterodimerization with Max and DNA binding. Myc-nick induces alpha-tubulin acetylation and altered cell morphology by recruiting histone acetyltransferase GCN5 to microtubules. During muscle differentiation, while the levels of full-length Myc diminish, Myc-nick and acetylated alpha-tubulin levels are increased. Ectopic expression of Myc-nick accelerates myoblast fusion, triggers the expression of myogenic markers, and permits Myc-deficient fibroblasts to transdifferentiate in response to MyoD. We propose that the cleavage of Myc by calpain abrogates the transcriptional inhibition of differentiation by full-length Myc and generates Myc-nick, a driver of cytoplasmic reorganization and differentiation.
Myc-nick: 一种Myc在细胞质中的剪切产物，能促进alpha-微管蛋白乙酰化和细胞分化。
Abstract
Myc癌蛋白家族包括一些控制多种细胞功能的转录因子，它们广泛参与肿瘤发生。这里我们报道了Myc-nick的确认，一种由钙蛋白酶依赖的在Myc全长第298位氨基酸裂解的Myc细胞质形式。 Myc-nick 保留了Myc盒区域但是缺少核定位信号和与Max形成异源二聚体以及和DNA结合的必须的bHLHZ域。Myc-nick引导alpha-微管蛋白乙酰化并通过募集组蛋白乙酰转移酶GCN5到微管上改变细胞形态。肌肉分化的过程中，当全长Myc消失时，Myc-nick和乙酰化的alpha-微管蛋白水平提高了。 Myc-nick的异位表达加速了成肌蛋白的融合，引发了生肌信号的表达，并允许Myc缺陷的纤维母细胞对MyoD应答以转移分化。我们认为钙蛋白酶对Myc的剪切消除了全长Myc的对分化的转录抑制作用，其产物Myc-nick是细胞质重组和分化的驱动器。
https://blog.sciencenet.cn/blog-464637-356657.html
上一篇：西行漫记03--迷路
下一篇：CNS翻译练习：深海喷油丰富了周围的石油降解细菌
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