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Stem Cell:SIRT1,P53和p38MAPK调节Max缺失时ESC的死亡

来源:生物谷 2012-06-17 22:06

近日,Stem Cell杂志在线报道了c-Myc基因重要伙伴蛋白Max基因缺失条件下胚胎干细胞丧失多能性并发生细胞死亡的机制研究进展。

c-Myc基因参与多种细胞过程,包括细胞周期调控,致瘤性转化和体细胞重编程为诱导多能干细胞。 c-Myc基因也是一个重要的调节自我更新和胚胎干细胞(ESCs)全能性的调节因子。

以往研究证实,Max基因(该基因编码Myc家族蛋白的最为人们熟知的合作伙伴因子)的缺失,首先导致胚胎干细胞的多能性的丧失,随后引起广泛的细胞死亡。

然而,负责这些表型的分子机制仍然在很大程度上模糊不清。本研究表明,SIRT1,P53和p38MAPK在导致Max基因缺失胚胎干细胞这些破坏性表型过程中,发挥重要作用。此外,研究者的分析显示,这些蛋白质在导致Max基因缺失胚胎干细胞细胞死亡的分子信号途径的不同层次,以不同水平互相作用。(生物谷bioon.com)

Sirt1, p53 and p38MAPK are Crucial Regulators of Detrimental Phenotypes of ESCs with Max Expression Ablation?

Tomoaki Hishida1,5,?, Yuriko Nozaki1,5, Yutaka Nakachi2,3, Yosuke Mizuno3, Hiroyoshi Iseki3,5, Miyuki Katano1, Masayoshi

c-Myc participates in diverse cellular processes including cell cycle control, tumorigenic transformation and reprogramming of somatic cells to induced pluripotent cells. c-Myc is also an important regulator of self-renewal and pluripotency of embryonic stem cells (ESCs). We recently demonstrated that loss of the Max gene, encoding the best characterized partner for all Myc family proteins, causes loss of the pluripotent state and extensive cell death in ESCs strictly in this order. However, the mechanisms and molecules that are responsible for these phenotypes remain largely obscure. Here, we show that Sirt1, p53 and p38MAPK are crucially involved in the detrimental phenotype of Max-null ESCs. Moreover, our analyses revealed that these proteins are involved at varying levels to one another in the hierarchy of the pathway leading to cell death in Max-null ESCs.

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