Bim and Bmf in tissue homeostasis and malignant disease.

Bim and Bmf in tissue homeostasis and malignant disease.
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DOI:
10.1038/onc.2009.42
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发表时间:
2008-12
期刊:
影响因子:
8
通讯作者:
Villunger, A.
Villunger, A.
中科院分区:
医学1区
文献类型:
--
作者:
Pinon, J. D.;Labi, V.;Egle, A.;Villunger, A.

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在迄今为止已知的所有 BH3 蛋白中,大多数信息都是关于 Bim(Bcl-2 细胞死亡相互作用介质)/BOD(Bcl-2 相关卵巢死亡激动剂)的生物学作用和功能,而对其最接近的 Bcl-2 修饰因子 (Bmf) 仍知之甚少。尽管 Bim 参与了多种细胞类型和组织响应大量刺激而诱导细胞死亡的调节,包括生长因子或细胞因子剥夺、钙流、T 细胞和 B 细胞上抗原受体的连接、糖皮质激素或粘附丧失,但 Bmf 似乎通过在其中一些细胞死亡过程中支持 Bim 来发挥更有限的作用。本综述旨在强调 Bim 和 Bmf 在细胞凋亡信号传导中的功能的相似性及其在正常发育和疾病中的作用。
Among all BH3-only proteins known to date, most information is available on the biological role and function of Bim (Bcl-2 interacting mediator of cell death)/BOD (Bcl-2 related ovarian death agonist), whereas little is still known about its closest relative, Bcl-2 modifying factor (Bmf). Although Bim has been implicated in the regulation of cell death induction in multiple cell types and tissues in response to a large number of stimuli, including growth factor or cytokine deprivation, calcium flux, ligation of antigen receptors on T and B cells, glucocorticoid or loss of adhesion, Bmf seems to play a more restricted role by supporting Bim in some of these cell death processes. This review aims to highlight similarities between Bim and Bmf function in apoptosis signaling and their role in normal development and disease.
吉非替尼诱导的表达突变体EGFR的NSCLC细胞系杀死需要BIM,并且可以通过BH3 Mimetics增强。
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