Akt和c-Jun氨基末端激酶2在白细胞介素-4缺乏诱导的细胞凋亡中的作用
Role of Akt and c-Jun N-terminal kinase 2 in apoptosis induced by interleukin-4 deprivation.
作者信息
Cerezo A, Martínez-A C, Lanzarot D, Fischer S, Franke T F, Rebollo A
机构信息
Department of Immunology and Oncology, Centro Nacional de Biotecnología, Universidad Autónoma, Campus de Cantoblanco, E-28049 Madrid, Spain.
出版信息
Mol Biol Cell. 1998 Nov;9(11):3107-18. doi: 10.1091/mbc.9.11.3107.
Abstract
We have shown previously that interleukin-4 (IL-4) protects TS1alphabeta cells from apoptosis, but very little is known about the mechanism by which IL-4 exerts this effect. We found that Akt activity, which is dependent on phosphatidylinositol 3 kinase, is reduced in IL-4-deprived TS1alphabeta cells. Overexpression of wild-type Akt or a constitutively active Akt mutant protects cells from IL-4 deprivation-induced apoptosis. Readdition of IL-4 before the commitment point is able to restore Akt activity. We also show expression and c-Jun N-terminal kinase 2 activation after IL-4 deprivation. Overexpression of the constitutively activated Akt mutant in IL-4-deprived cells correlates with inhibition of c-Jun N-terminal kinase 2 activity. Finally, TS1alphabeta survival is independent of Bcl-2, Bcl-x, or Bax.
摘要
我们之前已经表明，白细胞介素-4（IL-4）可保护TS1αβ细胞免于凋亡，但对于IL-4发挥这种作用的机制却知之甚少。我们发现，依赖磷脂酰肌醇3激酶的Akt活性在缺乏IL-4的TS1αβ细胞中降低。野生型Akt或组成型活性Akt突变体的过表达可保护细胞免于IL-4剥夺诱导的凋亡。在关键时间点之前重新添加IL-4能够恢复Akt活性。我们还显示了IL-4剥夺后c-Jun氨基末端激酶2的表达和激活。在缺乏IL-4的细胞中组成型激活的Akt突变体的过表达与c-Jun氨基末端激酶2活性的抑制相关。最后，TS1αβ细胞的存活独立于Bcl-2、Bcl-x或Bax。
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