The proapoptotic BH3-only protein bim is expressed in hematopoietic, epithelial, neuronal, and germ cells

被引:203
|
作者
O'Reilly, LA
Cullen, L
Visvader, J
Lindeman, GJ
Print, C
Bath, ML
Huang, DCS
Strasser, A [1 ]
机构
[1] Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, Melbourne, Vic 3050, Australia
[2] Royal Melbourne Hosp, Rotary Bone Marrow Res Labs, Melbourne, Vic 3050, Australia
来源
AMERICAN JOURNAL OF PATHOLOGY | 2000年 / 157卷 / 02期
基金
英国医学研究理事会;
关键词
D O I
10.1016/S0002-9440(10)64557-9
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Proapoptotic Bcl-2 family members activate cell death by neutralizing their anti-apoptotic relatives, which in turn maintain cell viability by regulating the activation of the cell death effecters, the caspases, Bim belongs to a distinct subgroup of proapoptotic proteins that only resemble other Bcl-2 family members within the short BH3 domain. Gene targeting experiments in mice have shown that him is essential for the execution of some but not all apoptotic stimuli, for hematopoietic cell homeostasis, and as a barrier against autoimmunity. There are three Bim isoforms, Bim(S), Bim(L), and Bim(EL), which have different proapoptotic potencies due at least in part to differences in interaction with the dynein motor complex. The expression pattern of Bim was investigated by immunohistochemical staining, immunoprecipitation followed by Western blotting, and in situ hybridization, him was found in hematopoietic, epithelial, neuronal, and germ cells. Bim(L) and Bim(EL) were coexpressed at similar levels In many cell types, but Bim(S) was not detected. Microscopic examination revealed a punctate pattern of Bim(L) and Bim(EL) immunostaining, indicating association with cytoplasmic structures. These results are discussed in the context of the phenotype of Bim-deficient mice and the post-translational regulation of Bim's pro-apoptotic activity.
引用
收藏
页码:449 / 461
页数:13
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