The proapoptotic BH3-only protein bim is expressed in hematopoietic, epithelial, neuronal, and germ cells
- Author(s)
- O'Reilly, LA; Cullen, L; Visvader, J; Lindeman, GJ; Print, C; Bath, ML; Huang, DCS; Strasser, A;
- Details
- Publication Year 2000-08,Volume 157,Issue #2,Page 449-461
- Journal Title
- AMERICAN JOURNAL OF PATHOLOGY
- Publication Type
- Journal Article
- Abstract
- 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.
- Publisher
- AMER SOC INVESTIGATIVE PATHOLOGY, INC
- Keywords
- BCL-2 FAMILY MEMBERS; IN-VIVO PATTERNS; IMMUNOHISTOCHEMICAL ANALYSIS; DEFICIENT MICE; NERVOUS-SYSTEM; LYMPHOID-CELLS; APOPTOSIS; DEATH; LINES; HAIR
- Publisher's Version
- https://doi.org/10.1016/S0002-9440(10)64557-9
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2000-08-01 12:00:00