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 effectors, 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 Bim 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, BimS, BimL, and BimEL, 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. Bim was found in hematopoietic, epithelial, neuronal, and germ cells. BimL and BimEL were coexpressed at similar levels in many cell types, but BimS was not detected. Microscopic examination revealed a punctate pattern of BimL and BimEL 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.
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Supported by grants and fellowships from AMRAD Biotech, the Leukemia and Lymphoma Society of America (New York), the Anti-Cancer Council of Victoria (Melbourne, Australia), the Dr. Josef Steiner Cancer Research Foundation (Bern, Switzerland), the National Health and Medical Research Council (Canberra, Australia), the Cancer Research Institute (New York), and the Victorian Breast Cancer Research Consortium (Melbourne, Australia).
Dr. Print’s present address is Department of Pathology, University of Cambridge, Cambridge, UK.
