PMID:12082633

Citation	Fleischer, A, Ayllón, V, Dumoutier, L, Renauld, JC and Rebollo, A (2002) Proapoptotic activity of ITM2B(s), a BH3-only protein induced upon IL-2-deprivation which interacts with Bcl-2. Oncogene 21:3181-9
Abstract	Growth factor deprivation is a physiological mechanism to induce apoptosis. We used an IL-2-dependent murine T cell line to identify proteins that trigger apoptosis. Here we report the identification, the cloning and characterization of ITM2B(s), a protein induced upon IL-2-deprivation. ITM2B(s), which shares the BH3 domain of Bcl-2 family members, is a cytoplasmic and mitochondrial protein. Expression of ITM2B(s) induces apoptosis in IL-2-stimulated cells, but not in IL-4-stimulated cells, while overexpression of the long form of the protein is not able to induce apoptosis. In IL-2-stimulated cells, ITM2B(s) interacts with the antiapoptotic protein Bcl-2, and does not interact with the proapoptotic Bad. Mutation of the critical L and D residues within the BH3 domain abolished the ability of ITM2B(s) to promote apoptosis.
Links	PubMed Online version:10.1038/sj.onc.1205464
Keywords	Alternative Splicing; Amino Acid Sequence; Amino Acid Substitution; Animals; Apoptosis/physiology; Carrier Proteins/metabolism; Cell Line/drug effects; Cell Line/metabolism; Cloning, Molecular; Gene Expression Profiling; Gene Expression Regulation/drug effects; Interleukin-2/pharmacology; Macromolecular Substances; Membrane Proteins/chemistry; Membrane Proteins/genetics; Membrane Proteins/physiology; Mice; Molecular Sequence Data; Protein Structure, Tertiary; Proto-Oncogene Proteins c-bcl-2/physiology; Recombinant Fusion Proteins/physiology; Sequence Alignment; Sequence Homology, Amino Acid; Subtraction Technique; T-Lymphocytes/drug effects; T-Lymphocytes/metabolism; Transfection; bcl-Associated Death Protein
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