| First Author | Fleischer A | Year | 2002 |
| Journal | Oncogene | Volume | 21 |
| Issue | 20 | Pages | 3181-9 |
| PubMed ID | 12082633 | Mgi Jnum | J:76678 |
| Mgi Id | MGI:2179928 | Doi | 10.1038/sj.onc.1205464 |
| Citation | Fleischer A, et al. (2002) Proapoptotic activity of ITM2B(s), a BH3-only protein induced upon IL-2-deprivation which interacts with Bcl-2. Oncogene 21(20):3181-9 |
| abstractText | 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. |
