| First Author | Alfredsson J | Year | 2005 |
| Journal | Cell Death Differ | Volume | 12 |
| Issue | 2 | Pages | 136-44 |
| PubMed ID | 15592435 | Mgi Jnum | J:106372 |
| Mgi Id | MGI:3618417 | Doi | 10.1038/sj.cdd.4401537 |
| Citation | Alfredsson J, et al. (2005) Proapoptotic Bcl-2 family member Bim is involved in the control of mast cell survival and is induced together with Bcl-XL upon IgE-receptor activation. Cell Death Differ 12(2):136-44 |
| abstractText | Mast cells play critical roles in the regulation of acute and chronic inflammations. Apoptosis is one of the mechanisms that limit and resolve inflammatory responses. Mast cell survival can be controlled by growth factors and activation of the IgE-receptor FcvarepsilonRI. Members of the Bcl-2 protein family are critical regulators of apoptosis and our study provides evidence that the proapoptotic BH3-only family member Bim is essential for growth factor deprivation-induced mast cell apoptosis and that Bim levels increase upon FcvarepsilonRI activation. Bim deficiency or Bcl-2 overexpression delayed or even prevented cytokine withdrawal-induced mast cell apoptosis in culture. The prosurvival protein Bcl-XL and the proapoptotic Bim were both induced upon FcvarepsilonRI activation. These results suggest that Bim and possibly also other BH3-only proteins control growth factor withdrawal-induced mast cell apoptosis and that the fate of mast cells upon FcvarepsilonRI activation depends on the relative levels of pro- and antiapoptotic Bcl-2 family members. |
