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Gene Review

Bcl2l11  -  BCL2-like 11 (apoptosis facilitator)

Mus musculus

Synonyms: 1500006F24Rik, Bcl-2-like protein 11, Bcl2-L-11, Bcl2-interacting mediator of cell death, Bim, ...
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Disease relevance of Bcl2l11


High impact information on Bcl2l11

  • Intracellular iron delivery blocks Bim induction and suppresses apoptosis due to 24p3 addition or IL-3 deprivation [6].
  • TCR ligation upregulated Bim expression and promoted interaction of Bim with Bcl-XL, inhibiting its survival function [7].
  • Thus, at least two mammalian BH3-only proteins, Bmf and Bim, function to sense intracellular damage by their localization to distinct cytoskeletal structures [8].
  • Proapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity [9].
  • Thus, Bim is required for hematopoietic homeostasis and as a barrier to autoimmunity [9].

Chemical compound and disease context of Bcl2l11


Biological context of Bcl2l11


Anatomical context of Bcl2l11


Associations of Bcl2l11 with chemical compounds

  • BH3-only proteins such as Bim, which are distant proapoptotic members of the Bcl-2 family, are essential initiators of programmed cell death and stress-induced apoptosis [18].
  • Moreover, small interfering RNA that reduces the expression level of Bim effectively rescues CML cells from apoptosis caused by imatinib [1].
  • In contrast, those cells isolated from our previously established CML model mice resist apoptosis in cytokine-free medium without the induction of Bim expression, and these effects are reversed by the Abl-specific kinase inhibitor imatinib mesylate [1].
  • These results implicate BH3-only proteins, in particular both Bik and Bim, as important mediators of the antitumor action of bortezomib and establish their role in its enhancement of TRAIL-induced apoptosis [2].
  • Here we tested the involvement of Bim in the rapid anoikis response of mouse mammary epithelial cells and discovered that Bim does not have a role in detecting integrin-mediated signals [19].

Physical interactions of Bcl2l11


Regulatory relationships of Bcl2l11


Other interactions of Bcl2l11

  • Consistent with this prediction, truncation of this short helix was required for Bim/Bax interaction and led to spontaneous activation of Bax [15].
  • Loss of Bim allows precursor B cell survival but not precursor B cell differentiation in the absence of interleukin 7 [16].
  • Loss of Bim increases T cell production and function in interleukin 7 receptor-deficient mice [18].
  • These data suggest an essential overlapping role for Bak or Bax and Bim in the intrinsic apoptotic pathway [25].
  • To investigate whether functional redundancy with Bim might obscure a significant role for Bik, we generated mice lacking both genes [12].

Analytical, diagnostic and therapeutic context of Bcl2l11


  1. Roles of Bim in apoptosis of normal and Bcr-Abl-expressing hematopoietic progenitors. Kuribara, R., Honda, H., Matsui, H., Shinjyo, T., Inukai, T., Sugita, K., Nakazawa, S., Hirai, H., Ozawa, K., Inaba, T. Mol. Cell. Biol. (2004) [Pubmed]
  2. The proteasome inhibitor bortezomib sensitizes cells to killing by death receptor ligand TRAIL via BH3-only proteins Bik and Bim. Nikrad, M., Johnson, T., Puthalalath, H., Coultas, L., Adams, J., Kraft, A.S. Mol. Cancer Ther. (2005) [Pubmed]
  3. Bim is a suppressor of Myc-induced mouse B cell leukemia. Egle, A., Harris, A.W., Bouillet, P., Cory, S. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  4. Proapoptotic BH3-only Bcl-2 family member Bik/Blk/Nbk is expressed in hemopoietic and endothelial cells but is redundant for their programmed death. Coultas, L., Bouillet, P., Stanley, E.G., Brodnicki, T.C., Adams, J.M., Strasser, A. Mol. Cell. Biol. (2004) [Pubmed]
  5. Loss of pro-apoptotic BH3-only Bcl-2 family member Bim does not protect mutant Lurcher mice from neurodegeneration. Bouillet, P., Robati, M., Adams, J.M., Strasser, A. J. Neurosci. Res. (2003) [Pubmed]
  6. A cell-surface receptor for lipocalin 24p3 selectively mediates apoptosis and iron uptake. Devireddy, L.R., Gazin, C., Zhu, X., Green, M.R. Cell (2005) [Pubmed]
  7. BH3-only Bcl-2 family member Bim is required for apoptosis of autoreactive thymocytes. Bouillet, P., Purton, J.F., Godfrey, D.I., Zhang, L.C., Coultas, L., Puthalakath, H., Pellegrini, M., Cory, S., Adams, J.M., Strasser, A. Nature (2002) [Pubmed]
  8. Bmf: a proapoptotic BH3-only protein regulated by interaction with the myosin V actin motor complex, activated by anoikis. Puthalakath, H., Villunger, A., O'Reilly, L.A., Beaumont, J.G., Coultas, L., Cheney, R.E., Huang, D.C., Strasser, A. Science (2001) [Pubmed]
  9. Proapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity. Bouillet, P., Metcalf, D., Huang, D.C., Tarlinton, D.M., Kay, T.W., Köntgen, F., Adams, J.M., Strasser, A. Science (1999) [Pubmed]
  10. A novel plant toxin, persin, with in vivo activity in the mammary gland, induces Bim-dependent apoptosis in human breast cancer cells. Butt, A.J., Roberts, C.G., Seawright, A.A., Oelrichs, P.B., Macleod, J.K., Liaw, T.Y., Kavallaris, M., Somers-Edgar, T.J., Lehrbach, G.M., Watts, C.K., Sutherland, R.L. Mol. Cancer Ther. (2006) [Pubmed]
  11. Loss of pro-apoptotic Bim promotes accumulation of pulmonary T lymphocytes and enhances allergen-induced goblet cell metaplasia. Pierce, J., Rir-Sima-Ah, J., Estrada, I., Wilder, J., Strasser, A., Tesfaigzi, Y. Am. J. Physiol. Lung Cell Mol. Physiol. (2006) [Pubmed]
  12. Concomitant loss of proapoptotic BH3-only Bcl-2 antagonists Bik and Bim arrests spermatogenesis. Coultas, L., Bouillet, P., Loveland, K.L., Meachem, S., Perlman, H., Adams, J.M., Strasser, A. EMBO J. (2005) [Pubmed]
  13. BH3-only proteins Puma and Bim are rate-limiting for gamma-radiation- and glucocorticoid-induced apoptosis of lymphoid cells in vivo. Erlacher, M., Michalak, E.M., Kelly, P.N., Labi, V., Niederegger, H., Coultas, L., Adams, J.M., Strasser, A., Villunger, A. Blood (2005) [Pubmed]
  14. Phagocytosis-induced apoptosis in macrophages is mediated by up-regulation and activation of the Bcl-2 homology domain 3-only protein Bim. Kirschnek, S., Ying, S., Fischer, S.F., Häcker, H., Villunger, A., Hochrein, H., Häcker, G. J. Immunol. (2005) [Pubmed]
  15. The structure of a Bcl-xL/Bim fragment complex: implications for Bim function. Liu, X., Dai, S., Zhu, Y., Marrack, P., Kappler, J.W. Immunity (2003) [Pubmed]
  16. Loss of Bim allows precursor B cell survival but not precursor B cell differentiation in the absence of interleukin 7. Oliver, P.M., Wang, M., Zhu, Y., White, J., Kappler, J., Marrack, P. J. Exp. Med. (2004) [Pubmed]
  17. Bim: a novel member of the Bcl-2 family that promotes apoptosis. O'Connor, L., Strasser, A., O'Reilly, L.A., Hausmann, G., Adams, J.M., Cory, S., Huang, D.C. EMBO J. (1998) [Pubmed]
  18. Loss of Bim increases T cell production and function in interleukin 7 receptor-deficient mice. Pellegrini, M., Bouillet, P., Robati, M., Belz, G.T., Davey, G.M., Strasser, A. J. Exp. Med. (2004) [Pubmed]
  19. Bim is an apoptosis sensor that responds to loss of survival signals delivered by epidermal growth factor but not those provided by integrins. Wang, P., Gilmore, A.P., Streuli, C.H. J. Biol. Chem. (2004) [Pubmed]
  20. Constitutive association of the proapoptotic protein Bim with Bcl-2-related proteins on mitochondria in T cells. Zhu, Y., Swanson, B.J., Wang, M., Hildeman, D.A., Schaefer, B.C., Liu, X., Suzuki, H., Mihara, K., Kappler, J., Marrack, P. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  21. Negative selection of semimature CD4(+)8(-)HSA+ thymocytes requires the BH3-only protein Bim but is independent of death receptor signaling. Villunger, A., Marsden, V.S., Zhan, Y., Erlacher, M., Lew, A.M., Bouillet, P., Berzins, S., Godfrey, D.I., Heath, W.R., Strasser, A. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  22. Smad3 potentiates transforming growth factor beta (TGFbeta )-induced apoptosis and expression of the BH3-only protein Bim in WEHI 231 B lymphocytes. Wildey, G.M., Patil, S., Howe, P.H. J. Biol. Chem. (2003) [Pubmed]
  23. Distinct activation signals determine whether IL-21 induces B cell costimulation, growth arrest, or Bim-dependent apoptosis. Jin, H., Carrio, R., Yu, A., Malek, T.R. J. Immunol. (2004) [Pubmed]
  24. Stem cell factor promotes mast cell survival via inactivation of FOXO3a-mediated transcriptional induction and MEK-regulated phosphorylation of the proapoptotic protein Bim. Möller, C., Alfredsson, J., Engström, M., Wootz, H., Xiang, Z., Lennartsson, J., Jönsson, J.I., Nilsson, G. Blood (2005) [Pubmed]
  25. Combined loss of proapoptotic genes Bak or Bax with Bim synergizes to cause defects in hematopoiesis and in thymocyte apoptosis. Hutcheson, J., Scatizzi, J.C., Bickel, E., Brown, N.J., Bouillet, P., Strasser, A., Perlman, H. J. Exp. Med. (2005) [Pubmed]
  26. Degradation of Mcl-1 by granzyme B: implications for Bim-mediated mitochondrial apoptotic events. Han, J., Goldstein, L.A., Gastman, B.R., Froelich, C.J., Yin, X.M., Rabinowich, H. J. Biol. Chem. (2004) [Pubmed]
  27. Microarray analysis uncovers the induction of the proapoptotic BH3-only protein Bim in multiple models of glucocorticoid-induced apoptosis. Wang, Z., Malone, M.H., He, H., McColl, K.S., Distelhorst, C.W. J. Biol. Chem. (2003) [Pubmed]
  28. The pro-apoptotic protein Bim is a convergence point for cAMP/protein kinase A- and glucocorticoid-promoted apoptosis of lymphoid cells. Zhang, L., Insel, P.A. J. Biol. Chem. (2004) [Pubmed]
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