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Gene Review

Bcl2l1  -  BCL2-like 1

Mus musculus

Synonyms: Apoptosis regulator Bcl-X, Bcl(X)L, Bcl-2-like protein 1, Bcl-XL, Bcl-Xs, ...
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Disease relevance of Bcl2l1


High impact information on Bcl2l1


Chemical compound and disease context of Bcl2l1

  • These data suggest that the responsiveness of ovarian cancer to paclitaxel and cisplatin in vivo, and therefore perhaps clinically, is influenced by levels of the antiapoptotic protein BclXL [10].

Biological context of Bcl2l1

  • Finally, overexpression of Bcl-XL effectively protected IL-3-dependent myeloid cells from apoptosis following removal of trophic factors [1].
  • Tumors harboring bcl-X insertions had altered bcl-X RNAs, expressed elevated levels of Bcl-XL protein, and lacked the requirements for cytokines normally essential for cell survival [1].
  • Therefore, Bcl-XL functions as a key cytokine regulated anti-apoptotic protein in myelopoiesis and contributes to leukemia cell survival [1].
  • To assess the role of Bcl-xL in thymocyte apoptosis, we generated mice overexpressing an E mu-bcl-x transgene within the T cell compartment [11].
  • The results demonstrated IL-3-independent growth by Ik6-transfected 32D clones coincident with up-regulation of the antiapoptotic protein Bcl-XL [12].

Anatomical context of Bcl2l1


Associations of Bcl2l1 with chemical compounds

  • These interactions have been considered promiscuous, but our analysis of the affinity of eight BH3 peptides for five Bcl-2-like proteins has revealed that the interactions vary over 10,000-fold in affinity, and accordingly, only certain protein pairs associate inside cells [17].
  • p21Cip1 protection against hyperoxia requires Bcl-XL and is uncoupled from its ability to suppress growth [18].
  • Oxidized low density lipoprotein inhibits macrophage apoptosis by blocking ceramide generation, thereby maintaining protein kinase B activation and Bcl-XL levels [19].
  • Here we demonstrate that expression of Bax, a Bcl-2-like protein, is increased at the blastocyst stage in the presence of high concentrations of glucose, and that these changes correlate morphologically with increased DNA fragmentation [20].
  • The PT pore complex is regulated by thiol-reactive agents, calcium, cyclophilin D ligands (cyclosporin A and a nonimmunosuppressive cyclosporin A derivative), ligands of the adenine nucleotide translocator, apoptosis-related endoproteases (caspases), and Bcl-2-like proteins [21].

Physical interactions of Bcl2l1


Enzymatic interactions of Bcl2l1

  • We found that Bcl-XL protein was cleaved by caspase-3/CPP32 at two sites in the loop domain (i.e., HLAD61/S and SSLD76/A) [25].
  • However, Bax with BH3 deleted did not form heterodimers with Bcl-XL, but retained its ability to counter the death repressor activity of Bcl-XL [26].

Regulatory relationships of Bcl2l1

  • c-Myc augments gamma irradiation-induced apoptosis by suppressing Bcl-XL [27].
  • Overexpression of Bad in murine FL5.12 cells demonstrated that the protein not only could abrogate the protective capacity of coexpressed Bcl-XL but could accelerate the apoptotic response to a death signal when it was expressed in the absence of exogenous Bcl-XL [28].
  • In this report, we examine whether Stat5 can induce transactivation of the bcl-x gene in response to Epo [29].
  • We now demonstrate that BTK regulates bcl-x expression by transcriptional control in response to BCR engagement [30].
  • Stable transfection of either bcl-2 or bcl-x expression plasmids promotes the survival of CTLL-2 cells in the setting of IL-2 withdrawal [31].

Other interactions of Bcl2l1

  • Bcl-XL and Bcl-2 repress a common pathway of cell death [32].
  • Among the Bcl-2 family proteins only Bid and Bcl-XL continue to be expressed at high levels in the adult brain [33].
  • Together, these results demonstrate that PU.1 and Ets2 dramatically increase bcl-x activation, which is necessary for the cytocidal function and survival of macrophages [34].
  • Bruton's tyrosine kinase targets NF-kappaB to the bcl-x promoter via a mechanism involving phospholipase C-gamma2 following B cell antigen receptor engagement [30].
  • Molecular linkage analysis using interspecific backcross mice revealed the murine Bcl2l locus at 0.7 cM terminal to D2Mit22, and the murine Bax locus at 0.8 cM terminal to D7Nds5 [35].

Analytical, diagnostic and therapeutic context of Bcl2l1

  • Elimination of Bclx by gene targeting dramatically shortens the survival of DP thymocytes but not the survival of SP thymocytes or peripheral SP T cells [36].
  • Immunoblotting analysis showed no upregulation of pro-apoptotic proteins (caspase-2L, -3, -6, -8, -9, and Bax) with age while all the anti-apoptotic proteins (caspase-2S, Bcl-2, and Bcl-XL) remained unchanged during aging [37].
  • The bcl-xS splice variant of bcl-x can promote cell death, and bcl-xL has a protective function in cell culture [38].
  • The drug effects on the expression of the beta-tubulin isotypes, Bcl-2, Bax, Bcl-XL and proteomic profiles were evaluated by immunobloting and SELDI mass spectrometry in tumor xenografts dosed at 0.5 MTDs [39].
  • Western blot analysis revealed decreased phosphorylation levels of STAT-5 and reduced expression of Bcl-XL in RGCs of axotomized tg21 animals, suggesting that the corresponding pathways are not crucial for Epo's neuroprotective activity [40].


  1. Selective regulation of Bcl-XL by a Jak kinase-dependent pathway is bypassed in murine hematopoietic malignancies. Packham, G., White, E.L., Eischen, C.M., Yang, H., Parganas, E., Ihle, J.N., Grillot, D.A., Zambetti, G.P., Nuñez, G., Cleveland, J.L. Genes Dev. (1998) [Pubmed]
  2. Bcl-XL disrupts death-inducing signal complex formation in plasma membrane induced by hypoxia/reoxygenation. Wang, X., Zhang, J., Kim, H.P., Wang, Y., Choi, A.M., Ryter, S.W. FASEB J. (2004) [Pubmed]
  3. Hepatocyte-specific disruption of Bcl-xL leads to continuous hepatocyte apoptosis and liver fibrotic responses. Takehara, T., Tatsumi, T., Suzuki, T., Rucker, E.B., Hennighausen, L., Jinushi, M., Miyagi, T., Kanazawa, Y., Hayashi, N. Gastroenterology (2004) [Pubmed]
  4. Bcl-x(L) prevents apoptosis of late-stage erythroblasts but does not mediate the antiapoptotic effect of erythropoietin. Rhodes, M.M., Kopsombut, P., Bondurant, M.C., Price, J.O., Koury, M.J. Blood (2005) [Pubmed]
  5. Bcl-XL is required for heme synthesis during the chemical induction of erythroid differentiation of murine erythroleukemia cells independently of its antiapoptotic function. Hafid-Medheb, K., Augery-Bourget, Y., Minatchy, M.N., Hanania, N., Robert-Lézénès, J. Blood (2003) [Pubmed]
  6. Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death. Yang, E., Zha, J., Jockel, J., Boise, L.H., Thompson, C.B., Korsmeyer, S.J. Cell (1995) [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. Massive cell death of immature hematopoietic cells and neurons in Bcl-x-deficient mice. Motoyama, N., Wang, F., Roth, K.A., Sawa, H., Nakayama, K., Nakayama, K., Negishi, I., Senju, S., Zhang, Q., Fujii, S. Science (1995) [Pubmed]
  9. Rel-dependent induction of A1 transcription is required to protect B cells from antigen receptor ligation-induced apoptosis. Grumont, R.J., Rourke, I.J., Gerondakis, S. Genes Dev. (1999) [Pubmed]
  10. Overexpression of BclXL in a human ovarian carcinoma cell line: paradoxic effects on chemosensitivity in vitro versus in vivo. Rogers, P.M., Beale, P.J., Al-Moundhri, M., Boxall, F., Patterson, L., Valenti, M., Raynaud, F., Hobbs, S., Johnston, S., Kelland, L.R. Int. J. Cancer (2002) [Pubmed]
  11. Bcl-XL displays restricted distribution during T cell development and inhibits multiple forms of apoptosis but not clonal deletion in transgenic mice. Grillot, D.A., Merino, R., Núñez, G. J. Exp. Med. (1995) [Pubmed]
  12. High frequency of Ikaros isoform 6 expression in acute myelomonocytic and monocytic leukemias: implications for up-regulation of the antiapoptotic protein Bcl-XL in leukemogenesis. Yagi, T., Hibi, S., Takanashi, M., Kano, G., Tabata, Y., Imamura, T., Inaba, T., Morimoto, A., Todo, S., Imashuku, S. Blood (2002) [Pubmed]
  13. p28 Bap31, a Bcl-2/Bcl-XL- and procaspase-8-associated protein in the endoplasmic reticulum. Ng, F.W., Nguyen, M., Kwan, T., Branton, P.E., Nicholson, D.W., Cromlish, J.A., Shore, G.C. J. Cell Biol. (1997) [Pubmed]
  14. Epistatic and independent functions of caspase-3 and Bcl-X(L) in developmental programmed cell death. Roth, K.A., Kuan, C., Haydar, T.F., D'Sa-Eipper, C., Shindler, K.S., Zheng, T.S., Kuida, K., Flavell, R.A., Rakic, P. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  15. tBid interaction with cardiolipin primarily orchestrates mitochondrial dysfunctions and subsequently activates Bax and Bak. Gonzalvez, F., Pariselli, F., Dupaigne, P., Budihardjo, I., Lutter, M., Antonsson, B., Diolez, P., Manon, S., Martinou, J.C., Goubern, M., Wang, X., Bernard, S., Petit, P.X. Cell Death Differ. (2005) [Pubmed]
  16. Apaf1-dependent programmed cell death is required for inner ear morphogenesis and growth. Cecconi, F., Roth, K.A., Dolgov, O., Munarriz, E., Anokhin, K., Gruss, P., Salminen, M. Development (2004) [Pubmed]
  17. Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function. Chen, L., Willis, S.N., Wei, A., Smith, B.J., Fletcher, J.I., Hinds, M.G., Colman, P.M., Day, C.L., Adams, J.M., Huang, D.C. Mol. Cell (2005) [Pubmed]
  18. p21Cip1 protection against hyperoxia requires Bcl-XL and is uncoupled from its ability to suppress growth. Vitiello, P.F., Staversky, R.J., Gehen, S.C., Johnston, C.J., Finkelstein, J.N., Wright, T.W., O'Reilly, M.A. Am. J. Pathol. (2006) [Pubmed]
  19. Oxidized low density lipoprotein inhibits macrophage apoptosis by blocking ceramide generation, thereby maintaining protein kinase B activation and Bcl-XL levels. Hundal, R.S., Gómez-Muñoz, A., Kong, J.Y., Salh, B.S., Marotta, A., Duronio, V., Steinbrecher, U.P. J. Biol. Chem. (2003) [Pubmed]
  20. Hyperglycemia induces apoptosis in pre-implantation embryos through cell death effector pathways. Moley, K.H., Chi, M.M., Knudson, C.M., Korsmeyer, S.J., Mueckler, M.M. Nat. Med. (1998) [Pubmed]
  21. The permeability transition pore complex: a target for apoptosis regulation by caspases and bcl-2-related proteins. Marzo, I., Brenner, C., Zamzami, N., Susin, S.A., Beutner, G., Brdiczka, D., Rémy, R., Xie, Z.H., Reed, J.C., Kroemer, G. J. Exp. Med. (1998) [Pubmed]
  22. Neurons exclusively express N-Bak, a BH3 domain-only Bak isoform that promotes neuronal apoptosis. Uo, T., Kinoshita, Y., Morrison, R.S. J. Biol. Chem. (2005) [Pubmed]
  23. Pim kinases phosphorylate multiple sites on Bad and promote 14-3-3 binding and dissociation from Bcl-XL. Macdonald, A., Campbell, D.G., Toth, R., McLauchlan, H., Hastie, C.J., Arthur, J.S. BMC Cell Biol. (2006) [Pubmed]
  24. Involvement of 5'-flanking kappaB-like sites within bcl-x gene in silica-induced Bcl-x expression. Chen, F., Demers, L.M., Vallyathan, V., Lu, Y., Castranova, V., Shi, X. J. Biol. Chem. (1999) [Pubmed]
  25. Acceleration of apoptotic cell death after the cleavage of Bcl-XL protein by caspase-3-like proteases. Fujita, N., Nagahashi, A., Nagashima, K., Rokudai, S., Tsuruo, T. Oncogene (1998) [Pubmed]
  26. Bax can antagonize Bcl-XL during etoposide and cisplatin-induced cell death independently of its heterodimerization with Bcl-XL. Simonian, P.L., Grillot, D.A., Merino, R., Nuñez, G. J. Biol. Chem. (1996) [Pubmed]
  27. c-Myc augments gamma irradiation-induced apoptosis by suppressing Bcl-XL. Maclean, K.H., Keller, U.B., Rodriguez-Galindo, C., Nilsson, J.A., Cleveland, J.L. Mol. Cell. Biol. (2003) [Pubmed]
  28. Bad is a BH3 domain-containing protein that forms an inactivating dimer with Bcl-XL. Kelekar, A., Chang, B.S., Harlan, J.E., Fesik, S.W., Thompson, C.B. Mol. Cell. Biol. (1997) [Pubmed]
  29. Erythropoietin can induce the expression of bcl-x(L) through Stat5 in erythropoietin-dependent progenitor cell lines. Silva, M., Benito, A., Sanz, C., Prosper, F., Ekhterae, D., Nuñez, G., Fernandez-Luna, J.L. J. Biol. Chem. (1999) [Pubmed]
  30. Bruton's tyrosine kinase targets NF-kappaB to the bcl-x promoter via a mechanism involving phospholipase C-gamma2 following B cell antigen receptor engagement. Petro, J.B., Castro, I., Lowe, J., Khan, W.N. FEBS Lett. (2002) [Pubmed]
  31. Expression of Bcl-2, Bcl-x, and Bax after T cell activation and IL-2 withdrawal. Broome, H.E., Dargan, C.M., Krajewski, S., Reed, J.C. J. Immunol. (1995) [Pubmed]
  32. Bcl-XL and Bcl-2 repress a common pathway of cell death. Chao, D.T., Linette, G.P., Boise, L.H., White, L.S., Thompson, C.B., Korsmeyer, S.J. J. Exp. Med. (1995) [Pubmed]
  33. Dynamics of expression of apoptosis-regulatory proteins Bid, Bcl-2, Bcl-X, Bax and Bak during development of murine nervous system. Krajewska, M., Mai, J.K., Zapata, J.M., Ashwell, K.W., Schendel, S.L., Reed, J.C., Krajewski, S. Cell Death Differ. (2002) [Pubmed]
  34. Bcl-XL expression correlates with primary macrophage differentiation, activation of functional competence, and survival and results from synergistic transcriptional activation by Ets2 and PU.1. Sevilla, L., Zaldumbide, A., Carlotti, F., Dayem, M.A., Pognonec, P., Boulukos, K.E. J. Biol. Chem. (2001) [Pubmed]
  35. Chromosomal assignment of the Bcl2-related genes, Bcl2l and Bax, in the mouse and rat. Matsuda, Y., Kusano, H., Tsujimoto, Y. Cytogenet. Cell Genet. (1996) [Pubmed]
  36. Bclx regulates the survival of double-positive thymocytes. Ma, A., Pena, J.C., Chang, B., Margosian, E., Davidson, L., Alt, F.W., Thompson, C.B. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  37. Changes of apoptosis-related proteins in hippocampus of SAM mouse in development and aging. Wu, Y., Zhang, A.Q., Wai, M.S., Lai, H.W., Wu, S.X., Yew, D.T. Neurobiol. Aging (2006) [Pubmed]
  38. Bax and Bcl-xs are induced at the onset of apoptosis in involuting mammary epithelial cells. Heermeier, K., Benedict, M., Li, M., Furth, P., Nuñez, G., Hennighausen, L. Mech. Dev. (1996) [Pubmed]
  39. Molecular determinants of differential sensitivity to docetaxel and paclitaxel in human pediatric cancer models. Izbicka, E., Campos, D., Marty, J., Carrizales, G., Mangold, G., Tolcher, A. Anticancer Res. (2006) [Pubmed]
  40. Erythropoietin protects from axotomy-induced degeneration of retinal ganglion cells by activating ERK-1/-2. Kilic, U., Kilic, E., Soliz, J., Bassetti, C.I., Gassmann, M., Hermann, D.M. FASEB J. (2005) [Pubmed]
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