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Gene Review

Bcl2a1a  -  B cell leukemia/lymphoma 2 related protein...

Mus musculus

Synonyms: A1, A1-A, BB218357, Bcl-2-related protein A1, Bcl2a1, ...
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Disease relevance of Bcl2a1a

  • Bcl-2-related protein A1 is an endogenous and cytokine-stimulated mediator of cytoprotection in hyperoxic acute lung injury [1].
  • Interestingly, a correlation was noted between the expression level of Bfl-1 gene and the development of stomach cancer in eight sets of clinical samples [2].
  • Although the TLR-9-mediated death of Nfkb1(-/-)C-Rel(-/-) pDCs, which coincided with a failure to up-regulate the prosurvival proteins B-cell lymphoma apoptosis regulator xL (Bcl-x(L)) and A1, was blocked by Bcl-2 transgene expression, this inhibition of apoptosis still failed to rescue the differentiation defects [3].
  • In contrast to Emu-Bcl-2 transgenes, A1 expression in pro-B cells did not rescue pre-B-cell development in SCID mice [4].
  • This study uncovers the importance of A1 for mast cell survival in allergic reactions, and it proposes A1 as a potential target for the treatment of allergic diseases [5].

High impact information on Bcl2a1a


Chemical compound and disease context of Bcl2a1a

  • By contrast, murine S49 lymphoma cells were able to generate the A1 subunit with a time course that closely resembled the kinetics of toxin-mediated cyclic AMP accumulation in these cells [9].

Biological context of Bcl2a1a

  • It is conceivable that Bfl-1 is involved in the promotion of the cell survival in the stomach cancer development or progression [2].
  • A new cDNA clone which is homologous to Bcl-2, named as Bfl-1 were isolated from a human fetal liver at 22 week of gestation [2].
  • The absence of mature B cells was associated with impaired survival that coincided with reduced expression of bcl-2 and A1. bcl-2 transgene expression not only prevented apoptosis and increased peripheral B-cell numbers, but also induced further maturation to an IgM(lo)IgD(hi) phenotype [10].
  • Bcl-2, Bcl-xL, and A1 are differentially expressed during B- and T-cell development, and they have shared and distinct roles in regulating cell death [4].
  • A1 gene expression was strongly but transiently induced during the first day of activation, with a peak at 2 to 6 hours, whereas Bcl-2 mRNA was simultaneously transiently down-regulated [11].

Anatomical context of Bcl2a1a


Associations of Bcl2a1a with chemical compounds


Physical interactions of Bcl2a1a

  • However, Bfl-1 remains tightly and selectively bound to tBid and blocks collaboration between tBid and Bax or Bak in the plane of the mitochondrial membrane, thereby preventing mitochondrial apoptotic activation [17].

Regulatory relationships of Bcl2a1a


Other interactions of Bcl2a1a

  • To test this, we characterized the expression of A1 and the oxygen susceptibility of WT and IL-11 Tg(+) mice with normal and null A1 loci [1].
  • We show that Bfl-1 undergoes constitutive ubiquitin/proteasome-mediated turnover [14].
  • The decreased expression observed with A1, a bcl-2 like gene, may account in part for the suppression of growth in cells from the null mice [20].
  • In addition to GM-CSF, a transient induction of A1 mRNA accumulation was observed in response to LPS in macrophages [18].
  • This induction is not mediated by IL-1 alpha or IL-6, neither of which stimulate A1 [18].

Analytical, diagnostic and therapeutic context of Bcl2a1a


  1. Bcl-2-related protein A1 is an endogenous and cytokine-stimulated mediator of cytoprotection in hyperoxic acute lung injury. He, C.H., Waxman, A.B., Lee, C.G., Link, H., Rabach, M.E., Ma, B., Chen, Q., Zhu, Z., Zhong, M., Nakayama, K., Nakayama, K.I., Homer, R., Elias, J.A. J. Clin. Invest. (2005) [Pubmed]
  2. A novel Bcl-2 related gene, Bfl-1, is overexpressed in stomach cancer and preferentially expressed in bone marrow. Choi, S.S., Park, I.C., Yun, J.W., Sung, Y.C., Hong, S.I., Shin, H.S. Oncogene (1995) [Pubmed]
  3. Distinct roles for the NF-kappaB1 and c-Rel transcription factors in the differentiation and survival of plasmacytoid and conventional dendritic cells activated by TLR-9 signals. O'Keeffe, M., Grumont, R.J., Hochrein, H., Fuchsberger, M., Gugasyan, R., Vremec, D., Shortman, K., Gerondakis, S. Blood (2005) [Pubmed]
  4. Perturbation of B-cell development in mice overexpressing the Bcl-2 homolog A1. Chuang, P.I., Morefield, S., Liu, C.Y., Chen, S., Harlan, J.M., Willerford, D.M. Blood (2002) [Pubmed]
  5. Essential role of the prosurvival bcl-2 homologue A1 in mast cell survival after allergic activation. Xiang, Z., Ahmed, A.A., Möller, C., Nakayama, K., Hatakeyama, S., Nilsson, G. J. Exp. Med. (2001) [Pubmed]
  6. Activated protein C blocks p53-mediated apoptosis in ischemic human brain endothelium and is neuroprotective. Cheng, T., Liu, D., Griffin, J.H., Fernández, J.A., Castellino, F., Rosen, E.D., Fukudome, K., Zlokovic, B.V. Nat. Med. (2003) [Pubmed]
  7. 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]
  8. 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]
  9. Human platelets are defective in processing of cholera toxin. Hughes, R.J., Insel, P.A. Biochem. J. (1983) [Pubmed]
  10. The anti-apoptotic activities of Rel and RelA required during B-cell maturation involve the regulation of Bcl-2 expression. Grossmann, M., O'Reilly, L.A., Gugasyan, R., Strasser, A., Adams, J.M., Gerondakis, S. EMBO J. (2000) [Pubmed]
  11. A1 is a growth-permissive antiapoptotic factor mediating postactivation survival in T cells. Gonzalez, J., Orlofsky, A., Prystowsky, M.B. Blood (2003) [Pubmed]
  12. A1/Bfl-1 expression is restricted to TCR engagement in T lymphocytes. Verschelde, C., Walzer, T., Galia, P., Biémont, M.C., Quemeneur, L., Revillard, J.P., Marvel, J., Bonnefoy-Berard, N. Cell Death Differ. (2003) [Pubmed]
  13. Accelerated neutrophil apoptosis in mice lacking A1-a, a subtype of the bcl-2-related A1 gene. Hamasaki, A., Sendo, F., Nakayama, K., Ishida, N., Negishi, I., Nakayama, K., Hatakeyama, S. J. Exp. Med. (1998) [Pubmed]
  14. Constitutive proteasome-mediated turnover of Bfl-1/A1 and its processing in response to TNF receptor activation in FL5.12 pro-B cells convert it into a prodeath factor. Kucharczak, J.F., Simmons, M.J., Duckett, C.S., Gélinas, C. Cell Death Differ. (2005) [Pubmed]
  15. bfl-1, a bcl-2 homologue, suppresses p53-induced apoptosis and exhibits potent cooperative transforming activity. D'Sa-Eipper, C., Subramanian, T., Chinnadurai, G. Cancer Res. (1996) [Pubmed]
  16. Retinoid x receptor agonists increase bcl2a1 expression and decrease apoptosis of naive T lymphocytes. Rasooly, R., Schuster, G.U., Gregg, J.P., Xiao, J.H., Chandraratna, R.A., Stephensen, C.B. J. Immunol. (2005) [Pubmed]
  17. Bcl-2 family member Bfl-1/A1 sequesters truncated bid to inhibit is collaboration with pro-apoptotic Bak or Bax. Werner, A.B., de Vries, E., Tait, S.W., Bontjer, I., Borst, J. J. Biol. Chem. (2002) [Pubmed]
  18. Characterization of A1, a novel hemopoietic-specific early-response gene with sequence similarity to bcl-2. Lin, E.Y., Orlofsky, A., Berger, M.S., Prystowsky, M.B. J. Immunol. (1993) [Pubmed]
  19. 4-1BB promotes the survival of CD8+ T lymphocytes by increasing expression of Bcl-xL and Bfl-1. Lee, H.W., Park, S.J., Choi, B.K., Kim, H.H., Nam, K.O., Kwon, B.S. J. Immunol. (2002) [Pubmed]
  20. STAT5A-deficient mice demonstrate a defect in granulocyte-macrophage colony-stimulating factor-induced proliferation and gene expression. Feldman, G.M., Rosenthal, L.A., Liu, X., Hayes, M.P., Wynshaw-Boris, A., Leonard, W.J., Hennighausen, L., Finbloom, D.S. Blood (1997) [Pubmed]
  21. A1 demonstrates restricted tissue distribution during embryonic development and functions to protect against cell death. Carrió, R., López-Hoyos, M., Jimeno, J., Benedict, M.A., Merino, R., Benito, A., Fernández-Luna, J.L., Núñez, G., García-Porrero, J.A., Merino, J. Am. J. Pathol. (1996) [Pubmed]
  22. The murine antiapoptotic protein A1 is induced in inflammatory macrophages and constitutively expressed in neutrophils. Orlofsky, A., Somogyi, R.D., Weiss, L.M., Prystowsky, M.B. J. Immunol. (1999) [Pubmed]
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