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Gene Review

BAK1  -  BCL2-antagonist/killer 1

Homo sapiens

Synonyms: Apoptosis regulator BAK, BAK, BAK-LIKE, BCL2L7, Bcl-2 homologous antagonist/killer, ...
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Disease relevance of BAK1


High impact information on BAK1

  • Furthermore, we modeled a complex of BCL-XL and BID by aligning the BID and BAK BH3 motifs in the known BCL-XL-BAK BH3 complex [5].
  • Thus, activation of a "multidomain" proapoptotic member, BAX or BAK, appears to be an essential gateway to mitochondrial dysfunction required for cell death in response to diverse stimuli [6].
  • BH3-only proteins in control: specificity regulates MCL-1 and BAK-mediated apoptosis [7].
  • Thus, MCL-1 may function by maintaining BAK in an inactive state, and the loss of MCL-1 upon activation of the DNA damage response, perhaps through replication stress induced in virus infected cells, may be required to initiate the apoptotic response [3].
  • BAK/BAX-mediated mitochondrial outer-membrane permeabilization (MOMP) drives cell death during development and tissue homeostasis from zebrafish to humans [8].

Chemical compound and disease context of BAK1


Biological context of BAK1


Anatomical context of BAK1


Associations of BAK1 with chemical compounds

  • Coexpression of BAD and NOXA killed wild-type but not Bax, Bak doubly deficient cells or Puma deficient cells with Bim knockdown, indicating that activator BH3-only molecules function downstream of inactivator BH3-only molecules to activate BAX-BAK [12].
  • However, in contrast to 5-FU, mithramycin A failed to activate p53 target genes including the cell cycle inhibitor p21Cip1 gene as well as the proapoptotic genes PUMA (p53-upregulated mediator of apotosis) and BAK (bcl2-homologous antagonist/killer) and blocked the induction of the above genes by 5-FU [18].
  • Despite the high spinning speeds employed during HRMAS (1)H NMR spectroscopy of one-half of the tumor samples, RT-PCR analysis of the pro-apoptotic transcripts Bcl-2, BAK-1, caspase-9 and FAS was possible, producing similar results to those detected in the unspun half of the tumors [19].
  • RESULTS: PS-341 decreased BCL-2, without effect on BAX or BAK [20].
  • Apoptosis inhibitors, i.e., IGFR type I and II were over-expressed, and apoptosis inducer, i.e., caspase 3 and BAK were underexpressed in highly cisplatin-resistant cell line, KFrP200 as compared to KFr [21].

Physical interactions of BAK1

  • BCL-2 selectively interacts with the BID-induced open conformer of BAK, inhibiting BAK auto-oligomerization [22].

Regulatory relationships of BAK1

  • This model suggests that the primary mechanism for BCL-2 blockade targets activated BAK rather than sequestering tBID [22].
  • Reversibly, overexpression of NOXA or PUMA induces apoptosis as evidenced by the activation of BAK and caspase-7 [23].

Other interactions of BAK1

  • Our results indicate that 4ICD is functionally similar to BH3-only proteins, proapoptotic members of the BCL-2 family required for initiation of mitochondrial dysfunction through activation of the proapoptotic multi-BH domain proteins BAX/BAK [24].
  • However, BCL-Xs and BAK were weakly expressed in K562, as were Bcl-X, BAD and BAK in the VAL line [25].
  • BAK overexpression mediates p53-independent apoptosis inducing effects on human gastric cancer cells [2].
  • Activated BRI1 or BAK1 then regulate, possibly indirectly, the activities of BIN2 kinase and/or BSU1 phosphatase, which directly regulate the phosphorylation status and nuclear accumulation of two homologous transcription factors, BZR1 and BES1 [13].
  • We first show that PrP is very specific for Bax and cannot prevent Bak (Bcl-2 antagonist killer 1)-, tBid-, staurosporine- or thapsigargin-mediated cell death [26].

Analytical, diagnostic and therapeutic context of BAK1


  1. Mechanisms of apoptosis regulation by viral oncogenes in infection and tumorigenesis. White, E. Cell Death Differ. (2006) [Pubmed]
  2. BAK overexpression mediates p53-independent apoptosis inducing effects on human gastric cancer cells. Tong, Q.S., Zheng, L.D., Wang, L., Liu, J., Qian, W. BMC Cancer (2004) [Pubmed]
  3. DNA damage response and MCL-1 destruction initiate apoptosis in adenovirus-infected cells. Cuconati, A., Mukherjee, C., Perez, D., White, E. Genes Dev. (2003) [Pubmed]
  4. Physical map of human 6p21.2-6p21.3: region flanking the centromeric end of the major histocompatibility complex. Tripodis, N., Mason, R., Humphray, S.J., Davies, A.F., Herberg, J.A., Trowsdale, J., Nizetic, D., Senger, G., Ragoussis, J. Genome Res. (1998) [Pubmed]
  5. Solution structure of BID, an intracellular amplifier of apoptotic signaling. Chou, J.J., Li, H., Salvesen, G.S., Yuan, J., Wagner, G. Cell (1999) [Pubmed]
  6. Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death. Wei, M.C., Zong, W.X., Cheng, E.H., Lindsten, T., Panoutsakopoulou, V., Ross, A.J., Roth, K.A., MacGregor, G.R., Thompson, C.B., Korsmeyer, S.J. Science (2001) [Pubmed]
  7. BH3-only proteins in control: specificity regulates MCL-1 and BAK-mediated apoptosis. Gélinas, C., White, E. Genes Dev. (2005) [Pubmed]
  8. The X-Ray Structure of a BAK Homodimer Reveals an Inhibitory Zinc Binding Site. Moldoveanu, T., Liu, Q., Tocilj, A., Watson, M., Shore, G., Gehring, K. Mol. Cell (2006) [Pubmed]
  9. Bi-directional regulation between tyrosine kinase Etk/BMX and tumor suppressor p53 in response to DNA damage. Jiang, T., Guo, Z., Dai, B., Kang, M., Ann, D.K., Kung, H.J., Qiu, Y. J. Biol. Chem. (2004) [Pubmed]
  10. Activation of natural killer cells by Bacillus Calmette-Guérin. Brandau, S., Böhle, A. Eur. Urol. (2001) [Pubmed]
  11. Apoptosis inhibition mediated by medroxyprogesterone acetate treatment of breast cancer cell lines. Ory, K., Lebeau, J., Levalois, C., Bishay, K., Fouchet, P., Allemand, I., Therwath, A., Chevillard, S. Breast Cancer Res. Treat. (2001) [Pubmed]
  12. Hierarchical regulation of mitochondrion-dependent apoptosis by BCL-2 subfamilies. Kim, H., Rafiuddin-Shah, M., Tu, H.C., Jeffers, J.R., Zambetti, G.P., Hsieh, J.J., Cheng, E.H. Nat. Cell Biol. (2006) [Pubmed]
  13. The brassinosteroid signal transduction pathway. Wang, Z.Y., Wang, Q., Chong, K., Wang, F., Wang, L., Bai, M., Jia, C. Cell Res. (2006) [Pubmed]
  14. VDAC2 inhibits BAK activation and mitochondrial apoptosis. Cheng, E.H., Sheiko, T.V., Fisher, J.K., Craigen, W.J., Korsmeyer, S.J. Science (2003) [Pubmed]
  15. Vaccination with dendritic cells transfected with BAK and BAX siRNA enhances antigen-specific immune responses by prolonging dendritic cell life. Peng, S., Kim, T.W., Lee, J.H., Yang, M., He, L., Hung, C.F., Wu, T.C. Hum. Gene Ther. (2005) [Pubmed]
  16. Regulation of endoplasmic reticulum Ca2+ dynamics by proapoptotic BCL-2 family members. Oakes, S.A., Opferman, J.T., Pozzan, T., Korsmeyer, S.J., Scorrano, L. Biochem. Pharmacol. (2003) [Pubmed]
  17. Over-expression of p53/BAK in aseptic loosening after total hip replacement. Landgraeber, S., Toetsch, M., Wedemeyer, C., Saxler, G., Tsokos, M., von Knoch, F., Neuhäuser, M., Löer, F., von Knoch, M. Biomaterials (2006) [Pubmed]
  18. Inhibition of p53-mediated transcriptional responses by mithramycin A. Koutsodontis, G., Kardassis, D. Oncogene (2004) [Pubmed]
  19. High-resolution magic angle spinning 1H NMR spectroscopy and reverse transcription-PCR analysis of apoptosis in a rat glioma. Griffin, J.L., Blenkiron, C., Valonen, P.K., Caldas, C., Kauppinen, R.A. Anal. Chem. (2006) [Pubmed]
  20. Chemosensitization of pancreatic cancer by inhibition of the 26S proteasome. Bold, R.J., Virudachalam, S., McConkey, D.J. J. Surg. Res. (2001) [Pubmed]
  21. Analysis of gene expression profiles associated with cisplatin resistance in human ovarian cancer cell lines and tissues using cDNA microarray. Sakamoto, M., Kondo, A., Kawasaki, K., Goto, T., Sakamoto, H., Miyake, K., Koyamatsu, Y., Akiya, T., Iwabuchi, H., Muroya, T., Ochiai, K., Tanaka, T., Kikuchi, Y., Tenjin, Y. Hum. Cell (2001) [Pubmed]
  22. BCL-2 selectively interacts with the BID-induced open conformer of BAK, inhibiting BAK auto-oligomerization. Ruffolo, S.C., Shore, G.C. J. Biol. Chem. (2003) [Pubmed]
  23. Endoplasmic reticulum stress-induced apoptosis: multiple pathways and activation of p53-up-regulated modulator of apoptosis (PUMA) and NOXA by p53. Li, J., Lee, B., Lee, A.S. J. Biol. Chem. (2006) [Pubmed]
  24. The ERBB4/HER4 intracellular domain 4ICD is a BH3-only protein promoting apoptosis of breast cancer cells. Naresh, A., Long, W., Vidal, G.A., Wimley, W.C., Marrero, L., Sartor, C.I., Tovey, S., Cooke, T.G., Bartlett, J.M., Jones, F.E. Cancer Res. (2006) [Pubmed]
  25. Expression of apoptosis-controlling proteins in acute leukemia cells. Campos, L., Sabido, O., Viallet, A., Vasselon, C., Guyotat, D. Leuk. Lymphoma (1999) [Pubmed]
  26. Cellular prion protein inhibits proapoptotic Bax conformational change in human neurons and in breast carcinoma MCF-7 cells. Roucou, X., Giannopoulos, P.N., Zhang, Y., Jodoin, J., Goodyer, C.G., LeBlanc, A. Cell Death Differ. (2005) [Pubmed]
  27. Immunogenetics of primary Sjögren's syndrome in Colombians. Anaya, J.M., Mantilla, R.D., Correa, P.A. Semin. Arthritis Rheum. (2005) [Pubmed]
  28. Role of endoplasmic reticulum depletion and multidomain proapoptotic BAX and BAK proteins in shaping cell death after hypericin-mediated photodynamic therapy. Buytaert, E., Callewaert, G., Hendrickx, N., Scorrano, L., Hartmann, D., Missiaen, L., Vandenheede, J.R., Heirman, I., Grooten, J., Agostinis, P. FASEB J. (2006) [Pubmed]
  29. EGR2 induces apoptosis in various cancer cell lines by direct transactivation of BNIP3L and BAK. Unoki, M., Nakamura, Y. Oncogene (2003) [Pubmed]
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