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Loss of Bif-1 Suppresses Bax/Bak Conformational Change and Mitochondrial Apoptosis
Open accessAbstract
Bif-1, a member of the endophilin B protein family, interacts with Bax and promotes interleukin-3 withdrawal-induced Bax conformational change and apoptosis when overexpressed in FL5.12 cells. Here, we provide evidence that Bif-1 plays a regulatory role in apoptotic activation of not only Bax but also Bak and appears to be involved in suppression of tumorigenesis. Inhibition of endogenous Bif-1 expression in HeLa cells by RNA interference abrogated the conformational change of Bax and Bak, cytochrome c release, and caspase 3 activation induced by various intrinsic death signals. Similar results were obtained in Bif-1 knockout mouse embryonic fibroblasts. While Bif-1 did not directly interact with Bak, it heterodimerized with Bax on mitochondria in intact cells, and this interaction was enhanced by apoptosis induction and preceded the Bax conformational change. Moreover, suppression of Bif-1 expression was associated with an enhanced ability of HeLa cells to form colonies in soft agar and tumors in nude mice. Taken together, these findings support the notion that Bif-1 is an important component of the mitochondrial pathway for apoptosis as a novel Bax/Bak activator, and loss of this proapoptotic molecule may contribute to tumorigenesis.
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Luo, X., Budihardjo, I., Zou, H., Slaughter, C., & Wang, X. (1998) · Cell · doi:10.1016/s0092-8674(00)81589-5 · Cited by 3,626
Direct Activation of Bax by p53 Mediates Mitochondrial Membrane Permeabilization and Apoptosis
Chipuk, J. E., Kuwana, T., Bouchier-Hayes, L., Droin, N. M., Newmeyer, D. D., Schuler, M., & Green, D. R. (2004) · Science · doi:10.1126/science.1092734 · Cited by 2,108 · cited 2×
“Several non-Bcl-2-related proteins, including Bif-1 (6), Ku70 (47), 14-3-3 theta (40), Humanin (HN) peptide (15), ASC (42), and p53 (4, 8, 29, 35, 60), have recently been shown to be involved in the regulation of Bax and/or Bak activity.”
The Role of Dynamin-Related Protein 1, a Mediator of Mitochondrial Fission, in Apoptosis
Frank, S., Gaume, B., Bergmann-Leitner, E. S., Leitner, W. W., Robert, E. G., Catez, F., Smith, C. L., & Youle, R. J. (2001) · Developmental Cell · doi:10.1016/s1534-5807(01)00055-7 · Cited by 1,755
Self-citationLetai, A., Bassik, M. C., Walensky, L. D., Sorcinelli, M. D., Weiler, S., & Korsmeyer, S. J. (2002) · Cancer Cell · doi:10.1016/s1535-6108(02)00127-7 · Cited by 1,677
Lindsten, T., Ross, A. J., King, A., Zong, W.-X., Rathmell, J. C., Shiels, H. A., Ulrich, E., Waymire, K. G., Mahar, P., Frauwirth, K., et al. (2000) · Molecular Cell · doi:10.1016/s1097-2765(00)00136-2 · Cited by 1,489
Kuwana, T., Bouchier-Hayes, L., Chipuk, J. E., Bonzon, C., Sullivan, B. A., Green, D. R., & Newmeyer, D. D. (2005) · Molecular Cell · doi:10.1016/j.molcel.2005.02.003 · Cited by 1,185
Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis
Yin, X.-M., Wang, K., Gross, A., Zhao, Y., Zinkel, S., Klocke, B., Roth, K. A., & Korsmeyer, S. J. (1999) · Nature · doi:10.1038/23730 · Cited by 1,004
Karbowski, M., Lee, Y.-J., Gaume, B., Jeong, S.-Y., Frank, S., Nechushtan, A., Santel, A., Fuller, M., Smith, C. L., & Youle, R. J. (2002) · The Journal of Cell Biology · doi:10.1083/jcb.200209124 · Cited by 846
Self-citation
Research works printed but not linked: 57
- 10.1074/jbc.M206069200 · DOI · Paper page
- 10.1038/sj.onc.1207234 · DOI
- 10.1038/sj.cdd.4401006 · DOI
- 10.1038/sj.onc.1207102 · DOI · Paper page
- 10.1074/jbc.M101527200 · DOI · Paper page
- 10.1074/jbc.M109939200 · DOI · Paper page
- 10.1038/ng1093 · DOI · Paper page
- 10.1128/MCB.20.3.929-935.2000 · DOI · Paper page
- 10.1083/jcb.200107075 · DOI · Paper page
- 10.1083/jcb.143.1.207 · DOI · Paper page
- 10.1016/S1535-6108(02)00024-7 · DOI · Paper page
- 10.1083/jcb.144.5.903 · DOI · Paper page
- 10.1038/nature01627 · DOI · Paper page
- 10.1038/sj.onc.1203592 · DOI · Paper page
- 10.1016/S0092-8674(00)81683-9 · DOI · Paper page
- 10.1074/jbc.M203079200 · DOI
- 10.1074/jbc.273.17.10777 · DOI · Paper page
- 10.1016/S1097-2765(02)00496-3 · DOI · Paper page
- 10.1016/S0959-4388(00)00126-4 · DOI
- 10.1038/nature03316 · DOI · Paper page
- 10.1083/jcb.200407046 · DOI · Paper page
- 10.1038/sj.cdd.4400783 · DOI · Paper page
- 10.1016/S0092-8674(02)01036-X · DOI · Paper page
- 10.1038/ncb1123 · DOI · Paper page
- 10.1016/S0092-8674(00)81590-1 · DOI · Paper page
- 10.1038/35036395 · DOI · Paper page
- 10.1128/MCB.22.11.3577-3589.2002 · DOI · Paper page
- 10.1016/S1097-2765(03)00050-9 · DOI · Paper page
- 10.1074/jbc.M203392200 · DOI · Paper page
- 10.1074/jbc.M208568200 · DOI
- 10.1093/emboj/18.9.2330 · DOI · Paper page
- 10.1101/gad.1204904 · DOI · Paper page
- 10.1074/jbc.M207880200 · DOI · Paper page
- 10.1038/ncb0403-281 · DOI
- 10.1038/ncb1087 · DOI · Paper page
- 10.1126/science.1092586 · DOI · Paper page
- 10.1006/geno.2000.6378 · DOI
- 10.1016/S1535-6108(02)00241-6 · DOI · Paper page
- 10.1042/bj20020972 · DOI · Paper page
- 10.1038/ncb950 · DOI · Paper page
- 10.1016/S1534-5807(01)00116-2 · DOI · Paper page
- 10.1126/science.1081208 · DOI · Paper page
- 10.1016/j.bbamcr.2003.10.016 · DOI · Paper page
- 10.1073/pnas.082117599 · DOI · Paper page
- 10.1016/S0092-8674(00)00167-7 · DOI · Paper page
- 10.1074/jbc.M313420200 · DOI · Paper page
- 10.1101/gad.10.22.2859 · DOI · Paper page
- Wang, X. 2001. The expanding role of mitochondria in apoptosis. Genes Dev. 15:2922–2933.
- 10.1101/gad.14.16.2060 · DOI · Paper page
- 10.1126/science.1059108 · DOI · Paper page
- 10.1083/jcb.139.5.1281 · DOI · Paper page
- Yamaguchi, H., K. Bhalla, and H. G. Wang. 2003. Bax plays a pivotal role in thapsigargin-induced apoptosis of human colon cancer HCT116 cells by controlling Smac/Diablo and Omi/HtrA2 release from mitochondria. Cancer Res. 63:1483–1489.
- 10.1074/jbc.M401530200 · DOI
- 10.1074/jbc.M207516200 · DOI
- 10.1074/jbc.M406933200 · DOI · Paper page
- 10.1038/sj.onc.1204984 · DOI · Paper page
- 10.1126/science.290.5493.989 · DOI · Paper page
Cited by
Mitochondrial membrane permeabilization in cell death
Kroemer, G., Galluzzi, L., & Brenner, C. (2007) · Physiological Reviews · doi:10.1152/physrev.00013.2006 · Cited by 3,598
Autophagic cell death: the story of a misnomer
Kroemer, G., & Levine, B. (2008) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2529 · Cited by 1,453
Mitochondrial dynamics and apoptosis
Suen, D.-F., Norris, K. L., & Youle, R. J. (2008) · Genes & Development · doi:10.1101/gad.1658508 · Cited by 1,270
Self-citationApoptosis and Molecular Targeting Therapy in Cancer
Hassan, M., Watari, H., AbuAlmaaty, A., Ohba, Y., & Sakuragi, N. (2014) · BioMed Research International · doi:10.1155/2014/150845 · Cited by 1,121
RetractedMitochondrial Dynamics in Mammalian Health and Disease
Liesa, M., Palacín, M., & Zorzano, A. (2009) · Physiological Reviews · doi:10.1152/physrev.00030.2008 · Cited by 953
Metadata
- Authors
- Takahashi, Y., Karbowski, M., Yamaguchi, H., Kazi, A., Wu, J., Sebti, S. M., Youle, R. J., & Wang, H.-G.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2005-11-01
- Volume
- 25
- Issue
- 21
- Pages
- 9369-9382
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- OpenAlex
- W2162378963
- Cited by
- 190
- References
- 8
- FWCI
- 6.22
- Type
- journal article
- Language
- en
- Open access
- green
- Licence
- journals.asm.org/non-commercial-tdm-license (tdm)
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- Takahashi, Y., Karbowski, M., Yamaguchi, H., Kazi, A., Wu, J., Sebti, S. M., Youle, R. J., & Wang, H.-G. (2005). Loss of Bif-1 Suppresses Bax/Bak Conformational Change and Mitochondrial Apoptosis. Molecular and Cellular Biology. https://doi.org/10.1128/mcb.25.21.9369-9382.2005
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.