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Loss of Bif-1 Suppresses Bax/Bak Conformational Change and Mitochondrial Apoptosis

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Takahashi, Yoshinori, Karbowski, Mariusz, Yamaguchi, Hirohito, Kazi, Aslamuzzaman, Wu, Jie, Sebti, Saïd M., Youle, Richard J., Wang, Hong-Gang·2005·Molecular and Cellular Biology

Abstract

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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Show all 8 references

Research works printed but not linked: 57

  1. 10.1074/jbc.M206069200 · DOI · Paper page
  2. 10.1038/sj.onc.1207234 · DOI
  3. 10.1038/sj.cdd.4401006 · DOI
  4. 10.1038/sj.onc.1207102 · DOI · Paper page
  5. 10.1074/jbc.M101527200 · DOI · Paper page
  6. 10.1074/jbc.M109939200 · DOI · Paper page
  7. 10.1038/ng1093 · DOI · Paper page
  8. 10.1128/MCB.20.3.929-935.2000 · DOI · Paper page
  9. 10.1083/jcb.200107075 · DOI · Paper page
  10. 10.1083/jcb.143.1.207 · DOI · Paper page
  11. 10.1016/S1535-6108(02)00024-7 · DOI · Paper page
  12. 10.1083/jcb.144.5.903 · DOI · Paper page
  13. 10.1038/nature01627 · DOI · Paper page
  14. 10.1038/sj.onc.1203592 · DOI · Paper page
  15. 10.1016/S0092-8674(00)81683-9 · DOI · Paper page
  16. 10.1074/jbc.M203079200 · DOI
  17. 10.1074/jbc.273.17.10777 · DOI · Paper page
  18. 10.1016/S1097-2765(02)00496-3 · DOI · Paper page
  19. 10.1016/S0959-4388(00)00126-4 · DOI
  20. 10.1038/nature03316 · DOI · Paper page
  21. 10.1083/jcb.200407046 · DOI · Paper page
  22. 10.1038/sj.cdd.4400783 · DOI · Paper page
  23. 10.1016/S0092-8674(02)01036-X · DOI · Paper page
  24. 10.1038/ncb1123 · DOI · Paper page
  25. 10.1016/S0092-8674(00)81590-1 · DOI · Paper page
  26. 10.1038/35036395 · DOI · Paper page
  27. 10.1128/MCB.22.11.3577-3589.2002 · DOI · Paper page
  28. 10.1016/S1097-2765(03)00050-9 · DOI · Paper page
  29. 10.1074/jbc.M203392200 · DOI · Paper page
  30. 10.1074/jbc.M208568200 · DOI
  31. 10.1093/emboj/18.9.2330 · DOI · Paper page
  32. 10.1101/gad.1204904 · DOI · Paper page
  33. 10.1074/jbc.M207880200 · DOI · Paper page
  34. 10.1038/ncb0403-281 · DOI
  35. 10.1038/ncb1087 · DOI · Paper page
  36. 10.1126/science.1092586 · DOI · Paper page
  37. 10.1006/geno.2000.6378 · DOI
  38. 10.1016/S1535-6108(02)00241-6 · DOI · Paper page
  39. 10.1042/bj20020972 · DOI · Paper page
  40. 10.1038/ncb950 · DOI · Paper page
  41. 10.1016/S1534-5807(01)00116-2 · DOI · Paper page
  42. 10.1126/science.1081208 · DOI · Paper page
  43. 10.1016/j.bbamcr.2003.10.016 · DOI · Paper page
  44. 10.1073/pnas.082117599 · DOI · Paper page
  45. 10.1016/S0092-8674(00)00167-7 · DOI · Paper page
  46. 10.1074/jbc.M313420200 · DOI · Paper page
  47. 10.1101/gad.10.22.2859 · DOI · Paper page
  48. Wang, X. 2001. The expanding role of mitochondria in apoptosis. Genes Dev. 15:2922–2933.
  49. 10.1101/gad.14.16.2060 · DOI · Paper page
  50. 10.1126/science.1059108 · DOI · Paper page
  51. 10.1083/jcb.139.5.1281 · DOI · Paper page
  52. 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.
  53. 10.1074/jbc.M401530200 · DOI
  54. 10.1074/jbc.M207516200 · DOI
  55. 10.1074/jbc.M406933200 · DOI · Paper page
  56. 10.1038/sj.onc.1204984 · DOI · Paper page
  57. 10.1126/science.290.5493.989 · DOI · Paper page

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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
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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CoChat. (2026). Citation check: Loss of Bif-1 Suppresses Bax/Bak Conformational Change and Mitochondrial Apoptosis. https://app.cochat.ai/papers/10.1128/mcb.25.21.9369-9382.2005
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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.