| First Author | Willis SN | Year | 2007 |
| Journal | Science | Volume | 315 |
| Issue | 5813 | Pages | 856-9 |
| PubMed ID | 17289999 | Mgi Jnum | J:182384 |
| Mgi Id | MGI:5315340 | Doi | 10.1126/science.1133289 |
| Citation | Willis SN, et al. (2007) Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak. Science 315(5813):856-9 |
| abstractText | A central issue in the regulation of apoptosis by the Bcl-2 family is whether its BH3-only members initiate apoptosis by directly binding to the essential cell-death mediators Bax and Bak, or whether they can act indirectly, by engaging their pro-survival Bcl-2-like relatives. Contrary to the direct-activation model, we show that Bax and Bak can mediate apoptosis without discernable association with the putative BH3-only activators (Bim, Bid, and Puma), even in cells with no Bim or Bid and reduced Puma. Our results indicate that BH3-only proteins induce apoptosis at least primarily by engaging the multiple pro-survival relatives guarding Bax and Bak. |
