AI Article Synopsis
- The Bcl-2 family regulates apoptosis, which can occur through direct binding of BH3-only proteins (Bim, Bid, Puma) to death mediators Bax and Bak, or through indirect interaction with pro-survival Bcl-2-like proteins.
- Research findings suggest that Bax and Bak can still trigger apoptosis even without significant interaction with BH3-only activators, especially in the absence of Bim or Bid and with low levels of Puma.
- The primary mechanism of BH3-only proteins appears to be their involvement in overcoming pro-survival signals that protect Bax and Bak, rather than directly activating them.
Article Abstract
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.
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| http://dx.doi.org/10.1126/science.1133289 | DOI Listing |
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