|PROSITE documentation PDOC00829 [for PROSITE entry PS01258]|
Active cell suicide (apoptosis) is induced by events such as growth factor withdrawal and toxins. It is controlled by regulators, which have either an inhibitory effect on programmed cell death (anti-apoptotic) or block the protective effect of inhibitors (pro-apoptotic) [1,2]. Many viruses have found a way of countering defensive apoptosis by encoding their own anti-apoptosis genes preventing their target-cells from dying too soon.
All proteins belonging to the Bcl-2 family  contain either a BH1, BH2, BH3, or BH4 motif. All anti-apoptotic proteins contain BH1 and BH2 motifs; some of them contain an additional N-terminal BH4 motif (Bcl-2, Bcl-x(L), Bcl-w), which is never seen in pro-apoptotic proteins, except for Bcl-x(S). On the other hand, all pro-apoptotic proteins contain a BH3 motif (except for Bad) necessary for dimerization with other proteins of Bcl-2 family and crucial for their killing activity; some of them also contain BH1 and BH2 motifs (Bax, Bak). The BH3 motif is also present in some anti-apoptotic protein, such as Bcl-2 or Bcl-x(L).
Some proteins that are known to contain these motifs are listed below.
We have developed patterns for the four BH motifs. There is also a profile for the BH4 motif as well as one profile for the bcl-2 family that spans part of BH3, BH1 and BH2 motifs.Last update:
March 2006 / Text revised.
PROSITE methods (with tools and information) covered by this documentation:
|Title||A boom time for necrobiology.|
|Source||Curr. Biol. 3:877-878(1993).|
|Source||Genes Dev. 10:2859-2869(1996).|
|3||Authors||Reed J.C. Zha H. Aime-Sempe C. Takayama S. Wang H.-G.|
|Title||Structure-function analysis of Bcl-2 family proteins. Regulators of programmed cell death.|
|Source||Adv. Exp. Med. Biol. 406:99-112(1996).|
|4||Authors||Inohara N. Ding L. Chen S. Nunez G.|
|Title||harakiri, a novel regulator of cell death, encodes a protein that activates apoptosis and interacts selectively with survival-promoting proteins Bcl-2 and Bcl-X(L).|
|Source||EMBO J. 16:1686-1694(1997).|