PMID- 18097445 OWN - NLM STAT- MEDLINE DCOM- 20080110 LR - 20240109 IS - 1471-0080 (Electronic) IS - 1471-0072 (Linking) VI - 9 IP - 1 DP - 2008 Jan TI - The BCL-2 protein family: opposing activities that mediate cell death. PG - 47-59 AB - BCL-2 family proteins, which have either pro- or anti-apoptotic activities, have been studied intensively for the past decade owing to their importance in the regulation of apoptosis, tumorigenesis and cellular responses to anti-cancer therapy. They control the point of no return for clonogenic cell survival and thereby affect tumorigenesis and host-pathogen interactions and regulate animal development. Recent structural, phylogenetic and biological analyses, however, suggest the need for some reconsideration of the accepted organizational principles of the family and how the family members interact with one another during programmed cell death. Although these insights into interactions among BCL-2 family proteins reveal how these proteins are regulated, a unifying hypothesis for the mechanisms they use to activate caspases remains elusive. FAU - Youle, Richard J AU - Youle RJ AD - Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, The National Institutes of Health, Bethesda, Maryland 20892, USA. youler@ninds.nih.gov FAU - Strasser, Andreas AU - Strasser A LA - eng PT - Journal Article PT - Review PL - England TA - Nat Rev Mol Cell Biol JT - Nature reviews. Molecular cell biology JID - 100962782 RN - 0 (Proto-Oncogene Proteins c-bcl-2) SB - IM MH - Animals MH - Apoptosis/*physiology MH - Humans MH - Mitochondria/physiology MH - Models, Molecular MH - Phylogeny MH - Protein Structure, Tertiary/physiology MH - Proto-Oncogene Proteins c-bcl-2/*physiology RF - 166 EDAT- 2007/12/22 09:00 MHDA- 2008/01/11 09:00 CRDT- 2007/12/22 09:00 PHST- 2007/12/22 09:00 [pubmed] PHST- 2008/01/11 09:00 [medline] PHST- 2007/12/22 09:00 [entrez] AID - nrm2308 [pii] AID - 10.1038/nrm2308 [doi] PST - ppublish SO - Nat Rev Mol Cell Biol. 2008 Jan;9(1):47-59. doi: 10.1038/nrm2308.