Heterodimerization with Bax is required for Bcl-2 to repress cell death.
Yin
X M
XM
Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110.
Oltvai
Z N
ZN
Korsmeyer
S J
SJ
D000595:Amino Acid Sequence; D000818:Animals; D017209:Apoptosis; D016384:Consensus Sequence; D006801:Humans; D008322:Mammals / Q000378:metabolism; D051379:Mice; D008969:Molecular Sequence Data; D016297:Mutagenesis, Site-Directed; D009363:Neoplasm Proteins / Q000737:chemistry / Q000502:physiology; D011487:Protein Conformation; D055503:Protein Multimerization; D017434:Protein Structure, Tertiary; D011518:Proto-Oncogene Proteins / Q000737:chemistry / Q000502:physiology*; D019253:Proto-Oncogene Proteins c-bcl-2; D011993:Recombinant Fusion Proteins / Q000378:metabolism; D016415:Sequence Alignment; D017386:Sequence Homology, Amino Acid; D013329:Structure-Activity Relationship; D051028:bcl-2-Associated X Protein
C494826:BAX protein, human; C494827:Bax protein, mouse; D009363:Neoplasm Proteins; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D011993:Recombinant Fusion Proteins; D051028:bcl-2-Associated X Protein