Coordinated regulation of life and death by RB.
Recent studies have shown that RB can inhibit apoptosis, independently of its ability to block cell proliferation. This poses the question of how cells choose to grow or to die when RB becomes inactivated. RB is phosphorylated following mitogenic stimulation, but it is degraded in response to death stimuli. Most sporadic cancers also inactivate RB by phosphorylation, rather than losing RB entirely--possibly to exploit the survival advantage conferred by RB under stress. Drawing from the different mechanisms of RB inactivation, we propose two models for ways in which cells use RB to make the choice of life versus death.
Chau
B Nelson
BN
Division of Biological Sciences and the Cancer Center, University of California, San Diego, La Jolla, California 92093-0322, USA.
Wang
Jean Y J
JY
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002453:Cell Cycle; D002470:Cell Survival; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D009369:Neoplasms / Q000401:mortality / Q000503:physiopathology; D016160:Retinoblastoma Protein / Q000172:deficiency / Q000235:genetics / Q000502:physiology*
D016160:Retinoblastoma Protein