Apoptosis, proliferation, differentiation: in search of the order.
In search of the order, we are tempted to universally link cell death, proliferation, differentiation, and senescence. Current models (classical, conflicting signal and quantitative signal models) are restricted, precisely because they attempt to hardware a plethora of end-points of cellular responses. By defining each cellular process in molecular term, one can disconnect proliferation (CDK activation), apoptosis (caspase activation), and differentiation (tissue function genes expression), even though these responses are linked by upstream signal transduction pathways. These ambivalent pathways (e.g. mitogen-activated pathways) simultaneously transduce opposite signals (for growth arrest and cycling, for cell death and survival), which are ultimately translated in all possible combinations of cellular responses. When depicted in multidimensional axis, this universal model may also include invasiveness, senescence, metastatic and angiogenic responses and even such integral characteristics as malignant transformation.
Blagosklonny
Mikhail V
MV
Department of Medicine, Brander Cancer Research Institute, New York Medical College, 19 Bradhurst Avenue, Hawthorne, NY 10532, USA. m_blagosklonny@nymc.edu
D000375:Aging / Q000502:physiology*; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002453:Cell Cycle / Q000502:physiology*; D002454:Cell Differentiation / Q000502:physiology*; D002455:Cell Division / Q000502:physiology; D006801:Humans; D008954:Models, Biological; D015398:Signal Transduction / Q000502:physiology*