Aging clock: the watchmaker's masterpiece.
The phenomenon of cellular senescence has been known for almost four decades. Yet, until very recently, the molecular mechanisms that lead to senescence have been poorly understood. However, substantial progress has been made in the last few years toward identifying the pathways executing senescence. This r view focuses on two major advances in this field, the telomere aging clock theory and the cell cycle regulatory mechanisms in senescent cells. These recent studies indicate that cellular senescence is a highly elaborate and active process, which presumably works as an anti-oncogenic mechanism.
Ishikawa
F
F
Tokyo Institute of Technology, Department of Life Science, Yokohama, Japan. fishikaw@bio.titech.ac.jp
D000375:Aging / Q000235:genetics / Q000502:physiology*; D000818:Animals; D001683:Biological Clocks / Q000235:genetics / Q000502:physiology*; D002352:Carrier Proteins / Q000235:genetics / Q000502:physiology; D016922:Cellular Senescence / Q000235:genetics / Q000502:physiology; D019941:Cyclin-Dependent Kinase Inhibitor p16; D016193:G1 Phase / Q000235:genetics / Q000502:physiology; D006801:Humans; D010641:Phenotype; D011506:Proteins / Q000235:genetics / Q000502:physiology; D016160:Retinoblastoma Protein / Q000235:genetics / Q000502:physiology; D019098:Telomerase / Q000235:genetics / Q000502:physiology; D016615:Telomere / Q000235:genetics / Q000502:physiology; D025803:Tumor Suppressor Protein p14ARF; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000502:physiology
D002352:Carrier Proteins; D019941:Cyclin-Dependent Kinase Inhibitor p16; D011506:Proteins; D016160:Retinoblastoma Protein; D025803:Tumor Suppressor Protein p14ARF; D016159:Tumor Suppressor Protein p53; D019098:Telomerase