title: p16 and ARF: activation of teenage proteins in old age.
abstract: Cellular senescence induced by different stresses and telomere shortening appears to play an important role in the aging process. The products of the INK4a/ARF locus--p16INK4a and ARF--arrest cell proliferation at the senescence stage by exerting their effects on retinoblastoma protein- and p53-mediated responsive pathways. A study in this issue of the JCI provides experimental evidence of a specific upregulation of these cell cycle inhibitors in a variety of organs during mammalian aging.
authors.affiliation: Department of Gastroenterology, Hepatology, and Endocrinology, Hannover Medical School, Hannover, Germany.
authors.forename: Ande
authors.initials: A
authors.lastname: Satyanarayana
authors.forename: K Lenhard
authors.initials: KL
authors.lastname: Rudolph
mesh_terms: D020823:ADP-Ribosylation Factor 1 / Q000502:physiology*; D000375:Aging; D000818:Animals; D015415:Biomarkers; D016922:Cellular Senescence; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000502:physiology*; D005786:Gene Expression Regulation; D006801:Humans; D008954:Models, Biological; D016160:Retinoblastoma Protein / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; D019941:Cyclin-Dependent Kinase Inhibitor p16; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53; D020823:ADP-Ribosylation Factor 1