P53-Mediated regulation of hepatic lipid metabolism: Forging links between metabolism, atherogenesis, and cancer

摘要

No discussion of cancer biology is complete without mention of tumor suppressor p53 and its stress-activated protection of the genome. A plethora of regulatory signaling impinges on p53 to either limit p53 protein levels, in the absence of stress signaling, or to rapidly induce protein levels and mediate cell cycle arrest or cell death in the face of threats to genome integrity [1,2]. Although reports of p53 regulation and functions in cellular surveillance add up to an astounding number, recent discoveries that illustrate functions of p53 in cellular metabolism reveal that much is left to learn [3,4]. The ability of the p53-null mouse to survive to adulthood with few apparent challenges to normal development casts a shadow over likely roles for p53 in normal, cellular homeostasis [5].