Abstract
The word senescence is derived from Latin word senex, meaning old age. It is a property of all living organisms and defined as a process that leads to functional decline, and hence an increase in vulnerability to a spectrum of diseases eventually leading to death. Evolutionarily, it is understood as a condition that allows continued survival of a population without exhaustive competition for resources. Senescence is widely accepted as an indispensable outcome of life and highly influenced by intrinsic and extrinsic environmental factors that orchestrate a complex network of signaling. The senescent cells show activation of major tumor suppressor proteins (p53 and pRB) and their regulators (p14ARF and p16INK4A). They are resistance to apoptosis, a process of programmed cell death. The present review is focused on the understanding of senescence as a tumor suppressor mechanism. We discuss the regulation of p53 signaling by ARF (alternate reading frame) and CARF (collaborator of ARF) to execute either senescence or apoptosis.
Keywords
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Wadhwa, R., Singh, R., Kaul, Z., Kaul, S.C. (2013). CARF Regulates Cellular Senescence and Apoptosis through p53-Dependent and -Independent Pathways. In: Lee, N., Cheng, C., Luk, J. (eds) New Advances on Disease Biomarkers and Molecular Targets in Biomedicine. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-62703-456-2_8
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