[HTML][HTML] p53 connects tumorigenesis and reprogramming to pluripotency
N Tapia, HR Schöler - The Journal of experimental medicine, 2010 - ncbi.nlm.nih.gov
N Tapia, HR Schöler
The Journal of experimental medicine, 2010•ncbi.nlm.nih.govThe tumor suppressor gene p53 prevents the initiation of tumor formation by inducing cell
cycle arrest, senescence, DNA repair, and apoptosis. Recently, the absence or mutation of
p53 was described to facilitate nuclear reprogramming. These findings suggest an influence
of p53 on the de-differentiation process, and highlight the similarities between induction of
pluripotency and tumor formation.
cycle arrest, senescence, DNA repair, and apoptosis. Recently, the absence or mutation of
p53 was described to facilitate nuclear reprogramming. These findings suggest an influence
of p53 on the de-differentiation process, and highlight the similarities between induction of
pluripotency and tumor formation.
Abstract
The tumor suppressor gene p53 prevents the initiation of tumor formation by inducing cell cycle arrest, senescence, DNA repair, and apoptosis. Recently, the absence or mutation of p53 was described to facilitate nuclear reprogramming. These findings suggest an influence of p53 on the de-differentiation process, and highlight the similarities between induction of pluripotency and tumor formation.
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