The DNA damage signaling pathway is a critical mediator of oncogene-induced senescence

Article Abstract:

The RNA interference against ATM inhibited accumulation in cells, which expresses oncogenic STAT5 and cooperated with Rb inactivation to suppress STAT5A-induced senescence, is reported. It is observed that bypassing oncogene-induced senescence by inactivation of p53 and Rb did not eliminate the accumulation of oncogene-induced DNA damage loci, thereby suggesting a mechanism that may limit transformation in immortalized cells.

Aging, Aging (Biology), RNA interference

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Poly(ADP-ribosyl)ation by PARP-1: 'Par-laying' NAD+ into a nuclear signal

Article Abstract:

Recent work on the biochemistry, biology, physiology and pathophysiology of poly(ADP-ribosyl)ation (PARylation) focusing the activity of poly(ADP-ribose) polymerase 1(PARP-1), the most abundantly expressed member of a family of PARP proteins is highlighted. Also, connections between nuclear nicotinamide adenine denucleotide (NAD(super +)) metabolism and nuclear signaling through PARP-1 is discussed.

New York, RNA polymerases, Structure

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RNPC1, an RNA-binding protein and a target of the p53 family, is required for maintaining the stability of the basal and stress induced p21 transcript

Article Abstract:

A study presents evidence that the RNPC1 gene is induced by the p53 family and by DNA damage in a p53-dependent manner. It is also shown that RNPC1 is required for the maintenance of the stability of p21 transcript induced by p53 and it is concluded that RNPC1 is a target of the p53 family and serves as a mediator of the p53 family to regulate p21 post-transcriptionally.

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