p16INK4a in cellular senescence

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p16INK4a in cellular senescence

senescence is the activation of the INK4/ARF locus, which is epigenetically regulated and under tight control of the Polycomb group (PcG) Trithorax group (TrxG) proteins [1]. In proliferating cells, the locus is silenced by Polycomb repressive complexes (PRCs), and the chromatin is enriched in H3K27me3 [2]. Upon senescence triggers, PRCs are displaced and the repressive H3K27me3 mark is removed...

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P16INK4a is required for hSNF5 chromatin remodeler-induced cellular senescence in malignant rhabdoid tumor cells.

The hSNF5 chromatin-remodeling factor is a tumor suppressor that is inactivated in malignant rhabdoid tumors (MRTs). A number of studies have shown that hSNF5 re-expression blocks MRT cell proliferation. However, the pathway through which hSNF5 acts remains unknown. To address this question, we generated MRT-derived cell lines in which restoration of hSNF5 expression leads to an accumulation in...

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Hypertension induces somatic cellular senescence in rats and humans by induction of cell cycle inhibitor p16INK4a.

There is increasing evidence for a role of somatic cellular senescence in physiological aging but also in injury and disease. Cell cycle inhibitor p16(INK4a) is the key mediator for stress and aberrant signaling induced senescence. Here we report that elevated blood pressure markedly induced p16(INK4a) expression in rat kidneys and hearts, as well as in human kidneys. In kidneys from deoxycorti...

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Loss of p16Ink4a Function Rescues Cellular Senescence Induced by Telomere Dysfunction

p16(Ink4a) is a tumor suppressor and a marker for cellular senescence. Previous studies have shown that p16(Ink4a) plays an important role in the response to DNA damage signals caused by telomere dysfunction. In this study, we crossed Wrn(-/-) and p16(Ink4a-/-) mice to knock out the p16(Ink4a) function in a Wrn null background. Growth curves showed that loss of p16(Ink4a) could rescue the growt...

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ژورنال

عنوان ژورنال: Aging

سال: 2013

ISSN: 1945-4589

DOI: 10.18632/aging.100592