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- W2158713934 abstract "The polycomb protein Bmi-1 represses the INK4a locus, which encodes the tumor suppressors p16 and p14(ARF). Here we report that Bmi-1 is downregulated when WI-38 human fibroblasts undergo replicative senescence, but not quiescence, and extends replicative life span when overexpressed. Life span extension by Bmi-1 required the pRb, but not p53, tumor suppressor protein. Deletion analysis showed that the RING finger and helix-turn-helix domains of Bmi-1 were required for life span extension and suppression of p16. Furthermore, a RING finger deletion mutant exhibited dominant negative activity, inducing p16 and premature senescence. Interestingly, presenescent cultures of some, but not all, human fibroblasts contained growth-arrested cells expressing high levels of p16 and apparently arrested by a p53- and telomere-independent mechanism. Bmi-1 selectively extended the life span of these cultures. Low O(2) concentrations had no effect on p16 levels or life span extension by Bmi-1 but reduced expression of the p53 target, p21. We propose that some human fibroblast strains are more sensitive to stress-induced senescence and have both p16-dependent and p53/telomere-dependent pathways of senescence. Our data suggest that Bmi-1 extends the replicative life span of human fibroblasts by suppressing the p16-dependent senescence pathway." @default.
- W2158713934 created "2016-06-24" @default.
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- W2158713934 date "2003-01-01" @default.
- W2158713934 modified "2023-09-30" @default.
- W2158713934 title "Control of the Replicative Life Span of Human Fibroblasts by p16 and the Polycomb Protein Bmi-1" @default.
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- W2158713934 doi "https://doi.org/10.1128/mcb.23.1.389-401.2003" @default.
- W2158713934 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/140680" @default.
- W2158713934 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12482990" @default.
- W2158713934 hasPublicationYear "2003" @default.
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