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- W2071776706 abstract "Fibroblasts from the progeroid Nijmegen breakage syndrome that express a truncated version of the nibrin protein (NBN(p70)) undergo premature senescence and have an enlarged morphology with high levels of senescence-associated β-galactosidase, although they do not have F-actin stress fibres. Growth of these fibroblasts in the continuous presence of p38 inhibitors resulted in a large increase in replicative capacity and changed the cellular morphology so that the cells resembled young normal fibroblasts. A similar effect was seen using an inhibitor of the p38 downstream effector kinase MK2. These data suggest that NBN(p70) expressing cells undergo a degree of stress-induced replicative senescence via p38/MK2 activation, potentially due to increased telomere dysfunction, that may play a role in the progeroid features seen in this syndrome." @default.
- W2071776706 created "2016-06-24" @default.
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- W2071776706 date "2014-09-12" @default.
- W2071776706 modified "2023-10-16" @default.
- W2071776706 title "Nijmegen breakage syndrome fibroblasts expressing the C-terminal truncated NBNp70 protein undergo p38/MK2-dependent premature senescence" @default.
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- W2071776706 doi "https://doi.org/10.1007/s10522-014-9530-3" @default.
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