Davis, Terence  ORCID: https://orcid.org/0000-0003-2780-0262, Tivey, Hannah S.E., Brook, Amy J.C. and Kipling, David
2015.
Nijmegen breakage syndrome fibroblasts expressing the C-terminal truncated NBNp70 protein undergo p38/MK2-dependent premature senescence.
Biogerontology
16
(1)
, pp. 43-51.
10.1007/s10522-014-9530-3
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Abstract
Fibroblasts from the progeroid Nijmegen breakage syndrome that express a truncated version of the nibrin protein (NBNp70) 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 NBNp70 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.
| Item Type: | Article |
|---|---|
| Date Type: | Publication |
| Status: | Published |
| Schools: | Schools > Medicine |
| Subjects: | R Medicine > R Medicine (General) |
| Publisher: | Springer |
| ISSN: | 1389-5729 |
| Date of First Compliant Deposit: | 30 March 2016 |
| Date of Acceptance: | 3 September 2014 |
| Last Modified: | 05 May 2023 07:49 |
| URI: | https://orca.cardiff.ac.uk/id/eprint/78966 |
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