Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/60027
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Type: Journal article
Title: A potential role for NEDD1 and the centrosome in senescence of mouse embryonic fibroblasts
Author: Manning, J.
Kumar, S.
Citation: Cell Death & Disease, 2010; 1(4):E35-1-E35-8
Publisher: Nature Publishing Group
Issue Date: 2010
ISSN: 2041-4889
2041-4889
Statement of
Responsibility: 
J.A. Manning and S. Kumar
Abstract: Mouse embryonic fibroblasts (MEFs) are commonly grown in cell culture and are known to enter senescence after a low number of passages as a result of oxidative stress. Oxidative stress has also been suggested to promote centrosome disruption; however, the contribution of this organelle to senescence is poorly understood. Therefore, this study aimed to assess the role of the centrosome in oxidative stress induced-senescence using MEFs as a model. We demonstrate here that coincident with the entry of late-passage MEFs into senescence, there was an increase in supernumerary centrosomes, most likely due to centrosome fragmentation. In addition, disrupting the centrosome in early-passage MEFs by depletion of neural precursor cell expressed developmentally downregulated gene 1 (NEDD1) also resulted in centrosomal fragmentation and subsequent premature entry into senescence. These data show that a loss of centrosomal integrity may contribute to the entry of MEFs into senescence in culture, and that centrosomal disruption can cause senescence.
Keywords: oxidative stress; senescence; mouse embryonic fibroblasts; NEDD1
Rights: This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits distribution and reproduction in any medium, provided the original author and source are credited. This license does not permit commercial exploitation without specific permission.
RMID: 0020100264
DOI: 10.1038/cddis.2010.12
Grant ID: http://purl.org/au-research/grants/nhmrc/399300
Appears in Collections:Medicine publications

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