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Cited by 255

The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.

Reversal of Senescence in Mouse Fibroblasts through Lentiviral Suppression of p53

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Dirac, Annette M.G., Bernards, René·2003·Journal of Biological Chemistry

Abstract

Senescence is generally defined as an irreversible state of G(1) cell cycle arrest in which cells are refractory to growth factor stimulation. In mouse embryo fibroblasts (MEFs), induction of senescence requires the presence of p19(ARF) and p53, as genetic ablation of either of these genes allows escape from senescence and leads to immortalization. We have developed a lentiviral vector that directs the synthesis of a p53-specific short hairpin transcript, which mediates stable suppression of p53 expression through RNA interference. We show that suppression of p53 expression in senescent MEFs leads to rapid cell cycle re-entry, is associated with loss of expression of senescence-associated genes, and leads to immortalization. These data indicate that senescence in MEFs is reversible and demonstrate that both initiation and maintenance of senescence is p53-dependent.

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Metadata

Authors
Dirac, A. M. G., & Bernards, R.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2003-04
Volume
278
Issue
14
Pages
11731-11734
ISSN
0021-9258 (ISSN-L)
OpenAlex
W2098995242
Cited by
255
References
36
FWCI
10.86
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Reversal of Senescence in Mouse Fibroblasts through Lentiviral Suppression of p53. https://app.cochat.ai/papers/10.1074/jbc.c300023200
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Dirac, A. M. G., & Bernards, R. (2003). Reversal of Senescence in Mouse Fibroblasts through Lentiviral Suppression of p53. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.c300023200

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.