p53 mutant mice that display early ageing-associated phenotypes

By Stuart D. Tyner, S. Venkatachalam, Jene Choi, Stephen N. Jones, N. Ghebranious, Herbert Igelmann, Xiongbin Lu, Gabrielle Soron, B. Cooper, C. Brayton and 5 more. Nature, 2002

1,479 citations recorded by the source corpus.

Subfields: Biotechnology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/e8e6740dcb3555660b47368b7a80fe59e79cbcc7

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In Biotechnology

1. J. Campisi
2. W. Gu
3. Scott W. Lowe

In Molecular Biology

1. J. Campisi
2. N. Sharpless
3. W. Gu
4. P. Desprez
5. Jean-Philippe Coppé
6. Derrick J. Rossi
7. C. Brooks
8. E. Verdin

In Oncology

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2. W. Gu
3. C. Brooks
4. Scott W. Lowe
5. J. Fridman
6. E. Verdin
7. Irving L. Weissman
8. S. Morrison

Citations in the corpus

• Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. (2005, background): “Cells from these modified mice were more susceptible to both p53-mediated apoptosis (Tyner et al., 2002) and p53-mediated senescence (Maier et al., 2004).”
• HERITABILITY OF NECTAR TRAITS: WHY DO WE KNOW SO LITTLE? (2004, background): “How- ever, experience with other traits (such as petal color; e.g., Glover and Martin 1998, Clegg and Durbin 2000, Irwin et al. 2003; see also Tyner et al. 2002) indicates that the effects of specific genes on labile physiological traits such as nectar will not be simple.”