p73-deficient mice have neurological, pheromonal and inflammatory defects but lack spontaneous tumours

By A. Yang, Nancy Walker, R. Bronson, M. Kaghad, M. Oosterwegel, J. Bonnin, C. Vagner, Hélène Bonnet, P. Dikkes, Arlene H. Sharpe and 2 more. Nature, 2000

1,072 citations recorded by the source corpus.

Subfields: Biotechnology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/36f93fca5189e9154d96483cc29234e8ca637e29

How researchers see this paper

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In Biotechnology

1. Scott W. Lowe

In Molecular Biology

1. Duojia Pan
2. K. Guan
3. Jixin Dong
4. Shian Wu
5. Scott W. Lowe
6. J. Fridman
7. Shomit Sengupta
8. A. Maitra

In Oncology

1. Scott W. Lowe
2. J. Fridman
3. Duojia Pan
4. T. Jacks
5. J. Campisi

Citations in the corpus

• Role of the reelin signaling pathway in central nervous system development. (2001, background): “…al 1997 Src Src proto-oncogene Howell et al 1997a Nuclear Emx2 Related to empty spiracles Mallamaci et al 2000 P73 Transformation-related protein 73 Yang et al 2000 Tbr-1 T-box brain-1 Bulfone et al 1995 large extracellular protein, Reelin, that is produced by discrete populations of cells in the…”
• Elucidation of a universal size-control mechanism in Drosophila and mammals. (2007, background): “Given that p73-deficient mice are viable (Yang et al., 2000) while YAP-deficient mice die at embryonic day 8.5 (Morin-Kensicki et al., 2006), p73 is unlikely to be a critical partner for YAP in mouse development.”
• p63 and p73 are required for p53-dependent apoptosis in response to DNA damage (2002, methodology): “The genotypes of the MEFs were determined by polymerase chain reaction (PCR) as described previously”
• Control of apoptosis by p53 (2003, background): “…of these genes in cancer development is unclear, in part, because inactivating mutations in tumors have not been identified (Yang et al., 2002) and p73-deficient mice are not tumor prone (Yang et al., 2000) (note that the early death of p63-null mice has precluded tumorigenicity studies to date).”