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Mechanisms of switching on p53: a role for covalent modification?
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Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
Mdm2 promotes the rapid degradation of p53
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“…to a region of the transactivation domain (Oliner et al., 1993; Zauberman et al., 1993) and mediates rapid turnover of p53 by targeting it to the 26S proteosome through a mechanism involving MDM2-mediated ubiquitination of p53 (Haupt et al., 1997; Honda and Yasuda, 1999; Kubbutat et al., 1997).”
BackgroundKastan, M. B., Zhan, Q., El-Deiry, W. S., Carrier, F., Jacks, T., Walsh, W. V., Plunkett, B. S., Vogelstein, B., & Fornace, A. J. (1992) · Cell · doi:10.1016/0092-8674(92)90593-2 · Cited by 3,047 · cited 1×
“ATM had long been suspected of being an upstream component of the p53 pathway on the basis that the induction of p53 in cells from AT patients showed a signi®cant delay in the response to IR (Kastan et al., 1992; Khanna and Lavin, 1993).”
BackgroundDNA damage-induced phosphorylation of p53 alleviates inhibition by MDM2
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Regulation and function of the p53 tumor suppressor protein
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Metadata
- Authors
- Meek, D. W.
- Venue
- Oncogene
- Published
- 1999-12-13
- Volume
- 18
- Issue
- 53
- Pages
- 7666-7675
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W1974836748
- Cited by
- 236
- References
- 20
- FWCI
- 9.78
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- www.springer.com/tdm (vor)
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