The p53-Mdm2 module and the ubiquitin system.

By D. Michael, Moshe Oren. Seminars in Cancer Biology, 2003

814 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/ab5d375c24bc26f59a0d87d68c35c1e677772ef9

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In Cancer Research

1. W. Gu

In Molecular Biology

1. W. Gu
2. Yingming Zhao
3. Yi Tang
4. Yue Chen
5. Wenhui Zhao
6. David P. Lane
7. Ronald T. Hay

In Oncology

1. W. Gu
2. Yingming Zhao
3. Yi Tang
4. Yue Chen
5. Wenhui Zhao
6. David P. Lane
7. Ronald T. Hay

Citations in the corpus

• Mdm2-mediated NEDD8 conjugation of p53 inhibits its transcriptional activity. (2004, background): “NEDDylated p53 was ated degradation of p53, including TSG101, the retinoblas- detected in the absence of coexpressed Mdm2 (Figure toma protein (pRb), the c-Abl protooncogene product, and 2A, lane 2); however, the amount of NEDDylated p53 was p300 (Vousden, 2002; Michael and Oren, 2003).”
• Ubiquitination regulates PTEN nuclear import and tumor suppression. (2007, neutral): “Monoubiquitination has previously been implied in p53 nuclear export (Li et al., 2003; Lohrum et al., 2001), but p53 also contains several well-characterized NLS and NES sequences that enhance transport (Michael and Oren, 2003).”
• The first 30 years of p53: growing ever more complex (2009, neutral): “By contrast, in cells exposed to various stress conditions (most notably those that put the cellular genome at risk) p53 is rapidly activate”
• Acetylation is indispensable for p53 activation. (2008, background): “Recent studies have established crucial roles for both Mdm2 and Mdmx in controlling p53 activity in vivo (Michael and Oren, 2003; Marine and Jochemsen, 2005).”
• Hydrogen peroxide sensing, signaling and regulation of transcription factors (2014, background): “Like it happens for NRF2, the cellular TP53 levels are mainly regulated by its ubiquitin-mediated proteasomal degradation [190][191].”
• A single nucleotide polymorphism in the MDM2 promoter attenuates the p53 tumor suppressor pathway and accelerates tumor formation in humans. (2004, positive): “In contrast, cells homozygous for SNP309 showed a much-weakened p53-dependent transcriptional re- binding (Michael and Oren, 2003).”