Post-translational modifications and activation of p53 by genotoxic stresses.

By E. Appella, C. Anderson. European Journal of Biochemistry, 2001

1,172 citations recorded by the source corpus.

Subfields: Biotechnology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/9d495d65e072934a7fedf4ae3175617372f3ee13

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Biotechnology

1. Guido Kroemer
2. W. Gu
3. Carol Prives
4. Karen H. Vousden
5. Sumit Ghosh

In Molecular Biology

1. Guido Kroemer
2. W. Gu
3. L. Galluzzi
4. Oliver Kepp
5. Karen H. Vousden
6. Sumit Ghosh
7. D. Reinberg
8. C. Brooks

In Oncology

1. W. Gu
2. Guido Kroemer
3. L. Galluzzi
4. Karen H. Vousden
5. Carol Prives
6. Oliver Kepp
7. C. Brooks
8. Yi Tang

Citations in the corpus

• USP10 Regulates p53 Localization and Stability by Deubiquitinating p53 (2010, neutral): “p53 activity, expression, and localization are mainly regulated by posttranslational modifications, such as phosphorylation, acetylation, and ubiquitination (Appella and Anderson, 2001).”
• Molecular mechanisms of cisplatin resistance (2012, background): “…checkpoint kinase 1 (CHEK1, the most prominent substrate and downstream effector of ATR), which in turn phosphorylates the tumor suppression protein TP53 on serine 20, allowing for its stabilization (Shieh et al., 2000; Appella and Anderson, 2001; Damia et al., 2001; Zhao and Piwnica-Worms, 2001).”
• Regulation of p53 activity through lysine methylation (2004, methodology): “Viral supernatants were collected from the transfected 293T cells 24, 36 and 48 h post-transfection, filtered and used for infection of ,5 £ 10(4) target U2OS cells grown on six-well plates in the presence of 4 mgml(21) of polybrene (Sigma).”
• Tip60-dependent acetylation of p53 modulates the decision between cell-cycle arrest and apoptosis. (2006, background): “A Regulatory Role for the DNA-Binding Domain in p53-Mediated Apoptosis Numerous studies have established that the N-terminal and C-terminal domains of p53 are subject to phosphorylation, acetylation, ubiquitination, sumoylation, neddylation, and methylation and that these modifications play an impor”
• Cisplatin: The first metal based anticancer drug. (2019, background): “Cisplatin first activates ATR kinase [69] which then activates p53 by phosphorylating at serine-15 [70].”
• The MAPK cascades: signaling components, nuclear roles and mechanisms of nuclear translocation. (2011, neutral): “hyper-mutagenized cells [163,164].”
• Blinded by the Light: The Growing Complexity of p53. (2009, background): “As there are a number of excellent reviews covering these aspects of p53 regulation (Appella and Anderson, 2001; Bode and Dong, 2004; Kruse and Gu, 2008; Olsson et al., 2007), we will focus on discussing findings relevant to a few key p53 modifications that selectively impact the cellular outcomes…”
• p53 polymorphisms: cancer implications (2009, background): “Numerous stress sensors that converge at p53 result in the phosphorylation, acetylation, ubiquitylation and methylation of specific p53 residue”
• Ubiquitination, phosphorylation and acetylation: the molecular basis for p53 regulation. (2003, background): “Post-translational modifications Post-translational modifications of p53 play an essential role in both stabilization and activation of the protein [5].”
• Pirh2, a p53-induced ubiquitin-protein ligase, promotes p53 degradation. (2003, positive): “Subsequent phosphorylation and acetylation leads to activation of the sequenceOntario Canada M5G 2C1 specific DNA binding and transcriptional activities of p53 (Appella and Anderson, 2001; Prives and Manley, 4 Department of Molecular Genetics The University of Texas 2001).”
• The complexity of p53 stabilization and activation (2006, background): “Ser15 phosphorylation of p53 occurs rapidly in response to DNA damage and appears to represent a ‘priming event’ for the subsequent series of modifications.(42) It acts as a”