p300/CBP‐mediated p53 acetylation is commonly induced by p53‐activating agents and inhibited by MDM2
By A. Ito, Chun‐Hsiang Lai, Xuan Zhao, Shinichi Saito, Maria H. Hamilton, E. Appella, T. Yao. EMBO Journal, 2001
609 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/262866924138500bba11f25fb1cfcc300153624d
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Citations in the corpus
- Human SIR2 deacetylates p53 and antagonizes PML/p53‐induced cellular senescence (2002, background): “This is consistent with a recent study which reports that p53 acetylation in vivo at this site is mediated by the p300/CBP acetyltransferases (Ito et al., 2001).”
- Blinded by the Light: The Growing Complexity of p53. (2009, background): “Nonetheless, Mdm2 has also been shown to reduce p53 acetylation by displacing p300 from p53 (Ito et al., 2001; Kobet et al., 2000; Teufel et al., 2007), as well as by inhibiting and degrading PCAF (Jin et al., 2004).”
- The world of protein acetylation. (2016, background): “terminus, acetylated mainly by p300/CBP, are part of the activity mechanism [256].”
- Post-translational modification of p53 in tumorigenesis (2004, background): “In some cases, previous phosphorylation might be required for subsequent acetylation of p53, and almost every type of cellular stress increases acetylation levels of p53 in a range of cell type”
- Tumour suppression by p53: a role for the DNA damage response? (2009, background): “Phosphorylation sites merit attention because of their specific association with DNA damage pathways, whereas acetylation events seem to be common to both the DNA damage- and ARF-mediated pathway”
- HDAC6 is a microtubule-associated deacetylase (2002, background): “Indeed, recent studies reveal that many non-histone nuclear transcription factors, such as p53, E2Fs and myoD, are regulated by acetylatio”
- The MDM2-p53 interaction. (2003, background): “In addition, MDM2 present in the ternary complex of MDM2-p53-p300 in HeLa cell nuclear extracts inhibits p300-mediated p53 acetylation and transcriptional activation (27, 28).”
- Lysine acetylation: codified crosstalk with other posttranslational modifications (2008, background): “In addition, oncogenic Ras and a variety of stress-inducing agents promote p53 acetylation (Pearson et al., 2000; Ito et al., 2001).”
- Acetylation is indispensable for p53 activation. (2008, background): “The acetylation levels of p53 are significantly enhanced in response to stress and correlate well with p53 activation and stabilization (Luo et al., 2000, 2001; Vaziri et al., 2001; Ito et al., 2001; Barlev et al., 2001; Knights et al., 2006; Li et al., 2007; Zhao et al., 2008; Kim et al., 2008).”
- Ubiquitination, phosphorylation and acetylation: the molecular basis for p53 regulation. (2003, background): “The acetylation levels of p53 are significantly enhanced in vivo in response to almost every type of stress, which correlates well with its activation and stabilization induced by stress [10 ].”
- Regulation of p53 activity by its interaction with homeodomain-interacting protein kinase-2 (2002, methodology): “c, GST–p53(1-80) or a point mutant of this fusion protein containing a Ser 46 to alanine exchange were employed as substrate proteins, typical autoradiograms are displayed.”