Acetylation of the p53 DNA-binding domain regulates apoptosis induction.
By Stephen M Sykes, H. Mellert, Marc A. Holbert, Keqin Li, R. Marmorstein, William Arbuthnot Sir Lane, S. McMahon. Molecules and Cells, 2006
776 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/57c122427f5734aa9db293aee7873de8b5177cc5
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Citations in the corpus
- Acetylation is indispensable for p53 activation. (2008, background): “Following our early findings of C terminus p53 acetylation, we and others recently showed that p53 is also acetylated by Tip60/hMOF at residue K120 within the DNA-binding domain (Tang et al., 2006; Sykes et al., 2006).”
- Tumor suppression in the absence of p53-mediated cell cycle arrest, apoptosis, and senescence (2012, neutral): “We and others recently showed that p53 is acetylated at K120 by Tip60/MOF (Sykes et al., 2006; Tang et al., 2006; Li et al., 2009), whereas K164 is acetylated by CBP and p300, but not Tip60/MOF (Tang et al.”
- Blinded by the Light: The Growing Complexity of p53. (2009, background): “Two MYST family histone acetyl transfereases (HATs)—Tip60 (Tang et al., 2006) and hMOF (Sykes et al., 2006)—are capable of acetylating K120.”
- The Cell-Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression. (2016, background): “Acetylation of K120 in the DNAbinding domain by acetylases Tip60 or hMOF specifically promotes apoptosis (Sykes et al. 2006; Tang et al. 2006).”
- HATs and HDACs: from structure, function and regulation to novel strategies for therapy and prevention (2007, background): “For example, p300, PCAF and two members of the MYST family acetylate p53 (Gu and Roeder, 1997; Sakaguchi et al., 1998; Liu et al., 1999; Sykes et al., 2006; Tang et al., 2006).”
- Lysine acetylation: codified crosstalk with other posttranslational modifications (2008, background): “Moreover, its acetylation lies at the nexus of apoptotic and cell-cycle control (Sykes et al., 2006; Tang et al., 2006), so it will be interesting to determine if K117R mutant mice display more dramatic phenotypes.”