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H2AFX — TP53
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Ye et al., DNA repair 2004
:
Like genistein, quercetin
induced phosphorylation of ATM on serine 1981, and ATM dependent phosphorylation of
histone H2AX on serine 139 ; however,
p53 accumulation and phosphorylation on serines 6, 9, 15, 20, 46, and 392 occurred in ATM-deficient cells, indicating that ATM is not required for quercetin induced phosphorylation of p53
Paulsen et al., Toxicol Appl Pharmacol 2005
(Necrosis) :
The natural toxin juglone causes degradation of
p53 and
induces rapid
H2AX phosphorylation and cell death in human fibroblasts
Chiu et al., Chem Biol Interact 2009
(Colorectal Neoplasms) :
Furthermore, inhibition of
p53 phosphorylation by pifithrin-alpha was
sufficient to reduce the oxaliplatin induced up-regulation of
gamma-H2AX and apoptosis
Atsumi et al., PloS one 2011
(Genomic Instability...) :
Onset of quiescence following
p53 mediated down-regulation of
H2AX in normal cells
Hiller et al., J Exp Med 2012
:
RNase H2-deficient cells proliferated slower than control cells and accumulated in G2/M phase due to chronic activation of a DNA damage response associated with an increased frequency of single-strand breaks, increased
histone H2AX phosphorylation, and
induction of
p53 target genes, most prominently the cyclin dependent kinase inhibitor 1 encoding cell cycle inhibitor p21
Osawa et al., Biochem Biophys Res Commun 2013
(Genomic Instability...) :
Normal cells undergo a growth arrested status that is produced by
p53 dependent down-regulation of
histone H2AX ... Here, we show that both Arf and
p53 are
required for the down-regulation of
H2AX and formation of the growth arrested state
Atsumi et al., J Biol Chem 2013
:
Here we show that
Arf/p53 dependent down-regulation of
H2AX induced the selective survival of normal cells after drug treatment, resulting in the preferential targeting of cancer cells