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AHSA1 — TP53

Text-mined interactions from Literome

Sanchez-Prieto et al., Cancer Res 2000 : Furthermore, we observed that p38 does not affect the accumulation of p53 in response to DNA damage or its nuclear localization
Chouinard et al., Biochem J 2002 : In these cells, UVB triggered a p38 dependent phosphorylation of p53 on Ser-15
Friis et al., J Physiol 2005 (Mechanotransduction, Cellular) : Inhibition of p38 in Rac cells reduced the activation of both p53 and caspase-3
Kim et al., Gastroenterology 2005 (MAP Kinase Signaling System) : The signaling pathway for colonocyte apoptosis following toxin A exposure involves p38 dependent activation of p53 and subsequent induction of p21 ( WAF1/CIP1 ), resulting in cytochrome c release and caspase-3 activation through Bak induction
Horikawa-Miura et al., Radiat Res 2007 : Furthermore, an inhibitor of p38 also blocked the phosphorylation of p53 at Ser-392
Lafarga et al., Cell cycle (Georgetown, Tex.) 2007 : Depending on the nature and the extent of the stress induced damage, cells may respond by arresting the cell cycle or by undergoing cell death, and these responses are usually associated with the phosphorylation of particular substrates by p38alpha as well as the activation of specific target genes by p53
Karunakaran et al., J Neurosci 2008 (Disease Models, Animal...) : p38 activation results in downstream phosphorylation of p53 and increased p53 mediated transcription of Bax and Puma in the ventral midbrain
Kwong et al., J Biol Chem 2009 (Inflammation) : Furthermore, upon activation by oncogenic ras, p38gamma stimulated the transcriptional activity of p53 by phosphorylating p53 at Ser ( 33 ), suggesting that the ability of p38gamma to mediate senescence is at least partly achieved through p53
Spallarossa et al., Am J Physiol Heart Circ Physiol 2009 : p38 modulates TRF2 expression, whereas JNK and cytoplasmic p53 regulate TRF1
Lee et al., Toxicol In Vitro 2011 (Mouth Neoplasms) : These results provide the first evidence that sappanchalcone suppresses oral cancer cell growth and induces apoptosis through the activation of p53 dependent mitochondrial, p38 , ERK, JNK, and NF-?B signaling
Ho et al., Life Sci 2012 : Inhibition of p38 activity reduced Taiwanin A-induced p53 phosphorylation on Ser15
Taylor et al., Molecular cancer 2013 (Lung Neoplasms...) : Collectively these data indicate that p38 and JNK MAP kinase signaling are important for eIF5A1 induced cell death and that induction of apoptosis was not dependent on p53 activity