◀ Back to GRAP2

GRAP2 — TP53

Text-mined interactions from Literome

Andrysík et al., Toxicol Appl Pharmacol 2006 : In contrast, the PAHs stimulating cell proliferation in WB-F344 cell line had no effect on activation of ERK1/2, p38 or JNKs. Synthetic inhibitors of ERK1/2 activation ( U0126 ) or p38 kinase activity ( SB203580 ) prevented both apoptosis and induction of p53 phosphorylation by DBalP ... Pifithrin-alpha, inhibitor of p53 transcriptional activity, prevented induction of apoptosis and activation of ERK1/2 and p38
Huang et al., J Pharmacol Sci 2008 (Carcinoma, Hepatocellular...) : Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53 , and the p38 inhibitor SB203580 reduced the activation of p53 as well
Zdanov et al., Biogerontology 2009 : In this work, p38 ( MAPK ) activation and increased DNA binding activities of ATF-2 and p53 are shown to mediate cyclooxygenase-2 overexpression in premature senescence
Bátor et al., Biochem Cell Biol 2013 : Cytotoxic concentrations of the nitric oxide donor sodium nitroprusside activated several proapoptotic mechanisms, including stimulation of the stress kinase pathways mediated by c-Jun N-terminal kinase (JNK) and p38 mitogen activated protein kinase ( MAPK ), inhibition of the translation initiation factor eIF2a, induction and phosphorylation of the p53 protein, and inhibited Akt mediated antiapoptotic signaling, independent of Ras function