Gene interactions and pathways from curated databases and text-mining

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GDF15 — TP53

Text-mined interactions from Literome

Baek et al., Carcinogenesis 2002 : Resveratrol increases the expression of p53, tumor suppressor protein, prior to NAG-1 induction, indicating that NAG-1 expression by resveratrol is mediated by p53 expression
Bottone et al., J Nutr 2002 (Colorectal Neoplasms) : DADS did not induce NAG-1 or p53 in p53 mutant cell lines ; however, NAG-1 expression was induced by sulindac sulfide
Newman et al., Mol Pharmacol 2003 (Adenocarcinoma...) : Although NAG-1 is a p53-responsive gene, AHPN induced NAG-1 expression does not require p53
Wilson et al., Int J Cancer 2003 (Carcinoma...) : The induction of p53 ( 3 hr ) precedes the induction of NAG-1 ( 12 hr ), suggesting that genistein induced NAG-1 expression is mediated by p53 ... The expression of p53 was critical for NAG-1 promoter activity since no promoter activity was observed with genistein treatment in HCT-15 cells
Shim et al., J Biol Chem 2005 (Inflammation...) : NAG-1 ( nonsteroidal anti-inflammatory drug activated gene ), a member of the transforming growth factor beta superfamily, is involved in cellular processes such as inflammation, apoptosis/survival, and tumorigenesis and is regulated by p53 , Sp1, and Egr-1
Agarwal et al., Proc Natl Acad Sci U S A 2006 : Expression of the secreted protein macrophage inhibitory cytokine 1 (MIC-1), a member of the TGF-beta superfamily, increases substantially after PALA treatment, and application of exogenous MIC-1 or its constitutive expression from a cDNA provides remarkable protection of p53-null cells from PALA mediated apoptosis, arguing that the p53 dependent secretion of MIC-1 provides a major part of such protection
Lim et al., Apoptosis 2007 (Colonic Neoplasms) : NAG-1 up-regulation mediated by EGR-1 and p53 is critical for quercetin induced apoptosis in HCT116 colon carcinoma cells ... Reporter assays using the luciferase constructs containing NAG-1 promoter region demonstrate that early growth response-1 (EGR-1) and p53 are required for quercetin mediated activation of the NAG-1 promoter
Soto-Cerrato et al., Mol Cancer Ther 2007 (Breast Neoplasms) : Our results show that prodigiosin triggers accumulation of the DNA-damage response tumor-suppressor protein p53 but that NAG-1 induction was independent of p53 accumulation
Miller et al., Biochem Biophys Res Commun 2009 : In the presence of palmitate, NRG-1beta caused an increase in p53 expression, bax multimer formation, concurrent with degradation of mdm2, a negative regulator of p53
Thapa et al., Biochem Pharmacol 2010 (Colonic Neoplasms) : The NAG-1 expression by LYR-8 was not blocked by pifithrin-alpha, a specific p53 inhibitor, which was different from doxorubicin that induced p53 dependent NAG-1 transcriptional activity
Kim et al., Arch Pharm Res 2011 (Colorectal Neoplasms) : Despite being a downstream target of p53, NAG-1 induction is both p53 dependent and p53 independent ... The present study demonstrates that p53 dependent NAG-1 induction is linked to cell death and that NAG-1 induction without accompanying alteration of antiapoptosis protein Bcl-2 family members may not lead to cancer cell death
Qian et al., Proc Natl Acad Sci U S A 2012 : Instead, we showed that DEC1 inhibits the ability of p53 to induce macrophage inhibitory cytokine-1 (MIC-1) , but not other prosurvival/proapoptotic targets, including p21 and Puma
Kang et al., J Nutr Biochem 2013 : Reporter assays, using the luciferase constructs containing the NAG-1 promoter, demonstrate that p53 is required for EGCG mediated activation of NAG-1 ... Taken together, these results demonstrate for the first time that EGCG induces apoptosis via ATM/p53 dependent NAG-1 expression in HNSCC, providing an additional mechanistic explanation for the apoptotic activity of EGCG
Li et al., PloS one 2013 : In the present study, we revealed that high glucose could induce GDF15 expression and secretion in cultured human umbilical vein endothelial cells in a ROS- and p53 dependent manner