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TNFRSF10B — TP53

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: TNFRSF10B → TP53 (increases, TNFRSF10B Activity)
  Evidence: NF?B family transcription factors can induce expression of antiapoptotic proteins that oppose the intrinsic (Bcl-XL, Bfl-1), extrinsic (FLIP), and convergence (cIAP2) pathways (Figure 2A), as well as suppressing expression of the death inducer Bax (intrinsic pathway) in some types of tumor cells (Karin and Lin, 2002). Further, hyperactivity of NF?B is now well documented in certain cancers (Karin et al., 2002).
• KEGG p53 signaling pathway: TP53 → TNFRSF10B (gene expression, expression)
• NCI Pathway Database Direct p53 effectors: p53 (tetramer) complex (TP53) → TRAILR2 (TNFRSF10B) (transcription, activates) Takimoto et al., Oncogene 2000*, Liu et al., Cancer Res 2004*
  Evidence: mutant phenotype, reporter gene, physical interaction
• WikiPathways miRNA Regulation of DNA Damage Response: TP53 → Complex of FAS-PIDD1-TNFRSF10B (activation)
  
• WikiPathways DNA Damage Response: TP53 → Complex of FAS-PIDD1-TNFRSF10B (activation)
  

Text-mined interactions from Literome

Tsai et al., J Biol Chem 2010 : CHM-1, a new vascular targeting agent, induces apoptosis of human umbilical vein endothelial cells via p53 mediated death receptor 5 up-regulation
Tseng et al., Mol Cancer Ther 2010 (Melanoma) : Nevertheless, nutlin-3 enhanced TRAIL induced apoptosis as a result of p53 mediated upregulation of TRAIL-R2
Tseng et al., Carcinogenesis 2012 (Melanoma...) : Regulation of TRAIL-R2 by MAGE-D2 appeared to be mediated by p53 , in that knockdown MAGE-D2 did not up-regulate TRAIL-R2 in p53-null or mutant p53 melanoma cells