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BID — TP53

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: BID → TP53 (increases, BID 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).
• FastForward regulation: TP53 → BID (transcriptional regulation, increase) Sax et al., Nat Cell Biol 2002*
  Evidence: DNABINDING, PROMACTIVITY

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Intact Interaction: Complex of TP53-BID-BCL2L1 (physical association, pull down) Chipuk et al., Science 2004*

Text-mined interactions from Literome

Sax et al., Nat Cell Biol 2002 : BID regulation by p53 contributes to chemosensitivity ... Here we show that BID , a member of the pro-apoptotic Bcl-2 family of proteins, is regulated by p53
Henry et al., EMBO J 2012 : Surprisingly, the key differential events in apoptotic cells are p53 dependent activation of the DR4 death receptor pathway, caspase 8-mediated cleavage of BID , and BID dependent activation of poised BAX at the mitochondria