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APP — NGFR

Pathways - manually collected, often from reviews:

• NCI Pathway Database p75(NTR)-mediated signaling: JNK family (MAPK8/MAPK9/MAPK10) → p75(NTR)/beta APP complex (NGFR-APP) (modification, collaborate)
  Troy et al., J Neurochem 2001, Yaar et al., J Biol Chem 2002
  Evidence: mutant phenotype, assay, other species
• NCI Pathway Database p75(NTR)-mediated signaling: p75(NTR) (NGFR) → beta APP (APP) (modification, collaborate) Yaar et al., J Biol Chem 2002
  Evidence: physical interaction, other species
• NCI Pathway Database p75(NTR)-mediated signaling: p75(NTR) (NGFR) → p75(NTR)/beta APP complex (NGFR-APP) (modification, collaborate)
  Yaar et al., J Biol Chem 2002
  Evidence: physical interaction, other species
• NCI Pathway Database p75(NTR)-mediated signaling: beta APP (APP) → p75(NTR)/beta APP complex (NGFR-APP) (modification, collaborate)
  Yaar et al., J Biol Chem 2002
  Evidence: physical interaction, other species

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

Studies that report less than 10 interactions are marked with *

• IRef Dip Interaction: APP — NGFR (direct interaction, pull down) Nikolaev et al., Nature 2009*
• IRef Dip Interaction: APP — NGFR (direct interaction, solid phase assay) Nikolaev et al., Nature 2009*
• IRef Intact Interaction: APP — NGFR (physical association, anti bait coimmunoprecipitation) Yaar et al., J Biol Chem 2002
• IRef Intact Interaction: APP — NGFR (direct interaction, enzyme linked immunosorbent assay) Nikolaev et al., Nature 2009*
• IRef Intact Interaction: APP — NGFR (direct interaction, pull down) Nikolaev et al., Nature 2009*

Text-mined interactions from Literome

Wallace et al., Brain Res Mol Brain Res 1997 : The neurotrophic activity of APP was independent of the TrkA NGF receptor because neither phospholipase C-gamma1 nor TrkA exhibited tyrosine phosphorylations with APP treatment
Rossner et al., Prog Neurobiol 1998 (Alzheimer Disease) : Recent experiments with NGF-responsive cells revealed a specific role for the high-affinity NGF receptor , TrkA, in the increases in secretory APP processing and a role for the low-affinity neurotrophin receptor, p75NTR, in the transcriptional regulation of APP