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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to MAPK1

ITGAV — MAPK1

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: MAPK1 → Complex of ITGAV-ITGB3 (increases, ITGAV/ITGB3 Activity) Bao et al., Mol Cell Biol 2002*
    Evidence: Cell attachment to fibronectin through ITGAV.ITGB3 activated the phosphorylation of ERK-2 within 60 minutes. ERK-2 activation was detected even in the presence of dn Cdc42 or dn Rac1 after attachment to fibronectin, indicating that these integrin-induced signaling components are still activated by attachment when Cdc42 and Rac1 are blocked.
  • OpenBEL Selventa BEL large corpus: MAPK1 → Complex of ITGAV-ITGB3 (increases, ITGAV/ITGB3 Activity, MAPK1 Activity) Rüegg et al., Biochim Biophys Acta 2004*
    Evidence: Activated ERK enters the nucleus to promote transcription [64]. The MAPK pathway is critically involved in controlling proliferation, survival, and migration of endothelial cells. Angiogenesis in the chorio-allantoid membrane (CAM) model requires two waves of ERK activation, the first one being dependent on FGF-2, and the second one on aVh3 integrin ligation [65].
  • OpenBEL Selventa BEL large corpus: MAPK1 → Complex of ITGAV-ITGB3 (increases) Bao et al., Mol Cell Biol 2002*
    Evidence: Cell attachment to fibronectin through ITGAV.ITGB3 activated the phosphorylation of ERK-2 within 60 minutes. ERK-2 activation was detected even in the presence of dn Cdc42 or dn Rac1 after attachment to fibronectin, indicating that these integrin-induced signaling components are still activated by attachment when Cdc42 and Rac1 are blocked.
  • NCI Pathway Database Integrins in angiogenesis: Erk1-2 (MAPK3/MAPK1) → alphav/beta3 Integrin/JAM-A complex (F11R-ITGAV-ITGB3) (modification, collaborate)
    Naik et al., J Cell Sci 2006
    Evidence: mutant phenotype, assay
  • NCI Pathway Database Integrins in angiogenesis: alphav/beta3 Integrin/JAM-A complex (F11R-ITGAV-ITGB3) → Erk1-2-active (MAPK3/MAPK1) (modification, activates)
    Naik et al., J Cell Sci 2006
    Evidence: mutant phenotype, assay
  • NCI Pathway Database Integrins in angiogenesis: Erk1-2 (MAPK3/MAPK1) → alphav/beta3 Integrin complex (ITGAV-ITGB3) (modification, collaborate)
    Naik et al., Blood 2003, Eliceiri et al., J Cell Biol 1998
    Evidence: mutant phenotype, assay, other species

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

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Roux et al., J Biol Chem 2005 (Edema) : The inhibitory effect of IL-1beta on alpha ENaC expression was mediated by the activation of p38 MAPK in both rat and human ATII cells and was independent of the activation of alpha v beta6 integrin and transforming growth factor-beta
Vellon et al., Mol Carcinog 2006 (Breast Neoplasms...) : Here, we have assessed the role of the extracellular signal regulated kinase ( ERK1 ) /ERK2, mitogen activated protein kinase ( MAPK ), and phospoinositide 3-kinase (PI-3'K) signaling pathways in the expression and function of alpha(v)beta(3) integrin in breast cancer models