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ICAM1 — ITGB2

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: Complex of ICAM1-ITGAM-ITGB2 → SPN (decreases, ICAM1/ITGAM/ITGB2 Activity)
  Evidence: Neutrophils are partially activated (primed) by the TNF and leukotrienes produced by mast cells and by other neutrophils, leading to release of small amounts of elastase. This cleaves the anti-adhesive coat of CD43 (leukosialin) from neutrophils, allowing their integrins to engage extracellular matrix proteins.
• OpenBEL Selventa BEL large corpus: Complex of ICAM1-ITGAL-ITGB2 → CCL2 (increases)
  Evidence: Strong adhesion between leukocytes and endothelial cells is promoted by the induction of ICAM-1 on inflamed endothelium and the activation of a conformational change in LFA-1 and Mac-1 in response to chemokines.
• OpenBEL Selventa BEL large corpus: Complex of ICAM1-ITGAM-ITGB2 → CCL2 (increases)
  Evidence: Strong adhesion between leukocytes and endothelial cells is promoted by the induction of ICAM-1 on inflamed endothelium and the activation of a conformational change in LFA-1 and Mac-1 in response to chemokines.
• KEGG Cell adhesion molecules (CAMs): Complex of ITGAL-ITGB2 → ICAM1/ICAM2/ICAM3 (protein-protein, activation)
• KEGG Cell adhesion molecules (CAMs): ICAM1/ICAM2/ICAM3 → Complex of ITGAL-ITGB2 (protein-protein, activation)
• KEGG Cell adhesion molecules (CAMs): ICAM1/ICAM2/ICAM3 → Complex of ITGAL-ITGB2 (protein-protein, activation)
• KEGG Cell adhesion molecules (CAMs): Complex of ITGAL-ITGB2 → ICAM1 (protein-protein, activation)
• KEGG Cell adhesion molecules (CAMs): Complex of ITGAM-ITGB2 → ICAM1 (protein-protein, activation)
• KEGG Cell adhesion molecules (CAMs): ICAM1/ICAM2/ICAM3 → Complex of ITGAL-ITGB2 (protein-protein, binding/association)
• KEGG Cell adhesion molecules (CAMs): ICAM1/ICAM2/ICAM3 → Complex of ITGAL-ITGB2 (protein-protein, binding/association)
• KEGG Natural killer cell mediated cytotoxicity: ICAM1/ICAM2 → Complex of ITGAL-ITGB2 (protein-protein, activation)
• KEGG Natural killer cell mediated cytotoxicity: ICAM1/ICAM2 → Complex of ITGAL-ITGB2 (protein-protein, activation)
• KEGG Leukocyte transendothelial migration: ICAM1 → Complex of ITGAL-ITGB2 (protein-protein, binding/association)
• KEGG Malaria: ITGAL/ITGB2 → ICAM1 (protein-protein, binding/association)
• KEGG Malaria: ITGAL/ITGB2 → ICAM1 (protein-protein, binding/association)
• KEGG Staphylococcus aureus infection: ICAM1 → Complex of ITGAL-ITGAM-ITGB2 (protein-protein, binding/association)
  
• KEGG Rheumatoid arthritis: ITGAL/ITGB2 → ICAM1 (protein-compound, binding/association)
• KEGG Viral myocarditis: ICAM1 → ITGAL/ITGB2 (protein-protein, activation)
• NCI Pathway Database Beta2 integrin cell surface interactions: ICAM1 (ICAM1) → alphaX/beta2 Integrin/ICAM1 complex (ICAM1-ITGAX-ITGB2) (modification, collaborate)
  Choi et al., Mol Cells 2010*
  Evidence: physical interaction
• NCI Pathway Database Beta2 integrin cell surface interactions: ICAM1 (ICAM1) → alphaX/beta2 Integrin complex (ITGAX-ITGB2) (modification, collaborate)
  Choi et al., Mol Cells 2010*
  Evidence: physical interaction
• NCI Pathway Database Beta2 integrin cell surface interactions: alphaX/beta2 Integrin/ICAM1 complex (ICAM1-ITGAX-ITGB2) → alphaX/beta2 Integrin complex (ITGAX-ITGB2) (modification, collaborate)
  Choi et al., Mol Cells 2010*
  Evidence: physical interaction
• NCI Pathway Database amb2 Integrin signaling: alphaM/beta2 Integrin/ICAM1 complex (ITGAM-ITGB2-ICAM1) → AKT1 (AKT1) (positive regulation of phagocytosis, collaborate) Lutz et al., J Leukoc Biol 2003
  Evidence: mutant phenotype, assay
• NCI Pathway Database amb2 Integrin signaling: alphaM/beta2 Integrin/ICAM1 complex (ITGAM-ITGB2-ICAM1) → PKC zeta (PRKCZ) (positive regulation of phagocytosis, collaborate) Lutz et al., J Leukoc Biol 2003
  Evidence: mutant phenotype, assay
• NCI Pathway Database Beta2 integrin cell surface interactions: ICAM1 (ICAM1) → alphaL/beta2 Integrin/ICAM1 complex (ICAM1-ITGAL-ITGB2) (modification, collaborate)
  Dransfield et al., J Cell Biol 1992*, Tang et al., J Biol Chem 2005*
  Evidence: physical interaction
• NCI Pathway Database Beta2 integrin cell surface interactions: ICAM1 (ICAM1) → alphaL/beta2 Integrin complex (ITGAL-ITGB2) (modification, collaborate)
  Dransfield et al., J Cell Biol 1992*, Tang et al., J Biol Chem 2005*
  Evidence: physical interaction
• NCI Pathway Database Beta2 integrin cell surface interactions: alphaL/beta2 Integrin/ICAM1 complex (ICAM1-ITGAL-ITGB2) → alphaL/beta2 Integrin complex (ITGAL-ITGB2) (modification, collaborate)
  Dransfield et al., J Cell Biol 1992*, Tang et al., J Biol Chem 2005*
  Evidence: physical interaction
• NCI Pathway Database Beta2 integrin cell surface interactions: alphaM/beta2 Integrin/ICAM1 complex (ITGAM-ITGB2-ICAM1) → ICAM1 (ICAM1) (modification, collaborate) Solovjov et al., J Biol Chem 2005, Diamond et al., J Cell Biol 1990*, Smith et al., J Clin Invest 1989*, Diamond et al., J Cell Biol 1993, Diamond et al., J Cell Biol 1993
  Evidence: physical interaction
• NCI Pathway Database Beta2 integrin cell surface interactions: alphaM/beta2 Integrin/ICAM1 complex (ITGAM-ITGB2-ICAM1) → alphaM/beta2 Integrin complex (ITGAM-ITGB2) (modification, collaborate)
  Solovjov et al., J Biol Chem 2005, Diamond et al., J Cell Biol 1990*, Smith et al., J Clin Invest 1989*, Diamond et al., J Cell Biol 1993, Diamond et al., J Cell Biol 1993
  Evidence: physical interaction
• NCI Pathway Database Beta2 integrin cell surface interactions: ICAM1 (ICAM1) → alphaM/beta2 Integrin complex (ITGAM-ITGB2) (modification, collaborate)
  Solovjov et al., J Biol Chem 2005, Diamond et al., J Cell Biol 1990*, Smith et al., J Clin Invest 1989*, Diamond et al., J Cell Biol 1993, Diamond et al., J Cell Biol 1993
  Evidence: physical interaction
• NCI Pathway Database amb2 Integrin signaling: alphaM/beta2 Integrin/ICAM1 complex (ITGAM-ITGB2-ICAM1) → ICAM1 (ICAM1) (modification, collaborate) Lutz et al., J Leukoc Biol 2003
  Evidence: assay
• NCI Pathway Database amb2 Integrin signaling: alphaM/beta2 Integrin/ICAM1 complex (ITGAM-ITGB2-ICAM1) → alphaM/beta2 Integrin complex (ITGAM-ITGB2) (modification, collaborate)
  Lutz et al., J Leukoc Biol 2003
  Evidence: assay
• NCI Pathway Database amb2 Integrin signaling: ICAM1 (ICAM1) → alphaM/beta2 Integrin complex (ITGAM-ITGB2) (modification, collaborate)
  Lutz et al., J Leukoc Biol 2003
  Evidence: assay
• Reactome Reaction: ICAM1 → ITGB2 (indirect_complex) Yusuf-Makagiansar et al., Med Res Rev 2002*
• Reactome Reaction: ICAM1 → ITGB2 (reaction) Yusuf-Makagiansar et al., Med Res Rev 2002*

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: ITGB2 — ICAM1 (direct interaction, pull down) Kotovuori et al., J Immunol 1999*
• IRef Biogrid Interaction: ITGB2 — ICAM1 (direct interaction, pull down) Lu et al., J Biol Chem 2001*
• IRef Biogrid Interaction: ITGB2 — ICAM1 (direct interaction, pull down) Huang et al., J Biol Chem 1995*
• IRef Biogrid Interaction: ITGB2 — ICAM1 (direct interaction, pull down) Rolén et al., J Cell Mol Med 2009*
• IRef Innatedb Interaction: ITGB2 — ICAM1 (unknown, -) Santoso et al., J Exp Med 2002
• IRef Ophid Interaction: ITGB2 — ICAM1 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005
• IRef Ophid Interaction: ITGB2 — ICAM1 (aggregation, confirmational text mining) Lu et al., J Biol Chem 2001*

Text-mined interactions from Literome

Yoshida et al., Aliment Pharmacol Ther 2000 (Helicobacter Infections...) : The expression of CD11b and CD18 on neutrophils and neutrophil dependent adhesion to endothelial cells elicited by HPE were inhibited by lansoprazole and omeprazole at clinical relevant doses, and the expression of ICAM-1 and VCAM-1 on endothelial cells and endothelial dependent neutrophil adherence induced by IL-1beta were also inhibited by lansoprazole and omeprazole at similar doses
Yoshida et al., Am J Physiol 1992 (Anoxia) : These studies indicate that A/R promotes neutrophil adherence via CD11a/CD18- and CD11b/CD18 dependent interactions with ICAM-1 that appear to be mediated by hydrogen peroxide and PAF
Yoshida et al., Dig Dis Sci 1995 (Gastritis) : These results suggest that neutrophil-endothelial adhesive interactions, which occur via CD11a/ CD18- and CD11b/CD18 dependent interactions with intercellular adhesion molecule-1 , and oxygen derived free radicals produced by neutrophils are implicated in the production of aspirin induced gastric mucosal injury
Yoshida et al., Gastroenterology 1993 (Duodenitis...) : These studies suggest that products of H. pylori elicit gastrointestinal inflammation by promoting PMN adhesion to endothelial cells via CD11a/CD18- and CD11b/CD18 dependent interactions with ICAM-1
Yoshida et al., Gastroenterology 1993 : These studies indicate that aspirin promotes neutrophil adherence to endothelium via CD11a/CD18- and CD11b/CD18 dependent interactions with intercellular adhesion molecule 1 ; the adhesion response is partially mediated by leukotriene B4
Zhou et al., Zhonghua Nei Ke Za Zhi 1995 (Lupus Erythematosus, Systemic) : Results demonstrated increase in CD8+ cell and decrease in CD4+ cell, CD4+/CD8+, and CD4+/CD45RA+ cell, as well as decrease in expression of CD11a and CD18 on CD4+ cell surface, Expression of CD11a and CD18 on CD8+ cell, and CD54 on CD20+ cell increased , Moreover, increase in CD18 on CD8+ cell correlated inversely with decrease in CD4+ CD45RA+ cell ( P < 0.05 ) and positively with increase in CD54 on CD20+ cell ( P < 0.01 )
Takaishi et al., Alcohol Clin Exp Res 1996 : The present study further supports that CD18/ ICAM-1 dependent leukocyte-endothelial adhesive interactions lead to macromolecular leakage in the postcapillary venules exposed to ethanol
Bavbek et al., Stroke 1998 (Disease Models, Animal...) : This study examined the effects of monoclonal antibodies on ICAM-1 and the effects of CD18 on cerebral vasospasm after SAH