◀ Back to ICAM1
ICAM1 — ITGAL
Pathways - manually collected, often from reviews:
-
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.
-
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):
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)
→
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
-
Reactome Reaction:
ICAM1
→
ITGAL
(indirect_complex)
Yusuf-Makagiansar et al., Med Res Rev 2002*
-
Reactome Reaction:
ICAM1
→
ITGAL
(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 Bind Interaction:
ITGAL
—
ICAM1
Shimaoka et al., Cell 2003*
-
IRef Bind_translation Interaction:
ITGAL
—
ICAM1
(x-ray crystallography)
Shimaoka et al., Cell 2003*
-
IRef Biogrid Interaction:
ICAM1
—
ITGAL
(direct interaction, pull down)
Lu et al., J Biol Chem 2001*
-
IRef Biogrid Interaction:
ICAM1
—
ITGAL
(association, x-ray crystallography)
Shimaoka et al., Cell 2003*
-
IRef Biogrid Interaction:
ICAM1
—
ITGAL
(direct interaction, pull down)
Yusuf-Makagiansar et al., Peptides 2001*
-
IRef Intact Interaction:
ITGAL
—
ICAM1
(direct interaction, x-ray crystallography)
Shimaoka et al., Cell 2003*
-
IRef Ophid Interaction:
ITGAL
—
ICAM1
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
-
IRef Ophid Interaction:
ITGAL
—
ICAM1
(aggregation, confirmational text mining)
Yusuf-Makagiansar et al., Peptides 2001*
Text-mined interactions from Literome
Chute et al., Exp Hematol 1999
:
Despite the high level of cellular activation and proliferation induced by PMVEC coculture, the surface expression of adhesion molecules
CD11a ( LFA-1 ), CD11b, CD15s ( sialyl-Lewis x ), CD43, and CD44 ( HCAM ) on the total CD34+ population was maintained, and the surface expression of CD49d ( VLA-4 ),
CD54 ( ICAM ), CD58, and CD62L ( L selectin )
increased after ex vivo expansion ... Despite the high level of cellular activation and proliferation induced by PMVEC coculture, the surface expression of adhesion molecules
CD11a ( LFA-1 ), CD11b, CD15s ( sialyl-Lewis x ), CD43, and CD44 ( HCAM ) on the total CD34+ population was maintained, and the surface expression of CD49d ( VLA-4 ), CD54 (
ICAM ), CD58, and CD62L ( L selectin )
increased after ex vivo expansion
Speer et al., Am J Obstet Gynecol 2002
:
Nicotine exerts inhibitory
effects on both endothelial cell surface
intercellular adhesion molecule expression and neutrophil integrin expressions of CD62L,
CD11a , and CD11b in vitro
Descamps et al., Ann Dermatol Venereol 2006
(Psoriasis) :
Binding of efalizumab to
CD11a prevents binding of LFA-1 to
ICAM-1 , thus inhibiting several steps in the immunological process responsible for formation of psoriatic plaque ( activation of naive T lymphocytes to memory T lymphocytes, lymphocyte migration and reactivation of T lymphocytes in skin )
Ren et al., Zhongguo Shi Yan Xue Ye Xue Za Zhi 2008
:
Confocal microscopy and FACS assay showed that blocking
CD11a and
CD54 could
inhibit exosome targeted DC and DC-embedded exosomes
Altomonte et al., Cancer Res 1993
(Melanoma) :
CD11a and CD2 were not
detected on melanoma cells while
CD54 and CD58 were coexpressed on the majority of the melanoma cell populations investigated
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 )