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Intercellular adhesion molecule 2

ICAM-2, CD102, intercellular adhesion molecule-2
The protein encoded by this gene is a member of the intercellular adhesion molecule (ICAM) family. All ICAM proteins are type I transmembrane glycoproteins, contain 2-9 immunoglobulin-like C2-type domains, and bind to the leukocyte adhesion LFA-1 protein. This protein may play a role in lymphocyte recirculation by blocking LFA-1-dependent cell adhesion. It mediates adhesive interactions important for antigen-specific immune response, NK-cell mediated clearance, lymphocyte recirculation, and other cellular interactions important for immune response and surveillance. Several transcript variants encoding the same protein have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Intercellular Adhesion Molecule-1, CD11b, ICAM-3, Vascular Cell Adhesion Molecule-1, CAN
Papers on ICAM-2
Inhibition of complement component C5 prevents clotting in an ex vivo model of xenogeneic activation of coagulation.
Tiede et al., Hannover, Germany. In Xenotransplantation, Feb 2016
The activation of PAEC (E-Selectin, tissue factor, ICAM-1, ICAM-2, VCAM-1) was studied after incubation with human serum.
PI3Kδ promotes CD4(+) T cell interactions with antigen presenting cells by increasing LFA-1 binding to ICAM-1.
Okkenhaug et al., Cambridge, United Kingdom. In Immunol Cell Biol, Feb 2016
Activation of the T cells increases the binding of the integrin LFA-1 expressed by T cells to ICAM-1 and ICAM-2 expressed by APCs.
Chemoattractant Signals and Adhesion Molecules Promoting Human Regulatory T Cell Recruitment to Porcine Endothelium.
Seebach et al., Genève, Switzerland. In Transplantation, Jan 2016
Under static conditions, transendothelial Treg migration was inhibited by blocking integrin sub-units (CD18, CD49d) on huTreg, or their respective porcine ligands intercellular adhesion molecule 2 (CD102) and vascular cell adhesion molecule 1 (CD106).
Association Between Intercellular Adhesion Molecule (Icam)-1, -2, -3 Plasma Levels and Disease Activity Of Ankylosing Spondylitis in The Chinese Han Population.
Wan et al., Zhengzhou, China. In Spine (phila Pa 1976), Jan 2016
RESULTS: Both ICAM-1 and ICAM-2 levels in plasma were markedly increased in AS patients compared to levels in the plasma of controls.
The physiological roles of ICAM-1 and ICAM-2 in neutrophil migration into tissues.
Enzmann et al., Bern, Switzerland. In Curr Opin Hematol, 2015
Endothelial intercellular cell adhesion molecule (ICAM)-1 and ICAM-2, in conjunction with ICAM-1 on pericytes, critically contribute to each step.
p53 siRNA - a therapeutic tool with significant implication in the modulation of apoptosis and angiogenic pathways.
Berindan-Neagoe et al., Cluj-Napoca / Kolozsvár, Romania. In Clujul Med, 2014
The downregulation of p53, PTEN, TNFα, NFkB, BCL-2, ICAM-2, VEGF, and FGFb was evidenced as response to p53 inhibition.
Intercellular adhesion molecules (ICAMs) and spermatogenesis.
Cheng et al., New York City, United States. In Hum Reprod Update, 2013
RESULTS: Members of the ICAM family, namely ICAM-1 and ICAM-2, and the biologically active soluble ICAM-1 (sICAM-1) are the likely regulatory molecules that co-ordinate these events.
CXCL17 and ICAM2 are associated with a potential anti-tumor immune response in early intraepithelial stages of human pancreatic carcinogenesis.
Kanai et al., Tokyo, Japan. In Gastroenterology, 2011
Immune surveillance occurs during the early intraepithelial stages of human pancreatic carcinogenesis and is mediated by expression of CXCL17 and ICAM2.
Differential roles for endothelial ICAM-1, ICAM-2, and VCAM-1 in shear-resistant T cell arrest, polarization, and directed crawling on blood-brain barrier endothelium.
Lyck et al., Bern, Switzerland. In J Immunol, 2010
a sequential involvement of endothelial ICAM-1 and VCAM-1 in mediating shear-resistant T cell arrest, followed by endothelial ICAM-1 and ICAM-2 in mediating T cell crawling to sites permissive for diapedesis across BBB endothelium.
C-type lectin DC-SIGN: an adhesion, signalling and antigen-uptake molecule that guides dendritic cells in immunity.
Obermajer et al., Ljubljana, Slovenia. In Cell Signal, 2010
Besides being an adhesion molecule, particularly in binding ICAM-2 and ICAM-3, it is also crucial in recognizing several endogenous and exogenous antigens.
Comprehensive analysis of lymph node stroma-expressed Ig superfamily members reveals redundant and nonredundant roles for ICAM-1, ICAM-2, and VCAM-1 in lymphocyte homing.
Stein et al., Bern, Switzerland. In Blood, 2010
unique role for ICAM-1 in intraluminal lymphocyte crawling but redundant roles for ICAM-1 and ICAM-2 in lymphocyte diapedesis and interstitial motility
The sequential expression of CD40 and Icam2 defines progressive steps in the formation of blood precursors from the mesoderm germ layer.
Kouskoff et al., Manchester, United Kingdom. In Stem Cells, 2010
show that the sequential expression of CD40 and Icam2 delineate a transition in the acquisition of the blood potential from hemangioblast to hemogenic endothelium leading to the formation of primitive and definitive hematopoietic progenitors.
Altered expression of glycoproteins on the cell surface of Jurkat cells during etoposide-induced apoptosis: shedding and intracellular translocation of glycoproteins.
Matsumoto et al., Funabashi, Japan. In Biochim Biophys Acta, 2009
Data show that The cell surface expression levels of (ICAM)-2 and -3 on the apoptotic cells were markedly lower, while those of calnexin, calreticulin, and (LAMP)-1 and -2 were significantly higher compared to non-apoptotic cells.
DC-SIGN: binding receptors for hepatitis C virus.
Zhou et al., Xi'an, China. In Chin Med J (engl), 2004
RESULTS: DC-SIGN, a dendritic cell-specific adhesion receptor and a type II transmembrane mannose-binding C-type lectin, is very important in the function of dendritic cells (DC), both in mediating naïve T cell interactions through ICAM-3 and as a rolling receptor that mediates the DC-specific ICAM-2-dependent migration processes.
DC-SIGN: binding receptor for HCV?
Zhou et al., Xi'an, China. In World J Gastroenterol, 2004
DC-SIGN, a dendritic Cell-specific adhesion receptor and a type II transmembrane mannose-binding C-type lectin, is very important in the function of DC, both in mediating naive T cell interactions through ICAM-3 and as a rolling receptor that mediates the DC-specific ICAM-2-dependent migration processes.
Locomotion of monocytes on endothelium is a critical step during extravasation.
Muller et al., New York City, United States. In Nat Immunol, 2004
Blocking CD11a-CD18 and CD11b-CD18 on human monocytes or adhesion molecules ICAM-1 and ICAM-2 on endothelial cells prevented the monocytes from reaching junctions.
Activation of the PKB/AKT pathway by ICAM-2.
Lorens et al., Stanford, United States. In Immunity, 2002
We identified intracellular adhesion molecule-2 (ICAM-2) in a genetic screen as an activator of the PI3K/AKT pathway leading to inhibition of apoptosis.
DC-SIGN-ICAM-2 interaction mediates dendritic cell trafficking.
van Kooyk et al., Nijmegen, Netherlands. In Nat Immunol, 2000
We now show that DC-SIGN, a DC-specific C-type lectin, supports tethering and rolling of DC-SIGN-positive cells on the vascular ligand ICAM-2 under shear flow, a prerequisite for emigration from blood.
FOG-2, a cofactor for GATA transcription factors, is essential for heart morphogenesis and development of coronary vessels from epicardium.
Orkin et al., Boston, United States. In Cell, 2000
Despite formation of an intact epicardial layer and expression of epicardium-specific genes, markers of cardiac vessel development (ICAM-2 and FLK-1) are not detected, indicative of failure to activate their expression and/or to initiate the epithelial to mesenchymal transformation of epicardial cells.
Prolonged eosinophil accumulation in allergic lung interstitium of ICAM-2 deficient mice results in extended hyperresponsiveness.
Gutierrez-Ramos et al., Cambridge, United States. In Immunity, 1999
ICAM-2-deficient mice exhibit prolonged accumulation of eosinophils in lung interstitium concomitant with a delayed increase in eosinophil numbers in the airway lumen during the development of allergic lung inflammation.
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