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Human F11R ELISA Kit for Sandwich ELISA - ABIN417734
Denk, Wiegner, Hönes, Messerer, Radermacher, Weiss, Kalbitz, Ehrnthaller, Braumüller, McCook, Gebhard, Weckbach, Huber-Lang: Early Detection of Junctional Adhesion Molecule-1 (JAM-1) in the Circulation after Experimental and Clinical Polytrauma. in Mediators of inflammation 2015
JAM family members differentially regulate CXCR4 (show CXCR4 ELISA Kits) function and CXCL12 (show CXCL12 ELISA Kits) secretion in the bone marrow niche.
Our observations suggest that increased expression of JAM-A promotes neoplasia of lung adenocarcinoma. In addition, an anti-JAM-A antibody efficiently reduced cell proliferation and provoked apoptosis, indicating the potential feasibility of JAM-A-inhibitory cancer therapy.
a new role for CD321 in endothelial cells
We have shown that tension on JAM-A activates RhoA (show RHOA ELISA Kits) to control cell stiffness. Phosphorylation of JAM-A at S284 is required for activation of RhoA (show RHOA ELISA Kits) and increased cell stiffness in response to tension on the protein
Using patient-derived glioblastoma cancer stem cells, we confirmed that JAM-A is suppressed by miR (show MLXIP ELISA Kits)-145
Screening of a library of human cell surface membrane proteins showed that the Hom-1 vesivirus could utilize human junctional adhesion molecule 1 as a receptor to enter cells and initiate replication.
Our results showed that APOC3 (show APOC3 ELISA Kits) was closely associated with the inflammatory process in ECs, and that this process was characterized by the increased expression of TNF-alpha (show TNF ELISA Kits). Inflammatory processes further disrupted the tight junctions (TJs) between HUVECs by causing increased expression of JAM-1.
High expression of junctional adhesion molecule-A and EphB2 (show EPHB2 ELISA Kits) can predict poor overall survival and high mortality rate, and EphB2 (show EPHB2 ELISA Kits) is an independent prognostic biomarker in lung adenocarcinoma patients.
JAM-A is one of the malignancy markers of HNSCC as well as beta-catenin (show CTNNB1 ELISA Kits) in histopathology, and the plasma-soluble JAM-A may contribute to a serum diagnosis of HNSCC. JAM-A is a promising molecular target for diagnosis and therapy in HNSCC.
F11R mrna expression was higher in rheumatoid arthritis patients, but promoter polymorphisms did not appear to be related to disease susceptibility.
Soluble JAM-A secreted from cardiac progenitor cells reduces infiltration of neutrophils after myocardial infarction and ameliorates tissue damage through prevention of excess inflammation.
JAM-A up-regulation can increase the proliferation, cytokine secretion and wound-homing ability of MSCs, thus accelerating the repair rate of full-thickness skin defects
Endothelial JAM-A but not hematopoietic JAM-A facilitates reovirus T1L bloodstream entry and egress.
Deletion of JAM-A causes a gain-of-function in platelets, with lower activation thresholds and increased inflammatory activities. This leads to an increase of plaque formation, particularly in early stages of the disease.
The F11r gene is directly regulated by retinoic acid in the embryonic mesoderm.
Redistribution of JAM-A in endothelial cells after stimulation with pro-atherogenic oxidized lipoproteins results in increased transmigration of mononuclear cells.
JAM-A has a prominent role in regulating leukocyte infiltration after brain I/R injury and could be a new target in limiting post-ischemic inflammation.
JAM-A regulates epithelial permeability via association with ZO-2 (show TJP2 ELISA Kits), afadin (show MLLT4 ELISA Kits), and PDZ-GEF1 (show RAPGEF2 ELISA Kits) to activate Rap2c (show RAP2C ELISA Kits) and control contraction of the apical cytoskeleton.
Cancer stem cells selectively express JAM-A, which regulates self-renewal.
These studies establish F11R as a novel monocyte prognostic marker for GBM critical for defining a subpopulation of stromal cells for future potential therapeutic intervention.
Tight junctions represent one mode of cell-to-cell adhesion in epithelial or endothelial cell sheets, forming continuous seals around cells and serving as a physical barrier to prevent solutes and water from passing freely through the paracellular space. The protein encoded by this immunoglobulin superfamily gene member is an important regulator of tight junction assembly in epithelia. In addition, the encoded protein can act as (1) a receptor for reovirus, (2) a ligand for the integrin LFA1, involved in leukocyte transmigration, and (3) a platelet receptor. Multiple 5' alternatively spliced variants, encoding the same protein, have been identified but their biological validity has not been established.
junctional adhesion molecule 1
, junctional adhesion molecule A
, platelet F11 receptor
, platelet adhesion molecule 1
, BV11 antigen
, F11 receptor/F11R
, junction cell adhesion molecule A
, junction cell adhesion molecule1