http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-2005025776-A1

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classificationCPCInventive http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K38-1709
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C07K14-705
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http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C07K14-705
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K38-17
filingDate 2003-04-11^^<http://www.w3.org/2001/XMLSchema#date>
inventor http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_e70e637af8e8332bcd9e683e65489f86
publicationDate 2005-02-03^^<http://www.w3.org/2001/XMLSchema#date>
publicationNumber US-2005025776-A1
titleOfInvention JAM-1 as ligand of the beta-2 integrin LFA-1
abstract Inflammatory recruitment of leukocytes is governed by dynamic interactions of integrins with endothelial immunglobulin superfamily (IgSF) proteins. We have identified the IgSF member junctional adhesion molecule-1 (JAM-1) as a ligand of the β 2 integrin lymphocyte function-associated antigen-1 (LFA-1). Under static and physiologic flow conditions, JAM-1 contributed to LFA-1-dependent transendothelial migration of T cells and neutrophils, and also to LFA-1-mediated arrest of T cells triggered by chemokines on endothelium co-stimulated with cytokines to re-distribute JAM-1 from the tight junctions. Transfectants expressing JAM-1 supported LFA-1-mediated adhesion of leukocytes which required the membrane-proximal Ig-like domain 2 of JAM-1. Thus, JAM-1 is a counter-receptor for LFA-1 ideally situated to guide and control transmigration during leukocyte recruitment.
isCitedBy http://rdf.ncbi.nlm.nih.gov/pubchem/patent/WO-2013116941-A1
priorityDate 2002-04-12^^<http://www.w3.org/2001/XMLSchema#date>
type http://data.epo.org/linked-data/def/patent/Publication

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