Description

PA007577.m2a?In Vivo Grade Recombinant Anti-human CD54 (ICAM-1) Monoclonal Antibody (Clone: R6-5-D6), Mouse IgG2a Kappa

Recombinant mouse Igg2a Monoclonal Antibody.

References of Anti-Human CD54 (ICAM-1) Monoclonal Antibody (Clone: R6-5-D6)

1. Cortactin regulates the activity of small GTPases and ICAM-1 clustering in endothelium: Implications for the formation of docking structures.
Schnoor, M., et al.Tissue Barriers. 2013 Jan 1;1(1):e23862. doi: 10.4161/tisb.23862. PMID: 24665381
“Additionally, we showed that RhoG cannot be activated upon ICAM-1 stimulation without cortactin leading to defective ICAM-1 clustering, reduced leukocyte adhesion to the apical endothelial surface and subsequently to reduced leukocyte transendothelial migration. …In addition, the defects in ICAM-1-triggered RhoG activation and ICAM-1 clustering corresponded with a reduced number of firmly adherent and transmigrated neutrophils as demonstrated by intravital microscopy of the TNF-inflamed cremaster. …Neutrophil transendothelial migration has previously been shown in vitro to be regulated by cortactin in an ICAM-1-dependent fashion. …We corroborated the findings of the Luscinskas group by also showing reduced formation of ICAM-1- and cortactin-dependent ring-like structures surrounding adherent neutrophils on the endothelial surface.Citation. …Using confocal and scanning electron microscopy, both HUVEC transfected with scrambled siRNA and primary MLEC derived from WT mice were observed to form docking structures comprised of ICAM-1-enriched microvilli-like protrusions that engulfed adherent neutrophils.”

2. Cortactin deficiency is associated with reduced neutrophil recruitment but increased vascular permeability in vivo.
Schnoor, M., et al.J Exp Med. 2011 Aug 1;208(8):1721-35. doi: 10.1084/jem.20101920. PMID: 21788407
“Silencing of cortactin by small interfering RNA (siRNA) was found to inhibit transmigration of neutrophils through endothelial cell monolayers, but although this was accompanied by reduced accumulation of ICAM-1 at sites of neutrophil attachment, it did not affect adhesion of neutrophils to the endothelial cell surface. …Because ICAM-1 is the major endothelial adhesion receptor relevant for firm neutrophil binding, we tested whether cortactin would influence neutrophil transmigration via ICAM-1. …To test this hypothesis, we used mouse endothelioma cells deficient for ICAM-1 and, as a control, the same cells retransfected for ICAM-1. …Therefore, we tested whether ICAM-1 clustering would be dependent on the expression of cortactin. …To determine whether the defect in ICAM-1–triggered RhoG activation in Cttndel/del MLECs would be responsible for impaired neutrophil transmigration, we tested whether transfection of CA-RhoG would rescue the phenotype.”

For more technical references or data sheets regarding the Recombinant Anti-Human CD54 (ICAM-1) Monoclonal Antibody (Clone: R6-5-D6) formats, please contact our scientific support team at message@sydlabs.com.

In Vivo Grade Recombinant Anti-human CD54 (ICAM-1) Monoclonal Antibody (Clone: R6-5-D6), Mouse IgG2a Kappa from: In Vivo Grade Recombinant Anti-human CD54 (ICAM-1) Monoclonal Antibody (Clone: R6-5-D6), Mouse IgG2a Kappa: PA007577.m2a