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Recombinant mouse IgG2a isotype controls are available. Condition of sample preparation and optimal sample dilution should be determined experimentally by the investigator.
Price/availability/specifications subject to change without notice. Unless otherwise indicated, our catalog and customized products are for research use only and not intended for human or animal diagnostic or therapeutic use.
Phone: 1-617-401-8149
Fax: 1-617-606-5019
Email: message@sydlabs.com
Or leave a message with a formal purchase
order (PO) Or credit card.
Recombinant mouse IgG2a Monoclonal Antibody.
Clone: R6-5-D6.
Isotype: Mouse IgG2a Kappa.
Source:The anti-human CD54 (ICAM-1) monoclonal antibody (clone: R6-5-D6) was produced in mammalian cells.
Specificity/Sensitivity: The in vivo grade recombinant mouse monoclonal antibody (clone: R6-5-D6) specifically binds to human CD54 (ICAM-1).
Applications:ELISA, neutralization, functional assays such as bioanalytical PK and ADA assays, and those assays for studying biological pathways affected by the human CD54 (ICAM-1) protein.
Form of Antibody: 0.2 uM filtered solution, pH 7.4, no stabilizers or preservatives.
Endotoxin: < 1 EU per 1 mg of the protein by the LAL method.
Purity: >95% by SDS-PAGE under reducing conditions and HPLC.
Shipping: The in vivo grade recombinant anti-human CD54 (ICAM-1) monoclonal antibody of clone R6-5-D6 is shipped with ice pack. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage: Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70°C as supplied.
1 month from date of receipt, 2 to 8°C as supplied.
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.
Tags: anti-human CD54 (ICAM-1); anti-human CD54 (ICAM-1) R6-5-D6 mAb
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.
Tags: anti-human CD54 (ICAM-1) R6-5-D6 antibody in cancer research; anti-human CD54 (ICAM-1) R6-5-D6 antibody in vivo
For more references about Anti-human CD54 (ICAM-1) Monoclonal Antibody please contact our scientific support team with message@sydlabs.com.
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