Anti-CD54/ICAM-1 Antibody (R6-5-D6)
Anti-CD54/ICAM-1 Antibody (R6-5-D6) is a kind of mouse IgG2a chimeric antibody inhibitor, targeting to human CD54/ICAM-1. Anti-CD54/ICAM-1 Antibody (R6-5-D6) can block CD54 binding to its ligand Lymphocyte Function-Associated Antigen 1 (LFA-1). Anti-CD54/ICAM-1 Antibody (R6-5-D6) can be used for the researches of inflammation and immunology.
For research use only. We do not sell to patients.
- Molecular Weight:150 kDa
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Isotype
Mouse IgG2a kappa
Recommend Isotype Controls
Species Reactivity
Human
IC50 & Target
CD54/ICAM-1
In Vitro
Anti-CD54/ICAM-1 Antibody (R6-5-D6) (10 μg/mL, 10 days) induces cells differentiate to Treg phenotype in human naïve CD4+ T cells[1].
Anti-CD54/ICAM-1 Antibody (R6-5-D6) (2-12 μg/mL, 15 mins) reduces baseline adherence and the enhancement caused by IL-l or LPS (HY-D1056) stimulation in human umbilical vein endothelial cells (HUVEC) [2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Gene ID
Accession
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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Product Image
Application
in vitro blocking of CD54; in vivo imaging; Functional Assays; Flow Cytometry; Immunofluorescenc
Chemical Information
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Molecular Weight 150 kDa
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SMILES
[Anti-CD54/ICAM-1 Antibody (R6-5-D6)]
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
References
[1]. Williams KM, et al. Choice of resident costimulatory molecule can influence cell fate in human naïve CD4+ T cell differentiation. Cell Immunol. 2011;271(2):418-27. [Content Brief]
[2]. Smith CW, et al. Recognition of an endothelial determinant for CD 18-dependent human neutrophil adherence and transendothelial migration. J Clin Invest. 1988 Nov;82(5):1746-56. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)