Anti-CD11a/LFA-1α Antibody (R7-1)
Anti-CD11a/LFA-1α Antibody (R7-1) is a kind of mouse IgG1 chimeric antibody inhibitor, targeting to human CD11a/LFA-1α. Anti-CD11a/LFA-1α Antibody (R7-1) can neutralize LFA-1α (lymphocyte function-associated antigen 1 alpha) also known as integrin alpha L chain and CD11a. Anti-CD11a/LFA-1α Antibody (R7-1) can be used for the research of inflammation.
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 IgG1 kappa
Recommend Isotype Controls
Species Reactivity
Human
IC50 & Target
CD11a/LFA-1α
In Vivo
Anti-CD11a/LFA-1α Antibody (R7-1) (1 mg/kg, i.v., 0.5 h before thioglycollate) reduces peritoneal accumulation of leukocytes in adult and neonatal rabbits 6 h after instillation of thioglycollate[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Adult and neonatal 6 h after instillation of thioglycollate[1]
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Dosage:1 mg/kg
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Administration:Intravenously injection, 0.5 h before thioglycollate
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Result:Increased blood neutrophili in adult rabbits.
Reduced peritoneal accumulation of leukocytes.
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
Functional assays; Flow cytometry
Chemical Information
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Molecular Weight 150 kDa
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SMILES
[Anti-CD11a/LFA-1aAntibody (R7-1)]
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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
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)