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CD11b Antibody [F15D4]

Cat.No.: F0040

Application: Reactivity: Mouse

Usage Information

Dilution
IHC1:100 FCM1:4000

Application
IP, IHC, FCM

Reactivity
Mouse

Source
Rat Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
165-170 kDa

Datasheet & SDS

Biological Description

Specificity
CD11b Antibody [F15D4] detects endogenous levels of total CD11b protein.

Clone
F15D4

Synonym(s)
CD11 antigen-like family member B; CD11B (p170); cell surface glycoprotein MAC-1 alpha subunit; cell surface glycoprotein MAC-1 subunit alpha; complement component receptor 3 alpha-a; Mac1A; Cd11b; CD11b/CD18; CR3; CR3A; F730045J24Rik; Ly-40; Mac-1; Mac-1a; MAC1

Background
CD11b, also known as integrin alpha M (ITGAM), is a transmembrane alpha chain protein that non-covalently heterodimerizes with the beta-2 chain CD18 to form the Mac-1 (αMβ2 or CR3) integrin, which is prominently expressed on myeloid cells such as neutrophils, monocytes, macrophages, and dendritic cells, serving as a key marker for these innate immune populations. This integrin contains a β-propeller domain and a ligand-binding inserted (I/A) domain in its alpha subunit, allowing interactions with diverse ligands including iC3b, ICAM-1, and fibrinogen. Disease-associated ITGAM variants such as R77H (rs1143679), P1146S (rs1143678), and A858V (rs1143683) subtly alter the β-propeller structure, reducing ligand affinity without significantly affecting surface expression. CD11b mediates proinflammatory processes like leukocyte adhesion, migration, transmigration, and phagocytosis of opsonized particles (apoptotic cells and immune complexes), while also exerting important anti-inflammatory effects by negatively regulating Toll-like receptor (TLR) signaling, via Src/Syk-mediated phosphorylation and Cbl-b-dependent ubiquitination and degradation of MyD88 and TRIF, to suppress NF-κB activation and proinflammatory cytokine production (IL-6, TNF-α, IL-1β). CD11b also curtails type I interferon (IFN-I) production through an AKT/FOXO3/IRF3/7 pathway, maintaining nuclear FOXO3 to repress IRF7 and IFN-β/IRF7 expression; this mechanism is defective in ITGAM variant carriers, leading to elevated basal IFN-I, uncontrolled TLR responses, impaired B-cell tolerance, enhanced autoreactive B-cell activation, and increased Th17 differentiation. These immune dysregulations confer a high genetic risk for systemic lupus erythematosus (SLE) and lupus nephritis (LN), with ITGAM variants being associated with higher IFN-I serum levels, renal involvement, autoantibody production, glomerular injury, and poor immune complex clearance.

Background

CD11b, also known as integrin alpha M (ITGAM), is a transmembrane alpha chain protein that non-covalently heterodimerizes with the beta-2 chain CD18 to form the Mac-1 (αMβ2 or CR3) integrin, which is prominently expressed on myeloid cells such as neutrophils, monocytes, macrophages, and dendritic cells, serving as a key marker for these innate immune populations. This integrin contains a β-propeller domain and a ligand-binding inserted (I/A) domain in its alpha subunit, allowing interactions with diverse ligands including iC3b, ICAM-1, and fibrinogen. Disease-associated ITGAM variants such as R77H (rs1143679), P1146S (rs1143678), and A858V (rs1143683) subtly alter the β-propeller structure, reducing ligand affinity without significantly affecting surface expression. CD11b mediates proinflammatory processes like leukocyte adhesion, migration, transmigration, and phagocytosis of opsonized particles (apoptotic cells and immune complexes), while also exerting important anti-inflammatory effects by negatively regulating Toll-like receptor (TLR) signaling, via Src/Syk-mediated phosphorylation and Cbl-b-dependent ubiquitination and degradation of MyD88 and TRIF, to suppress NF-κB activation and proinflammatory cytokine production (IL-6, TNF-α, IL-1β). CD11b also curtails type I interferon (IFN-I) production through an AKT/FOXO3/IRF3/7 pathway, maintaining nuclear FOXO3 to repress IRF7 and IFN-β/IRF7 expression; this mechanism is defective in ITGAM variant carriers, leading to elevated basal IFN-I, uncontrolled TLR responses, impaired B-cell tolerance, enhanced autoreactive B-cell activation, and increased Th17 differentiation. These immune dysregulations confer a high genetic risk for systemic lupus erythematosus (SLE) and lupus nephritis (LN), with ITGAM variants being associated with higher IFN-I serum levels, renal involvement, autoantibody production, glomerular injury, and poor immune complex clearance.

References
https://pubmed.ncbi.nlm.nih.gov/30568188/ https://pubmed.ncbi.nlm.nih.gov/16857989/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%