Recombinant Human Integrin alpha M beta 2 Protein, CF

R&D Systems, part of Bio-Techne | Catalog # 4047-AM

R&D Systems, part of Bio-Techne
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4047-AM-050
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Key Product Details

Source

CHO

Accession #

NP_001139280 (Integrin alphaM) & P05107 (Integrin beta2)

Conjugate

Unconjugated

Applications

Bioactivity

View all Integrin alpha M beta 2 Proteins and Enzymes »

Product Specifications

Source

Chinese Hamster Ovary cell line, CHO-derived human Integrin alpha M beta 2 protein
Human Integrin alphaM
(Phe17-Asn1105)
Accession # NP_001139280		 acidic tail
Human Integrin beta2
(Gln23-Asn700)
Accession # P05107		 basic tail
N-terminus C-terminus

Purity

>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.

Endotoxin Level

<1.0 EU per 1 μg of the protein by the LAL method.

N-terminal Sequence Analysis

Phe17 (Integrin alphaM) & No results obtained: Gln23 predicted (Integrin beta2)

Predicted Molecular Mass

124.7 kDa (Integrin alphaM), 79 kDa (Integrin beta2)

SDS-PAGE

165 kDa and 100 kDa, reducing conditions

Activity

Measured by the ability of the immobilized protein to support the adhesion of CHO Chinese hamster ovary cells transfected with ICAM-1.
The ED50 for this effect is 0.25-1.5 μg/mL.

Formulation, Preparation and Storage

4047-AM
Formulation Lyophilized from a 0.2 μm filtered solution in Tris, NaCl and MgCl2.
Reconstitution
Reconstitute at 100 μg/mL in sterile PBS.

Reconstitution Buffer Available:
Size / Price
Qty
Shipping The product is shipped at ambient temperature. 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, 2 to 8 °C under sterile conditions after reconstitution.
  • 3 months, -20 to -70 °C under sterile conditions after reconstitution.

Background: Integrin alpha M beta 2

Integrin alphaM beta2, also called MAC-1 or complement receptor type 3 (CR3), is one of three leukocyte beta2 integrins. The non-covalent heterodimer of 170 kDa alphaM/CD11b and 95 kDa beta2/CD18 integrin subunits is expressed mainly on myeloid and natural killer cells (1-6). The alphaM vWFA or I-domain, which contains adhesion sites, forms the N-terminal head region with the alphaM beta-propeller and the beta2 vWFA domain. Unlike most integrins, the calf domain of alphaM is lectin-like and binds carbohydrates (7). Each subunit has a transmembrane sequence and a short cytoplasmic tail. The 1088 amino acid (aa) human alphaM/CD11b ECD shares 73-76% aa sequence identity with mouse, rat, bovine, and canine alphaM, while the 678 aa human beta2/CD18 ECD shares 81 - 83% aa sequence identity with mouse, rat, bovine, canine, goat, sheep, and porcine beta2. Like other integrins, alphaM beta2 has multiple activation states (1-3). In the presence of divalent cations and "inside-out" signaling, alphaM beta2 is fully active and extended. In the inactive state, the heterodimer flexes in the center at the alphaM thigh and calf domains and beta2 I-EGF domains, impeding access to adhesion sites. Active alphaM beta2 binds an unusually large number of adhesion partners, including the complement opsonin fragment iC3b, coagulation proteins fibrinogen, plasminogen and factor X, extracellular matrix (ECM) proteins fibronectin, laminin and collagen, and cell surface ICAMs, myelin basic protein and DC-SIGN (3, 4, 7). alphaM beta2 lectin-like adhesion partners include heparin, bacterial lipopolysaccharides, and GPI-linked glycoproteins such as uPAR and Fc gammaRIIIB (3, 7). Binding of platelet JAM-C links platelets with myeloid and dendritic cell (DC) alphaM beta2 and recruits these cells to inflamed or injured endothelium, while neutrophil alphaM beta2 adheres to RAGE on inflamed endothelium; both are atherogenic events (3, 8, 9). However, activation of alphaM beta2 inhibits alternative activation of macrophages and atherosclerotic foam cell formation (3, 10). alphaM beta2 can either suppress or allow constitutive neutrophil apoptosis, depending on its ligand and activation state (3, 11, 12). Deletion of mouse alphaM causes defects in neutrophil adhesion and degranulation, while mutations of human or mouse beta2 cause leukocyte adhesion deficiency (LAD-1) and susceptibility to bacterial infections (3, 12, 13).

References

  1. Takada, Y. et al. (2007) Genome Biol. 8:215.
  2. Luo, B-H. et al. (2007) Annu. Rev. Immunol. 25:619.
  3. Tan, S.M. (2012) Biosci. Rep. 32:241.
  4. Corbi, A.L. et al. (1988) J. Biol. Chem. 263:12403.
  5. Kishimoto, T. K. et al. (1987) Cell 48:681.
  6. Muto, S. et al. (1993) J. Clin. Immunol. 13:175.
  7. Xia, Y. et al. (2002) J. Immunol. 169:6417.
  8. Santoso, S. et al. (2002) J. Exp. Med. 196:679.
  9. Langer, H.F. et al. (2007) Arterioscler. Thromb. Vasc. Biol. 27:1463.
  10. Yakubenko, V.P. et al. (2011) Circ. Res. 108:544.
  11. Pluskota, E. et al. (2008) J. Immunol. 181:3609.
  12. Coxon, A. et al. (1996) Immunity 5:653.
  13. Lu, H. et al. (1997) J. Clin. Invest. 99:1340.

Entrez Gene IDs

3684 (Human)

Gene Symbol

ITGAM

UniProt

NP_001139280 (Integrin alphaM) & P05107 (Integrin beta2)

Additional Integrin alpha M beta 2 Products

Product Documents for Recombinant Human Integrin alpha M beta 2 Protein, CF

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Product Specific Notices for Recombinant Human Integrin alpha M beta 2 Protein, CF

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