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Recombinant Mouse Integrin alpha M beta 2 Protein, CF 50 UG

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產(chǎn)品介紹

    基本參數(shù)

    詳細(xì)說明

    • Purity

      >95%, by SDS-PAGE with silver staining

    • Endotoxin Level

      <0.01 EU per 1 μg of the protein by the LAL method.  

    • Activity

      Measured by the ability of the immobilized protein to support the adhesion of CHO Chinese hamster ovary cells transfected with ICAM-1. The ED    50 for this effect is 0.4-1.6 μg/mL.

    • Source

      Chinese Hamster Ovary cell line, CHO-derived

      Mouse Integrin alpha M
      (Phe17-Asn1105)
      Accession # NP_032427
      His-ProGGGSGGGSAcidic Tail6-His tag
      Mouse Integrin beta 2
      (Gln24-Asn702)
      Accession # P11835
      His-ProGGGSGGGSBasic Tail
      N-terminus


      C-terminus
    • Accession #

    • N-terminal Sequence    
      Analysis

      Phe17 (Integrin alpha M) & Gln24 predicted, No results obtained: sequencing might be blocked (Integrin beta 2)

    • Structure / Form

      Noncovalently-linked heterodimer

    • Predicted Molecular Mass

      130 kDa (Integrin alpha M) & 83 kDa (Integrin beta 2)

    • SDS-PAGE

      155-180 kDa & 95-105 kDa, reducing conditions

    7959-AM

     

    Formulation Lyophilized from a 0.2 μm filtered solution in PBS.


    Reconstitution Reconstitute at 400 μg/mL in PBS.



    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  alpha M beta 2, also called MAC?1 or complement receptor type 3 (CR3), is one of three leukocyte  beta 2 integrins. The non?covalent heterodimer of 170 kDa alpha M/CD11b and 95 kDa beta 2/CD18 integrin subunits is expressed mainly on myeloid and natural killer cells (1?6). The alpha M vWFA or I?domain, which contains adhesion sites, forms the N?terminal head region with the alpha M beta ?propeller and the beta 2 vWFA domain. Unlike most integrins, the calf domain of alpha M is lectin?like and binds carbohydrates (7). Each subunit has a transmembrane sequence and a short cytoplasmic tail. The 1089 amino acid (aa) mouse alpha M/CD11b ECD shares 87% aa sequence identity with rat, and 70?74% with human, equine, bovine, feline, and canine  alpha M ECD. A potential mouse alpha M isoform lacks 117 aa within the beta ?propeller. The 679 aa mouse  beta 2/CD18 ECD shares 91% aa sequence identity with rat, and 80?82% with human, bovine, canine, and porcine beta 2 ECD. Like other integrins, alpha M beta 2 has multiple activation states (1?3). In the presence of divalent cations and "inside?out" signaling, alpha M beta 2 is fully active and extended. In the inactive state, the heterodimer flexes in the center at the alpha M thigh and calf domains and beta 2 I?EGF domains, impeding access to adhesion sites. Active alpha M beta 2 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). alpha M beta 2 lectin-like adhesion partners include heparin, bacterial lipopolysaccharides, and GPI?linked glycoproteins such as uPAR and Fc gamma RIIIB (3, 7). Binding of platelet JAM?C links platelets with myeloid and dendritic cell (DC) alpha M beta 2 and recruits these cells to inflamed or injured endothelium, while neutrophil alpha M beta 2 adheres to RAGE on inflamed endothelium; both are atherogenic events (3, 8, 9). However, activation of alpha M beta 2 inhibits alternative activation of macrophages and atherosclerotic foam cell formation (3, 10). alpha M beta 2 can either suppress or allow constitutive neutrophil apoptosis, depending on its ligand and activation state (3, 11, 12). Deletion of mouse  alpha M causes defects in neutrophil adhesion and degranulation, while mutations of human or mouse  beta 2 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. Pytela, R. (1988) EMBO J. 7:1371.

      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)

    • Alternate Names:

      Integrin alpha M beta 2








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