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Human Complement Component C5/C5a Antibody

Catalog #: AF2037
3 Citations Datasheet / COA / SDS
Catalog # Availability Size / Price Qty
AF2037
AF2037-SP
N-Acetyl-beta -D-Glucosamini-dase Release Induced by Complement Component C5a and Neutralization by Human Complement Component C5a Antibody.
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Citations (3)
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Summary Data Examples Preparation and Storage Reconstitution Calculator Background Product Datasheets Related Research Areas

Human Complement Component C5/C5a Antibody Summary

Species Reactivity
Human
Specificity
Detects human Complement Component C5/C5a in direct ELISAs and Western blots. In Western blots, approximately 5% cross-reactivity with recombinant mouse Complement Component C5a is observed.
Source
Polyclonal Goat IgG
Purification
Antigen Affinity-purified
Immunogen
E. coli-derived recombinant human Complement Component C5a
Thr678-Arg751
Accession # P01031
Formulation
Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied either lyophilized or as a 0.2 µm filtered solution in PBS.
Endotoxin Level
<0.10 EU per 1 μg of the antibody by the LAL method.
Label
Unconjugated

Applications

Recommended Concentration
Sample
Western Blot
0.1 µg/mL
Recombinant Human Complement Component C5a (Catalog # 2037-C5)
Neutralization
Measured by its ability to neutralize Complement ComponentC5a-induced N-acetyl-beta -D-glucosaminidase release in the dibutyryl cyclic-AMPdifferentiated U937 human histiocytic lymphoma cell line. Gerard, NP and Gerard, C. (1990) Biochemistry29:9274. The Neutralization Dose (ND50) istypically 0.15-0.75 μg/mL in the presence of 15 ng/mL Recombinant HumanComplement Component C5a and cytochalasin‑B.

Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.

Scientific Data

Neutralization N-Acetyl-beta -D-Glucosamini-dase Release Induced by Complement Component C5a and Neutralization by Human Complement Component C5a Antibody. View Larger

N-Acetyl-beta -D-Glucosamini-dase Release Induced by Complement Component C5a and Neutralization by Human Complement Component C5a Antibody. Recombinant Human Complement Component C5a (Catalog # 2037-C5) induces N-acetyl- beta -D-glucosaminidase release in the the dibutyryl cyclic-AMP differentiated U937 human histiocytic lymphoma cell line in a dose-dependent manner (orange line). N-Acetyl-beta -D-Glucosamin-idase Release elicited by Recombinant Human Complement Component C5a (15 ng/mL) is neutralized (green line) by increasing concen-trations of Goat Anti-Human Complement Component C5a Antigen Affinity-purified Polyclonal Antibody (Catalog # AF2037). The ND50 is typically 0.15-0.75 µg/mL in the presence of cytochalasin-B.

Reconstitution Calculator

Reconstitution Calculator

The reconstitution calculator allows you to quickly calculate the volume of a reagent to reconstitute your vial. Simply enter the mass of reagent and the target concentration and the calculator will determine the rest.

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Preparation and Storage

Reconstitution
Reconstitute at 0.2 mg/mL in sterile PBS.
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Shipping
Lyophilized product is shipped at ambient temperature. Liquid small pack size (-SP) is shipped with polar packs. Upon receipt, store 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.
  • 6 months, -20 to -70 °C under sterile conditions after reconstitution.

Background: Complement Component C5/C5a

Human complement 5a (C5a) is an enzymatically generated glycoprotein that belongs to a family of structurally and functionally related proteins known as anaphylatoxins. C5a is a 74 amino acid (aa) peptide that is created by the activity of C5a convertase on the C5 alpha -chain (1, 2). Human C5a has four alpha -helices plus three intrachain disulfide bonds that create a triple loop structure (3). In serum, proteolytic processing removes the C-terminal arginine, creating a low activity C5adesArg74 molecule (1). Human C5a is 60% and 54% aa identical to mouse and rat C5a, respectively. C5a binds to a signaling G-protein coupled receptor (C5aR/CD88) and a nonsignaling GPCR termed C5L2 (4). Activation of Cd88 results in neutrophil chemotaxis and endothelial cell activation (1, 5). It also triggers an oxidative burst in macrophages and neutrophils, and induces release of histamine in basophils and mast cells.

References
  1. Gerard, C. and N.P. Gerard (1994) Annu. Rev. Immunol. 12:775.
  2. DiScipio, R.G. et al. (1983) J. Biol. Chem. 258:10629.
  3. Huber-Lang, M.S. et al. (2003) J. Immunol. 170:6115.
  4. Okinaga, S. et al. (2003) Biochemistry 42:9406.
  5. Gerard, N.P. and C. Gerard (2002) Curr. Opin. Immunol. 14:705.
Entrez Gene IDs
727 (Human); 15139 (Mouse)
Alternate Names
C5; C5a;C5b;C5D;Complement C5;CPAMD4;ECLZB; Complement Component C5/C5a

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Citations for Human Complement Component C5/C5a Antibody

R&D Systems personnel manually curate a database that contains references using R&D Systems products. The data collected includes not only links to publications in PubMed, but also provides information about sample types, species, and experimental conditions.

3 Citations: Showing 1 - 3
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  1. Sexual dimorphism of liver metastasis by murine pancreatic neuroendocrine tumors is affected by expression of complement C5
    Oncotarget, 2016-05-24;7(21):30585-96.
    Species: Human
    Sample Types: Cell Lysates
    Applications: Western Blot
  2. Production of C5a by ASP, a serine protease released from Aeromonas sobria.
    Authors: Nitta H, Imamura T, Wada Y, Irie A, Kobayashi H, Okamoto K, Baba H
    J. Immunol., 2008-09-01;181(5):3602-8.
    Species: Human
    Sample Types: Plasma
    Applications: Western Blot
  3. Absent C3a and C5a receptor signaling into CD4+ T cells enables auto-inductive TGF-beta 1 signaling and induction of Foxp3+ T regulatory cells
    Authors: Michael G. Strainic, Ethan M. Shevach, Fengqi An, Feng Lin, M. Edward Medof
    Nature Immunology

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