Overview

  • Product name

    Anti-C3b / iC3b antibody [1H8]
    See all C3b / iC3b primary antibodies
  • Description

    Mouse monoclonal [1H8] to C3b / iC3b
  • Host species

    Mouse
  • Specificity

    This monoclonal binds to C3b and iC3b fragments of complement 3. C3b is deposited on the cell surface during complement activation to mark cells for destruction by opsonization. Cell-bound C3b can be degraded to iC3b and C3dg inactive forms to cease complement activation and this may be exploited by cancer cells to avoid complement-mediated destruction (PubMed IDs: 2786912, 20068220, 14978136, 12393727).

  • Tested applications

    Suitable for: WBmore details
  • Species reactivity

    Reacts with: Human
  • Immunogen

    Other Immunogen Type. C3b(i)-Sepharose. C3bi was deposited on Sepharose 4B via the alternative pathway of complement activation in normal human serum.

  • Positive control

    • WB: Human serum and plasma lysates
  • General notes

    This antibody clone is manufactured by Abcam. If you require a different buffer formulation or a particular conjugate for your experiments, please contact orders@abcam.com.

Properties

  • Form

    Liquid
  • Storage instructions

    Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
  • Storage buffer

    Preservative: 0.02% Sodium azide
    Constituent: PBS
  • Concentration information loading...
  • Purity

    Protein G purified
  • Clonality

    Monoclonal
  • Clone number

    1H8
  • Isotype

    IgG2
  • Light chain type

    kappa

Applications

Our Abpromise guarantee covers the use of ab231080 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
WB Use at an assay dependent concentration. Predicted molecular weight: 68 kDa.

Target

  • Function

    C3 plays a central role in the activation of the complement system. Its processing by C3 convertase is the central reaction in both classical and alternative complement pathways. After activation C3b can bind covalently, via its reactive thioester, to cell surface carbohydrates or immune aggregates.
    Derived from proteolytic degradation of complement C3, C3a anaphylatoxin is a mediator of local inflammatory process. In chronic inflammation, acts as a chemoattractant for neutrophils (By similarity). It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes.
    C3-beta-c: Acts as a chemoattractant for neutrophils in chronic inflammation.
    Acylation stimulating protein: adipogenic hormone that stimulates triglyceride (TG) synthesis and glucose transport in adipocytes, regulating fat storage and playing a role in postprandial TG clearance. Appears to stimulate TG synthesis via activation of the PLC, MAPK and AKT signaling pathways. Ligand for C5AR2. Promotes the phosphorylation, ARRB2-mediated internalization and recycling of C5AR2 (PubMed:8376604, PubMed:2909530, PubMed:9059512, PubMed:10432298, PubMed:15833747, PubMed:16333141, PubMed:19615750).
  • Tissue specificity

    Plasma. The acylation stimulating protein (ASP) is expressed in adipocytes and released into the plasma during both the fasting and postprandial periods.
  • Involvement in disease

    Complement component 3 deficiency
    Macular degeneration, age-related, 9
    Hemolytic uremic syndrome atypical 5
    Increased levels of C3 and its cleavage product ASP, are associated with obesity, diabetes and coronary heart disease. Short-term endurance training reduces baseline ASP levels and subsequently fat storage.
  • Sequence similarities

    Contains 1 anaphylatoxin-like domain.
    Contains 1 NTR domain.
  • Post-translational
    modifications

    C3b is rapidly split in two positions by factor I and a cofactor to form iC3b (inactivated C3b) and C3f which is released. Then iC3b is slowly cleaved (possibly by factor I) to form C3c (beta chain + alpha' chain fragment 1 + alpha' chain fragment 2), C3dg and C3f. Other proteases produce other fragments such as C3d or C3g. C3a is further processed by carboxypeptidases to release the C-terminal arginine residue generating the acylation stimulating protein (ASP). Levels of ASP are increased in adipocytes in the postprandial period and by insulin and dietary chylomicrons.
    Phosphorylated by FAM20C in the extracellular medium.
  • Cellular localization

    Secreted.
  • Information by UniProt
  • Database links

  • Alternative names

    • ASP antibody
    • C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1 antibody
    • C3 antibody
    • C3adesArg antibody
    • C3bc antibody
    • CO3_HUMAN antibody
    • Complement C3c alpha'' chain fragment 2 antibody
    see all

Images

  • All lanes :

    Lane 1 : human serum diluted 1/100
    Lane 2 : Human plasma diluted 1/100

    Lysates/proteins at 5 µl per lane.

    Performed under reducing conditions.

    Predicted band size: 68 kDa
    Observed band size: 68 kDa



    This blot was produced using a 4-12% Bis-tris gel under the MOPS buffer system. The gel was run at 200V for 55 minutes before being transferred onto a Nitrocellulose membrane at 30V for 70 minutes. The membrane was then blocked for an hour using 5% milk before being incubated with ab231080 overnight at 4°C. Antibody binding was detected using Goat anti-Rabbit IgG H&L (IRDye® 800CW) preadsorbed (ab216773) at 1/20000 dilution for 1 hour at room temperature before imaging.

References

This product has been referenced in:

  • Lindorfer MA  et al. A novel approach to preventing the hemolysis of paroxysmal nocturnal hemoglobinuria: both complement-mediated cytolysis and C3 deposition are blocked by a monoclonal antibody specific for the alternative pathway of complement. Blood 115:2283-91 (2010). Read more (PubMed: 20068220) »
  • Kennedy AD  et al. Rituximab infusion promotes rapid complement depletion and acute CD20 loss in chronic lymphocytic leukemia. J Immunol 172:3280-8 (2004). Read more (PubMed: 14978136) »
See all 4 Publications for this product

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