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Anti-Complement C3d Antibody LS-C44975

Catalog Size Price
LS-C44975-100 100 µl (1 mg/ml) Unavailable

Related Products

8 Complement C3d Antibodies

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Immunohistochemistry Image
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100% Guaranteed
Mouse Monoclonal (IgG1) to Human Complement C3d
Human
IHC - Frozen, Western blot, Flow Cytometry, ELISA
Unconjugated

Details

Human Complement C3d
Mouse
Human (tested or 100% immunogen sequence identity)
IgG1 Monoclonal
Unconjugated
Protein A purified
Unmodified

Applications

  • IHC - Frozen
  • Western blot (1:5000)
  • Flow Cytometry
  • ELISA

Specificity and Use

Complement C3d antibody was raised against purified C3d from human plasma.
Specific for human complement component 3d (C3d), a 33kD polypeptide fragment generated over the course of complement activation where complement 3 (C3) convertases cleave C3 to C3b, which is further degraded into iC3b and C3dg/C3d. C3d is involved in the regulation of many aspects of the immune response, including antigen processing and presentation. The C3d/antigen complex mediates B cell activation by simultaneously binding antigen-specific surface bound immunoglobulin and CD21, lowering the complement activation threshold. C3 is crucial in the induction of tolerance generated when an antigen is introduced into immunoprivileged sites and this is exploited by pathogens and cancer cells to evade the immune system by inhibiting complement activation.

Packaging

Borate buffered saline, 0.1% sodium azide.
Short term 4°C, long term aliquot and store at -20°C, avoid freeze thaw cycles. Store undiluted.
For research use only.

About Complement C3d

Complement C3 plays a central role in the activation of complement system. Its activation is required for both classical and alternative complement activation pathways. One form of C3-convertase, also known as C4b2a, is formed by a heterodimer of activated forms of C4 and C2. It catalyzes the proteolytic cleavage of C3 into C3a and C3b, generated during activation through the classical pathway as well as the lectin pathway.

Requested From: 
Date Requested: 8/18/2017

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