Complement C3, C3a, Monoclonal Antibody

Anti -Complement C3, C3a

For Research Use Only. Not for use in diagnostic procedures.

Chromosome: 19; NC_000019.9 (6677846..6720662, complement). Location: 19p13.3-p13.2

Monoclonal

IgG1

6A526

Mouse

Reacts with an epitope on C3a. Reacts both with intact C3 as with C3a.

Affinity Purified
Purified IgG

Supplied as a liquid in PBS, containing 0.02% sodium azide and 0.1% BSA.

May be stored at 4 degree C for short-term only. For long-term storage and to avoid repeated freezing and thawing, aliquot and add glycerol (40-50%). Store at -20 degree C or colder. Aliquots are stable for at least 12 months at -20 degree C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.

Small volumes of anti-C3 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

The complement system is an important factor in innate immunity. The third complement component, C3, is central to the classical, alternative and lectin pathways of complement activation. The synthesis of C3 is tissue-specific and is modulated in response to a variety of stimulatory agents. An inherited deficiency of C3 predisposes the person to frequent assaults of bacterial infections. Proteolysis by certain enzymes results in the cleavage of C3 into C3a and C3b. C3a is a mediator of local inflammatory processes. C3a does induce smooth muscle contraction, increases vascular permeability, and causes histamine release from mast cells and basophilic leukocytes.

Antibodies; Abs to Complement

Western Blot (WB)

Can be used for Western Blot and immunoassays.
Dilution: Western Blot: 1:10

187,148 Da[Similar Products]

complement component 3

complement C3; OTTHUMP00000197086; complement component C3; acylation-stimulating protein cleavage product; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1

Complement C3

CPAMD1  [Similar Products]

CO3_HUMAN

Complement component C3 plays a central role in the activation of complement system. Its activation is required for both classical and alternative complement activation pathways. People with C3 deficiency are susceptible to bacterial infection. [provided by RefSeq]

C3: 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. Defects in C3 are the cause of complement component 3 deficiency (C3D). A rare defect of the complement classical pathway. Patients develop recurrent, severe, pyogenic infections because of ineffective opsonization of pathogens. Some patients may also develop autoimmune disorders, such as arthralgia and vasculitic rashes, lupus-like syndrome and membranoproliferative glomerulonephritis. Genetic variation in C3 is associated with susceptibility to age-related macular degeneration type 9 (ARMD9). ARMD is a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid that lie beneath the retinal pigment epithelium and within an elastin- containing structure known as Bruch membrane. Defects in C3 are a cause of susceptibility to hemolytic uremic syndrome atypical type 5 (AHUS5). An atypical form of hemolytic uremic syndrome. It is a complex genetic disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, renal failure and absence of episodes of enterocolitis and diarrhea. In contrast to typical hemolytic uremic syndrome, atypical forms have a poorer prognosis, with higher death rates and frequent progression to end-stage renal disease. Susceptibility to the development of atypical hemolytic uremic syndrome can be conferred by mutations in various components of or regulatory factors in the complement cascade system. Other genes may play a role in modifying the phenotype. 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.

Protein type: Secreted, signal peptide; Inhibitor; Secreted

Chromosomal Location of Human Ortholog: 19p13.3-p13.2

Cellular Component: extracellular space; plasma membrane; extracellular region

Molecular Function: protein binding; endopeptidase inhibitor activity; C5L2 anaphylatoxin chemotactic receptor binding; receptor binding

Biological Process: regulation of immune response; complement activation, alternative pathway; signal transduction; fatty acid metabolic process; complement activation; G-protein coupled receptor protein signaling pathway; positive regulation of angiogenesis; positive regulation of activation of membrane attack complex; positive regulation of type IIa hypersensitivity; positive regulation of G-protein coupled receptor protein signaling pathway; regulation of complement activation; innate immune response; immune response; positive regulation of protein amino acid phosphorylation; inflammatory response; complement activation, classical pathway

Disease: Complement Component 3 Deficiency, Autosomal Recessive; Hemolytic Uremic Syndrome, Atypical, Susceptibility To, 5; Macular Degeneration, Age-related, 9

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