Mouse anti-Human Complement C3, C3d Monoclonal Antibody | anti-C3 antibody

Complement C3, C3d (Complement C3d Fragment, Complement Component C3d, C3/C3d, Complement Component 3, Complement Factor 3, CPAMD1)

Cat. Num. AAA632466

• Gene Names: C3; ASP; AHUS5; ARMD9; CPAMD1
• Reactivity: Human
• Applications: ELISA, Western Blot, Immunohistochemistry, Flow Cytometry, Functional Assay
• Purity: Affinity Purified; Purified by Protein A affinity chromatography.
• Synonyms: Complement C3; C3d; Monoclonal Antibody; C3d (Complement C3d Fragment; Complement Component C3d; C3/C3d; Complement Component 3; Complement Factor 3; CPAMD1); Anti -Complement C3; anti-C3 antibody

• Host: Mouse
• Reactivity: Human
• Clonality: Monoclonal
• Isotype: IgG1
• Clone Number: 10B388
• Specificity: Recognizes human complement component 3d (C3d) at ~33kD.
• Purity/Purification: Affinity Purified; Purified by Protein A affinity chromatography.
• Form/Format: Supplied as a liquid in borate buffered saline, 0.1% sodium azide.

• Applicable Applications for anti-C3 antibody: ELISA (EL/EIA), Western Blot (WB), Immunohistochemistry (IHC), Flow Cytometry (FC/FACS)
• Application Notes: Suitable for use in ELISA, Flow Cytometry, Immunohistochemistry and Western Blot.; Dilution: Western Blot: 1:5000; Immunohistochemistry: frozen sections
• Immunogen: Purified C3d from human plasma.
• Preparation and Storage: May be stored at 4 degree C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20 degree C. Aliquots are stable for 12 months. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Related Product Information for anti-C3 antibody

Human complement component 3d (C3d) is 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.

Product Categories/Family for anti-C3 antibody

Antibodies; Abs to Complement

NCBI and Uniprot Product Information

• NCBI GI #: 115298678
• NCBI GeneID: 718
• NCBI Accession #: NP_000055.2
• NCBI GenBank Nucleotide #: NM_000064.2
• UniProt Accession #: P01024; A7E236; Q6LDJ0
• Molecular Weight: 187,148 Da
• NCBI Official Full Name: complement C3
• NCBI Official Synonym Full Names: complement component 3
• NCBI Official Symbol: C3
• NCBI Official Synonym Symbols: ASP; AHUS5; ARMD9; CPAMD1
• NCBI Protein Information: complement C3; OTTHUMP00000197086; complement component C3; acylation-stimulating protein cleavage product; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1
• UniProt Protein Name: Complement C3
• Protein Family: Complement C3
• UniProt Gene Name: C3
• UniProt Synonym Gene Names: CPAMD1
• UniProt Entry Name: CO3_HUMAN

NCBI Description

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]

Uniprot Description

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; Secreted, signal peptide; Inhibitor

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

Cellular Component: extracellular space; extracellular region; plasma membrane

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