antibody

MOUSE ANTI HUMAN iC3b (NEOANTIGEN)

MBS212912

0.1 mg

635 USD

monoclonal

mouse

nonconjugated

013III-1.16

western blot, ELISA, flow cytometry, FACS, enzyme immunoassay

Antibody

MOUSE ANTI HUMAN iC3b (NEOANTIGEN)

iC3b

complement C3; Complement C3; complement C3; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1; C3a anaphylatoxin; acylation-stimulating protein cleavage product; complement component C3; complement component C3a; complement component C3b; epididymis secretory sperm binding protein Li 62p; prepro-C3; complement component 3; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1Cleaved into the following 12 chains:Complement C3 beta chain; C3-beta-c; C3bc; Complement C3 alpha chain; C3a anaphylatoxin; Acylation stimulating protein; ASPAlternative name(s):C3adesArg

iC3b

C3; C3; ASP; C3a; C3b; AHUS5; ARMD9; CPAMD1; HEL-S-62p; CPAMD1; C3bc; ASP

CO3_HUMAN

Monoclonal

IgG2b

013III-1.16

Mouse

1663

This item recognises 42kDa human inactive complement component 3b (iC3b) neoantigen present in blood serum. Cleavage of C3b into iC3b by the protease factor I, in the presence of cofactors, changes the structure and resulting binding properties, preventing binding by complement factor B and properdin. This prevents further progression of the complement pathway, providing another mechanism by which the complement pathway may be regulated. iC3b is thought to play a role in inducing tolerance, binding complement receptor type 3 on antigen presenting cells and stimulating them to produce transforming growth factor beta2 and interleukin-10. It is thought to stimulate B-cells via the CD21 receptor providing a link between the innate and adaptive immune responses. Additionally iC3b acts as an opsonin which is recognised by complement receptor 3 expressed on leukocytes or complement receptor of the immunoglobulin superfamily (CRIg) on Kupffer cells, stimulating phagocytosis of the tagged cells. iC3b levels are often elevated in diseases such as Systemic Lupus Erythematosis and Rheumatoid arthritis.

Purified. Purified IgG - liquid

IgG concentration 1.0mg/ml

Store at 4 degree C or at -20 degree C if preferred. Storage in frost-free freezers is not recommended. This product should be stored undiluted. Avoid repeated freezing and thawing as this may denature the antibody. Should this product contain a precipitate we recommend microcentrifugation before use. Shelf Life: 18 months from date of despatch.

Immunohistology Frozen, ELISA (EIA), Flow cytometry (FC/FACS), Western Blot (WB)

Perservative Stabilisers: 0.09% Sodium Azide (NaN3) . Preparation: Purified IgG prepared by affinity chromatography on Protein A

Immunogen: Purified human iC3b. Histology Positive Control Tissue: Kidney from post streptoccal glomerulonephritis patients. Buffer Solution: Borate buffered saline. Target Species: Human

MBS212912 recognises 42kDa human inactive complement component 3b (iC3b) neoantigen present in blood serum. Cleavage of C3b into iC3b by the protease factor I, in the presence of cofactors, changes the structure and resulting binding properties, preventing binding by complement factor B and properdin. This prevents further progression of the complement pathway, providing another mechanism by which the complement pathway may be regulated. iC3b is thought to play a role in inducing tolerance, binding complement receptor type 3 on antigen presenting cells and stimulating them to produce transforming growth factor beta2 and interleukin-10. It is thought to stimulate B-cells via the CD21 receptor providing a link between the innate and adaptive immune responses. Additionally iC3b acts as an opsonin which is recognised by complement receptor 3 expressed on leukocytes or complement receptor of the immunoglobulin superfamily (CRIg) on Kupffer cells, stimulating phagocytosis of the tagged cells. iC3b levels are often elevated in diseases such as Systemic Lupus Erythematosis and Rheumatoid arthritis.

115298678

NP_000055.2

NM_000064.3

P01024

187,148 Da

Activation Of C3 And C5 Pathway (106412); Adaptive Immune System Pathway (366160); Alternative Complement Activation Pathway (106410); Chagas Disease (American Trypanosomiasis) Pathway (147809); Chagas Disease (American Trypanosomiasis) Pathway (147795); Class A/1 (Rhodopsin-like Receptors) Pathway (106357); Complement Activation, Classical Pathway (198823); Complement And Coagulation Cascades Pathway (198880); Complement And Coagulation Cascades Pathway (83073); Complement And Coagulation Cascades Pathway (484)

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. A peptide (C3a) derived from the encoded protein has antimicrobial activity, so people with C3 deficiency are susceptible to bacterial infection. [provided by RefSeq, Nov 2014]

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; Secreted; Inhibitor. 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: G-protein coupled receptor protein signaling pathway; regulation of immune response; positive regulation of angiogenesis; positive regulation of activation of membrane attack complex; positive regulation of G-protein coupled receptor protein signaling pathway; positive regulation of type IIa hypersensitivity; complement activation, alternative pathway; regulation of complement activation; innate immune response; immune response; positive regulation of protein amino acid phosphorylation; signal transduction; fatty acid metabolic process; inflammatory response; complement activation, classical pathway; complement activation. Disease: Complement Component 3 Deficiency, Autosomal Recessive; Hemolytic Uremic Syndrome, Atypical, Susceptibility To, 5; Macular Degeneration, Age-related, 9

0.1 mg

635 USD