Mouse monoclonal (KT17) antibody to C3 from Absea Biotechnology (010113E09).
|Description:||Mouse monoclonal (KT17) antibody to C3.|
|Immunogen:||Purified C3 from human blood.|
|Purification:||IgG is purified through a Protein A column.|
|Concentration:||1 mg/ml in PBS containing 0.09% sodium azide as a preservative.|
|Storage:||4 °C for 1 month, -20 °C or -80°C in aliquots. Avoid repeated freeze/thaw cycles.|
|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.|
|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: 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.
Macular degeneration, age-related, 9: A form of age-related macular degeneration, 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.
Hemolytic uremic syndrome atypical 5: 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.
|Post-Translational Modification:||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.|
|Synonyms:||Acylation stimulating protein cleavage product Antibody
acylation-stimulating protein cleavage product Antibody
C3 and PZP like alpha 2 macroglobulin domain containing protein 1 Antibody
C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1 Antibody
C3a anaphylatoxin Antibody
Complement C3 Antibody
Complement C3 alpha chain Antibody
Complement C3b alpha' chain Antibody
Complement C3c Antibody
Complement C3c alpha' chain fragment 1 Antibody
Complement C3c alpha' chain fragment 2 Antibody
Complement C3c alpha'' chain fragment 2 Antibody
Complement C3d fragment Antibody
Complement C3dg fragment Antibody
Complement C3f fragment Antibody
Complement C3g fragment Antibody
Complement component 3 Antibody
Complement component C3 Antibody
Complement component C3a Antibody
Complement component C3b Antibody
Complement factor 3 Antibody
HEL S 62p Antibody
omplement C3 beta chain Antibody
Prepro C3 Antibody
|Information:||Target information shown above is from the UniProt Consortium.|
Please Note: Anti-C3 Antibody is for research use only. It is not intended for diagnostic of therapeutic use.