Rat Plasma.
Complement C3, C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1, C3, CPAMD1.
Sterile filtered solution.
Greater than 95.0% as determined by SDS-PAGE.
Rat Complement C3 produced in Rat plasma having a molecular weight of 187kDa.
Complement component 3 (C3) plays a critical role in the activation of the complement system, a vital part of the innate immune response. The complement system can be activated through three pathways, all of which converge on C3. Activation of each pathway leads to the formation of enzyme complexes on the target surface. These enzymes cleave C3, releasing the anaphylatoxin C3a and generating activated C3b. The majority of activated C3 does not bind to the target surface because its thioester group reacts with water, forming fluid-phase C3b, which is rapidly inactivated by factors H and I, resulting in iC3b. Surface-bound C3b is essential for all three pathways to effectively activate C5 and subsequently form the membrane attack complex (MAC, C5b-9), which lyses the target cell membrane.
Rat Complement C3 is purified from rat plasma and has a molecular weight of 187 kDa.
Sterile filtered liquid.
C3 solution is supplied in phosphate buffered saline (PBS).
C3 Rat is stable for 2-4 weeks at 4°C. For long-term storage, freeze at -20°C or colder. Addition of a carrier protein (0.1% HSA or BSA) is recommended for long-term storage. Avoid repeated freeze-thaw cycles.
Purity is determined to be greater than 95.0% by SDS-PAGE analysis.
Complement C3, C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1, C3, CPAMD1.
Rat Plasma.
Complement C3 is a large protein composed of 1663 amino acids . It is synthesized primarily in the liver and then secreted into the bloodstream. The protein exists in an inactive form until it is cleaved by proteolytic enzymes known as C3 convertases. This cleavage results in the formation of two fragments: C3a and C3b .
Classical Pathway: This pathway is initiated by the binding of antibodies to antigens on the surface of pathogens. The antibody-antigen complex then interacts with the C1 complex, leading to the activation of C3 convertase, which cleaves C3 into C3a and C3b .
Alternative Pathway: This pathway is activated directly on the surface of pathogens without the need for antibodies. It involves the spontaneous hydrolysis of C3, forming C3(H2O), which then interacts with factor B and factor D to form C3 convertase .
Lectin Pathway: This pathway is initiated by the binding of mannose-binding lectin (MBL) to carbohydrate structures on the surface of pathogens. This binding activates MBL-associated serine proteases (MASPs), which then cleave C4 and C2 to form C3 convertase .
Complement C3 is essential for the effective functioning of the immune system. The activation of C3 leads to a cascade of events that result in the formation of the membrane attack complex (MAC), which can lyse and kill pathogens. Additionally, the fragments of C3, particularly C3b, play a critical role in enhancing phagocytosis and promoting the clearance of immune complexes and apoptotic cells .
Research on Complement C3 in rats has provided valuable insights into the functioning of the immune system and the mechanisms of immune response. Studies have shown that the complement system, including C3, is involved in various diseases and conditions, such as autoimmune diseases, infections, and inflammatory disorders .
In experimental settings, rat models are often used to study the complement system due to their physiological similarities to humans. For instance, the development of a complement C3 humanized rat model has been instrumental in evaluating the efficacy of complement inhibitors and understanding the role of C3 in human diseases .