C1Q Mouse
Mouse Plasma.
Component C1q, Complement C1q, Complement Component C1q, C1q.
Sterile filtered solution.
Greater than 92.0% as determined by SDS-PAGE.
Description
Mouse Complement C1Q produced in Mouse plasma having a molecular weight of 439.5kDa.
Product Specs
C1q, the initial component in the classical complement pathway, forms the C1 complex with C1r and C1s, its enzymatically active counterparts. Upon binding to immune complexes via immunoglobulins, C1 activates, triggering the C1r and C1s proteases and initiating the complement cascade. This glycoprotein, a member of the collectin family, weighs approximately 410-462 kDa and comprises six globular heads linked to collagen-like triple-helix tails. The globular heads exhibit specific binding to the CH2 domain of IgG or the CH3 domain of IgM. Activation requires C1q to bind at least two immunoglobulin heavy chains, inducing a conformational change that activates C1r and C1s. Consequently, activation is contingent upon C1q binding to multivalent antigen-bound immunoglobulin immune complexes. A key physiological role of C1q is clearing immune complexes and apoptotic bodies. Disruption of this process can trigger autoimmunity. Genetic deficiencies in C1q or other classical pathway components increase susceptibility to Systemic Lupus Erythematosus (SLE). C1q demonstrates specific binding to apoptotic bodies from human keratinocytes, vascular endothelial cells, and lymphocytes. Complement components C1q and C3, when bound, mediate apoptotic body clearance. Thus, C1q contributes to autoantigen removal, mitigating immune system stimulation. However, prolonged exposure to the neoepitope on immune complex-bound or apoptotic body-bound C1q can elicit an autoimmune response against C1q itself, disrupting complement function. C1q deficiency can also hinder the negative selection of autoreactive B cells. C1q, along with other recognition proteins, binds to conserved lupus antigens like dsDNA and nuclear proteins, activating the complement system. Anti-C1q autoantibodies are found in various autoimmune and infectious diseases, including glomerulonephritis (GN) and SLE, and hold clinical significance due to their negative predictive value.
Mouse Complement C1Q, with a molecular weight of 439.5 kDa, is produced in Mouse plasma.
The product is a sterile-filtered solution.
The C1Q solution is formulated in 10mM HEPES buffer with 300mM NaCl, at a pH of 7.2.
Mouse C1Q remains stable at 4°C for 2-4 weeks, provided the entire vial is used within this period. For extended storage, freezing below -20°C is recommended. Adding a carrier protein (0.1% HSA or BSA) is advisable for long-term storage. Repeated freezing and thawing cycles should be avoided.
The purity of the product is greater than 92.0% as determined by SDS-PAGE analysis.
Component C1q, Complement C1q, Complement Component C1q, C1q.
Mouse Plasma.
Product Science Overview
C1q is the recognition component of the C1 complex, which also includes the proteases C1r and C1s . When C1q binds to antibodies that are complexed with antigens, it triggers a cascade of events leading to the activation of the complement system . This activation results in the cleavage of C4 and C2, forming the C3/C5 convertase, which is essential for the downstream effects of the complement system .
Interestingly, C1q can also bind directly to the surface of certain pathogens, initiating the complement activation in the absence of antibodies . This ability highlights its role in innate immunity, providing a first line of defense against infections.
In mice, C1q is purified from pooled normal mouse serum and is a part of the C1 complex . The study of C1q in mice is crucial for understanding its role in immune responses and its potential implications in various diseases. Mice models are often used to study the genetic and molecular mechanisms of C1q, providing insights that can be translated to human health.
Research on C1q has revealed its involvement in various physiological and pathological processes. For instance, C1q has been linked to the clearance of apoptotic cells and the modulation of immune responses . Its deficiency or dysfunction can lead to autoimmune diseases, highlighting its importance in maintaining immune homeostasis .
