C1q, Mouse, mAb JL-1
Referencia HM1096-500UG
embalaje : 500ug
Marca : Hycult Biotech
C1q, Mouse, mAb JL-1
The monoclonal antibody JL-1 recognizes the collagen-like region (CLR) of mouse C1q, a 459 kDa molecule consisting of three individual polypeptide chains.
The monoclonal antibody JL-1 is highly specific for the collagen-like region (CLR) of mouse C1q, a key component of the classical complement pathway. C1q is a large molecule (459 kDa) composed of three distinct polypeptide chains and plays a central role in immune recognition. The JL-1 antibody was developed by immunizing C1q-deficient (C1q-/-) mice (C57BL/6 strain) with purified mouse C1q, ensuring targeted immune response toward this specific region of C1q.
C1q in the Classical Complement Pathway
C1q is part of the C1 complex, which also includes C1r and C1s, forming the initial component of the classical complement pathway. Upon interaction with immune complexes, C1q undergoes a conformational shift that activates this pathway, essential for immune defense. As the recognition unit, C1q binds to the Fc region of IgG or IgM, provided they are attached to an antigen. Additionally, C1q identifies molecular patterns on pathogens and apoptotic cells, activating the pathway and facilitating phagocytosis. This function is crucial for clearing apoptotic cells, preventing the exposure of autoantigens, and reducing immune system activation.
Importance of C1q in Immune Regulation
C1q is primarily produced by macrophages, but it is also synthesized by follicular dendritic cells and other cells in the monocyte-macrophage lineage. Deficiency in C1q can lead to impaired clearance of immune complexes and apoptotic cells, contributing to autoimmune conditions such as systemic lupus erythematosus (SLE). Inherited C1q deficiency has been strongly linked to the development of SLE, as the absence of C1q disrupts normal immune regulation.
JL-1 Antibody and Its Role in Research
The monoclonal antibody JL-1 specifically targets the collagen-like region of C1q, where autoantibodies bind in both mice and humans. These anti-C1q antibodies are often present in SLE patients and contribute to renal disease, especially in the context of glomerular immune complex disease. This makes JL-1 a valuable tool in studying autoimmune conditions like SLE and the mechanisms of C1q-related immune dysfunction.
By focusing on C1q and its pivotal role in the immune system, JL-1 provides insight into immune regulation, complement activation, and the potential development of autoimmune disorders.
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