Hycult Biotech

A-FABP, Human, pAb – The A-FABP protein is derived from the human FABP4 gene. FABPs are small intracellular proteins (~13-14 kDa) with a high degree of tissue specificity that bind long chain fatty acids. They are abundantly present in various cell types and play an important role in the intracellular utilization of fatty acids, transport and metabolism. There are at least nine distinct types of FABP, each showing a specific pattern of tissue expression.

Activated C1s, Human, mAb M241 – Monoclonal antibody M241 reacts with an epitope on human C protein activated C1s, a subcomponent of the first component of C (C1). Activated C1s is a glycosylated single-polypeptide zymogen of 85 kD. Activation of the proenzyme C1s occurs through cleavage by the active form of C1r. The activated protease, activated C1s, consists of a disulfide-linked H chain and a L chain. Activated C1s is a serine protease and its catalytic site is located in the L chain. Activation of the classical C pathway is triggered by activated C1s which cleaves C4 and C2 to form the C3 convertase, C4bC2a. The epitope recognised by the antibody M241 is domain IV and/or V of the gamma-domain of activated C1s. Monoclonal antibody M241 blocks C4 activation and C4 binding to activated C1s. The antibody binds specifically to the active centre of C1s.

Alternative Complement Pathway, Human, Assay – The Human Alternative Complement Pathway ELISA kit is to be used for the in vitro quantitative determination of Alternative Complement Pathway activity in serum samples.

C1q, Human, Natural – Human complement protein C1q forms together with C1r and C1s the C1 macromolecule, the first component of the classical complement pathway. Interaction of immune complexes with C1q induces a conformational change within the C1 complex, which results in activation of the classical pathway. C1q functions as recognition unit by binding to the heavy chain of IgG or IgM (Fc gamma and Fc micro) provided that the immunoglobulins are bound to their antigen. Furthermore, C1q can bind to apoptotic blebs, where it activates the classical complement pathway and mediates phagocytosis. As such, C1q promotes the clearance of apoptotic cells and subsequent exposure of auto antigens, thereby preventing stimulation of the immune system.