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Complement C1q tumor necrosis factor-related protein 6 (C1QTNF6, CTRP6) is a secreted multimeric protein of the CTRP family, structurally similar to adiponectin and containing a C-terminal globular C1q domain homologous to tumor necrosis factor family proteins[1][2]. It is widely expressed in multiple tissues and circulates in oligomeric form. C1QTNF6 acts as a regulator of the alternative pathway of the complement system by competitively inhibiting factor B binding to C3(H2O), thereby suppressing C3 convertase formation and dampening complement activation[3]. It is involved in processes such as immune and inflammatory responses, metabolic regulation (e.g., promoting fatty acid oxidation via AMPK activation), cell cycle control, and anti-apoptosis[1][2]. Elevated expression and activity have been observed in several cancer types and inflammatory diseases, making it of interest both as a potential therapeutic target and biomarker[2][3][4]. Recombinant CTRP6 has shown experimental efficacy in suppressing autoimmunity and inflammation in mouse models. Excessive suppression or activation of C1QTNF6 may carry risks of immune dysregulation, autoimmunity, or tumorigenesis[1][2][3][4].
Competitive inhibition of complement factor B binding to C3(H2O) during alternative pathway activation; Suppression of the formation of C3 convertase, reducing complement-mediated inflammation and autoimmunity
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