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Probable ATP-dependent RNA helicase DDX60 (DDX60) is a large member of the DEAD (Asp-Glu-Ala-Asp) box family of RNA helicases, crucial for innate antiviral immunity[1][3][5]. It is induced by interferons and acts as an antiviral factor by binding to double-stranded and single-stranded viral RNA and DNA, thereby enhancing the recognition and signaling by the cytosolic pattern recognition receptors RIG-I and MDA5 (members of the RIG-I-like receptor family)[1][3][5]. DDX60 thereby promotes type I interferon and interferon-stimulated gene expression, contributing to cellular defense against a broad spectrum of viruses, including hepatitis C virus and vesicular stomatitis virus[1][3][5]. Unlike some related helicases, DDX60 does not act directly as a pattern recognition receptor but augments the sensitivity and effectiveness of the canonical RLR pathway. The protein contains the conserved helicase motifs necessary for ATP binding and hydrolysis and is capable of remodeling nucleic acid-protein complexes. It is not presently a direct therapeutic target for any approved drugs but is a subject of active investigation as a key factor in antiviral responses, with implications for understanding immune regulation and potential relevance to autoimmunity and cancer[1][3][5].
Enhancement of RIG-I/MDA5-mediated signaling leading to type I interferon production; binding and remodeling of viral nucleic acids
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