Melanoma differentiation-associated protein 5 (MDA5)

Melanoma differentiation-associated protein 5 (MDA5) is a pattern recognition receptor belonging to the RIG-I-like receptor family encoded by the IFIH1 gene[1][3]. It functions as a cytoplasmic RNA helicase that detects long double-stranded RNA, often of viral origin or endogenous sources, to trigger antiviral and inflammatory responses through the induction of type I interferons and other cytokines[1][3][6]. MDA5 activates the mitochondrial antiviral signaling protein (MAVS) pathway via its N-terminal CARD domains, leading to downstream activation of transcription factors such as IRF3/7 and NF-κB[1][4]. Beyond its antiviral role, MDA5 contributes to cell death/apoptosis of malignantly transformed cells and is being investigated as a therapeutic target for cancers such as pancreatic cancer, via agents like poly(I:C)[2][4]. Mutations or aberrant activation of MDA5 are implicated in various autoimmune conditions (e.g., type 1 diabetes, dermatomyositis, Aicardi–Goutières syndrome), and excessive interferon signaling mediated by MDA5 is linked to pathological inflammation and tissue damage[3][5][12]. While “MDA-5 signaling pathway” describes the downstream functional cascade, the actual target molecule for structured data is MDA5 itself. Therefore, the entry “MDA-5 signaling pathway” is not a molecule but a pathway, so the query as written is partially incorrect for a list of molecular targets[6][15]. **Key Points on Naming and Query Accuracy:** - The canonical molecular target is MDA5 (melanoma differentiation-associated protein 5), not "MDA-5 signaling pathway," which refers to the collection of cellular events downstream of MDA5 activation. - For databases of molecular targets, use the molecule name (MDA5, IFIH1), not the signaling pathway, as the canonical entry[1][6]. - Consider this query **is_incorrect: true** per target annotation conventions.

Other names

IFIH1Interferon induced with helicase C domain 1MDA-5

Immune activation via double-stranded RNA sensing, Induction of type I interferon signaling, Sensitization to apoptosis