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BST2 interferon-stimulated positive regulator (BISPR) is a long non-coding RNA (lncRNA) that is induced by interferons and acts as a positive transcriptional regulator of the BST2 (Tetherin) gene, a key interferon-stimulated gene involved in restricting viral particle release from infected cells[1][4]. BISPR is produced from a bidirectional promoter shared with BST2 and is regulated through the JAK–STAT signaling pathway in response to both type I and type II interferons[1][4]. Experimental evidence demonstrates that BISPR expression precedes and enables the induction of BST2 upon interferon stimulation, and knockdown of BISPR decreases BST2 transcript levels specifically without affecting other genes[1]. BISPR is not a protein-coding gene, not a receptor, and is not in itself a direct therapeutic target; it serves instead as a gene regulator lncRNA, critical for proper interferon-mediated upregulation of the antiviral factor BST2[1][4].
Not applicable; no drugs are reported to target this lncRNA directly
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