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Endogenous bornavirus-like nucleoprotein 1 (EBLN1) is a host-derived, protein-coding gene in humans, originating from the ancient integration of bornavirus N gene sequences into the genome[1][2][3]. Evolved beyond its viral origin, EBLN1 encodes a protein primarily localized in the cytoplasm that is required to facilitate proper cell cycle progression, maintain the integrity of the genome, and support the organization of microtubules[1]. Loss of EBLN1 leads to increased accumulation of DNA damage, cell cycle abnormalities, disruption of microtubule arrays, and premature centrosome splitting—functions partly mediated through interaction with the nuclear envelope protein TPR, but not with Cyclin B1-CDK1[1]. There is currently no evidence that EBLN1 acts as a direct therapeutic target (e.g., a receptor, enzyme, or transporter), nor are any drugs known to target this protein, but it represents an example of endogenized viral elements that have acquired essential cellular roles over vertebrate evolution[1][3][2][5].
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