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Proof-of-concept is provided in a human FcRn and human albumin double transgenic mouse model (AlbuMus) 27 with bispecific anti-EGFR x anti-CD3 LiTE fusions (Albu-LiTE) engineered for null (Albu-LiTE-NB), wild-type (Albu-LiTE-WT) or high (Albu-LiTE-HB) FcRn binding (Fig

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In addition, most of the variable SSRs were predicted to induce phenotypic changes by modulating gene expression at a transcriptional level or by producing different protein isoforms rather than mediating on/off translational switching through frameshifts as previously known (Siena et al., 2016)

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Why did NMDA receptor antagonists fail clinical trials for stroke and traumatic brain injury