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In rabies virus G protein, two modalities of neutralization were described: (1) targeting an epitope on a single domain that is fully accessible only in prefusion is enough to lock the protein in prefusion conformation, hence inhibiting the fusion process 44 and (2) recognition of an epitope that spans more than three domains, including one on an adjacent protomer, prevents the conformational changes required for fusion 45
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By integrating insights across molecular, cellular, and clinical dimensions, this review offers a strategic framework for understanding and tackling cancer drug resistance, with important translational implications for the future of precision oncology
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