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Simultaneously, through the extrinsic pathway, the infection induced an increase in the expression of death receptors targeted by TNF-α on tumor cell surface, thereby activating caspase-8 and the apoptotic machinery from the outside-in (59, 60)

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In contrast, deletion of domain 3 (CSQ(ΔD3)-anti-VEGF-scFv) dramatically reduced solubility to ~13%, whereas deletion of domain 2 (CSQ(ΔD2)-anti-VEGF-scFv) resulted in intermediate solubility of ~76%