Abstract
We demonstrate here that the genetic incorporation of the fusogenic peptide HA2 into a CXCR4-targeted protein nanoparticle dramatically reduces the specificity of the interaction between nanoparticles and cell receptors, a factor to be considered when designing tumor-homing drug vehicles displaying endosomal-escape agents. The loss of specificity is concomitant with enhanced cell penetrability.
MeSH terms
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Drug Carriers / chemistry
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Drug Carriers / metabolism
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Endosomes / chemistry
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Endosomes / metabolism
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Fluorescence
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HeLa Cells
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Hemagglutinins, Viral / chemistry*
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Hemagglutinins, Viral / genetics
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Hemagglutinins, Viral / metabolism
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Humans
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Nanoparticles / chemistry*
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Nanoparticles / metabolism
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Receptors, CXCR4 / chemistry*
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Receptors, CXCR4 / metabolism
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Receptors, Cell Surface / chemistry*
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Receptors, Cell Surface / metabolism
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Tumor Cells, Cultured
Substances
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CXCR4 protein, human
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Drug Carriers
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Hemagglutinins, Viral
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Receptors, CXCR4
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Receptors, Cell Surface
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hemagglutinin HA-2 fusogenic peptide, Influenza virus