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Enhanced complement susceptibility of avidin-biotin-treated human erythrocytes is a consequence of neutralization of the complement regulators CD59 and decay accelerating factor.

Biotinylation of erythrocytes (E) followed by avidin cross-linking at specific sites has been suggested as a novel means of drug delivery. Upon avidin cross-linking, biotinylated E become complement-activating and highly susceptible to complement lysis, thus bringing about release of entrapped drug....

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Detalles Bibliográficos
Main Authors: Zaltzman, A B, Van den Berg, C W, Muzykantov, V R, Morgan, B P
Formato: Artigo
Idioma:Inglês
Publicado: 1995
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Acceso en liña:https://ncbi.nlm.nih.gov/pmc/articles/PMC1136700/
https://ncbi.nlm.nih.gov/pubmed/7537958
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