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• W2010980121 abstract "Protein C deficiency results in a thrombotic disorder that might be treated by expressing a normal human protein C (hPC) gene in patients. An amphotropic retroviral vector with a liver-specific promoter and the hPC cDNA was delivered to rat hepatocytes in vivo during liver regeneration. Expression of hPC varied from 55 to 203 ng/ml (1.3-5.0% of normal) for 2 wk after transduction. Expression increased to an average of 900 ng/ml (22% of normal) in some rats and was maintained at stable levels for 1 yr. All of these rats developed anti-hPC antibodies and exhibited a prolonged hPC half-life in vivo. The hPC was functional as determined by a chromogenic substrate assay after immunoprecipitation. We conclude that most rats achieved hPC levels that would prevent purpura fulminans, and that hepatic gene therapy might become a viable treatment for patients with severe homozygous hPC deficiency. Anti-hPC antibodies increased the hPC half-life and plasma levels in some rats, but did not interfere with its functional activity. Thus, the development of antibodies against a plasma protein does not necessarily abrogate its biological effect in gene therapy experiments." @default.
• W2010980121 created "2016-06-24" @default.
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• W2010980121 date "1998-06-15" @default.
• W2010980121 modified "2023-09-25" @default.
• W2010980121 title "Therapeutic levels of human protein C in rats after retroviral vector-mediated hepatic gene therapy." @default.
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• W2010980121 doi "https://doi.org/10.1172/jci1880" @default.
• W2010980121 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/508874" @default.
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