Correction of the UDP-glucuronosyltransferase gene defect in the Gunn rat model of Crigler–Najjar syndrome type I with a chimeric oligonucleotide
Crigler–Najjar syndrome type I is characterized by unconjugated hyperbilirubinemia resulting from an autosomal recessive inherited deficiency of hepatic UDP-glucuronosyltransferase (UGT) 1A1 activity. The enzyme is essential for glucuronidation and biliary excretion of bilirubin, and its absence can...
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| Vydáno v: | Proc Natl Acad Sci U S A |
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| Hlavní autoři: | , , , , , |
| Médium: | Artigo |
| Jazyk: | Inglês |
| Vydáno: |
National Academy of Sciences
1999
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| Témata: | |
| On-line přístup: | https://ncbi.nlm.nih.govhttps://pmc.ncbi.nlm.nih.gov/articles/PMC17891/ https://ncbi.nlm.nih.govhttps://pubmed.ncbi.nlm.nih.gov/10468611/ https://ncbi.nlm.nih.govhttps://doi.org/10.1073/pnas.96.18.10349 |
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