Advances in understanding disease mechanisms and potential treatments for Crigler–Najjar syndrome
Author:
Affiliation:
1. Mouse Molecular Genetics Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), Trieste, Italy
Funder
Beneficentia Stiftung, Vaduz, Lichtenstein
Publisher
Informa UK Limited
Subject
Pharmacology (medical),Health Policy,Pharmacology, Toxicology and Pharmaceutics (miscellaneous)
Link
https://www.tandfonline.com/doi/pdf/10.1080/21678707.2018.1495558
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1. THE ENZYMATIC FORMATION OF BILIRUBIN
2. ATP-dependent transport of bilirubin glucuronides by the multidrug resistance protein MRP1 and its hepatocyte canalicular isoform MRP2
3. Functionally Overlapping Roles of Abcg2 (Bcrp1) and Abcc2 (Mrp2) in the Elimination of Methotrexate and Its Main Toxic Metabolite 7-Hydroxymethotrexate In vivo
4. Intestinal Absorption of Bile Pigments
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4. CRISPR-Cas9-mediated somatic correction of a one-base deletion in the Ugt1a gene ameliorates hyperbilirubinemia in Crigler-Najjar syndrome mice;Molecular Therapy - Methods & Clinical Development;2023-12
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