A novel biochemically salvageable animal model of hyperammonemia devoid of N-acetylglutamate synthase

All knockout mouse models of urea cycle disorders die in the neonatal period or shortly thereafter. Since N-acetylglutamate synthase (NAGS) deficiency in humans can be effectively treated with N-carbamyl-L-glutamate (NCG), we sought to develop a mouse model of this disorder that could be rescued by...

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Bibliographic Details
Main Authors: Senkevitch, Emilee, Cabrera-Luque, Juan, Morizono, Hiroki, Caldovic, Ljubica, Tuchman, Mendel
Format: Artigo
Language:Inglês
Published: 2012
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Article
Online Access:https://ncbi.nlm.nih.gov/pmc/articles/PMC3356441/
https://ncbi.nlm.nih.gov/pubmed/22503289
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.ymgme.2012.03.004
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