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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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| Main Authors: | , , , , |
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| Format: | Artigo |
| Jezik: | Inglês |
| Izdano: |
2012
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| Teme: | |
| Online dostop: | 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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