A potential animal model for Lesch–Nyhan syndrome through introduction of HPRT mutations into mice View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1987-03

AUTHORS

Michael R. Kuehn, Allan Bradley, Elizabeth J. Robertson, Martin J. Evans

ABSTRACT

The human Lesch-Nyhan syndrome is a rare neurological and behavioural disorder, affecting only males, which is caused by an inherited deficiency in the level of activity of the purine salvage enzyme hypoxanthine-guanosine phosphoribosyl transferase (HPRT). How the resulting alterations in purine metabolism lead to the severe symptoms characteristic of Lesch-Nyhan patients is still not understood. No mutations at the Hprt locus leading to loss of activity have been described in laboratory animals. To derive an animal model for the Lesch-Nyhan syndrome, we have used cultured mouse embryonic stem cells, mutagenized by retroviral insertion and selected for loss of HPRT activity, to construct chimaeric mice. Two clonal lines carrying different mutant Hprt alleles have given rise to germ cells in chimaeras, allowing the derivation of strains of mutant mice having the same biochemical defect as Lesch-Nyhan patients. Male mice carrying the mutant alleles are viable and analysis of their cells shows a total lack of HPRT activity. More... »

PAGES

295-298

Journal

TITLE

Nature

ISSUE

6110

VOLUME

326

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/326295a0

    DOI

    http://dx.doi.org/10.1038/326295a0

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1030310246

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/3029599


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