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1 d neurometabolic conditions, such as classic Lesch-Nyhan syndrome.
2  the behavioral symptoms associated with the Lesch-Nyhan syndrome.
3 ute to their toxicity and to the symptoms of Lesch-Nyhan syndrome.
4 act on the use of female hiPSCs for modeling Lesch-Nyhan syndrome.
5 me (DS)/trisomy 21, and the carrier state of Lesch-Nyhan syndrome.
6  pathological conditions such as cholera and Lesch-Nyhan syndrome.
7  of non-dopaminergic neuronal development in Lesch-Nyhan syndrome.
8 l to HPRT1, the housekeeping gene underlying Lesch-Nyhan syndrome, an X-linked recessive disorder.
9 h inborn errors of purine metabolism such as Lesch-Nyhan syndrome, and metabolic diseases with a life
10 behavioral abnormalities associated with the Lesch-Nyhan syndrome as previously suggested.
11  are unlikely to contribute substantially to Lesch-Nyhan syndrome burden.
12 rited mutations in the human HPRT leading to Lesch-Nyhan syndrome (D193N) or gout (S103R or S109L), a
13                                              Lesch-Nyhan syndrome encompasses a host of neurological
14 at directly contacts the Mg(2+) ions, causes Lesch-Nyhan syndrome (HGPRT(Kinston), D193N).
15  a disorder in the HPRT gene (leading to the Lesch-Nyhan syndrome) is unique to human, chimpanzee, an
16 s with 6-hydroxydopamine (6-OHDA; a model of Lesch-Nyhan syndrome (LNS)) or vehicle (unlesioned rats)
17 pectively model Parkinson's disease (PD) and Lesch-Nyhan syndrome (LNS).
18  from germ-line HPRT mutations identified in Lesch-Nyhan syndrome or hyperuricemia patients.
19 ibosyltransferase (HGPRTase) is the locus of Lesch-Nyhan syndrome, the activator of the prodrugs 6-me
20 e (HPRT) deficiency in humans results in the Lesch-Nyhan syndrome which is characterized, among other