2010, ISBN: 1617374466

[EAN: 9781617374463], Neubuch, [PU: SPRINGER NATURE Nov 2010], MEDICAL / NURSING; MICROBIOLOGY NATUROPATHY; NEUROLOGY; SCIENCE LIFE SCIENCES CELL BIOLOGY, This item is printed on demand -… More...

[EAN: 9781617374463], Neubuch, [PU: SPRINGER NATURE Nov 2010], MEDICAL / NURSING; MICROBIOLOGY NATUROPATHY; NEUROLOGY; SCIENCE LIFE SCIENCES CELL BIOLOGY, This item is printed on demand - it takes 3-4 days longer - Neuware -Trinucleotide repeats are relatively common in the human genome. These simple repeats have received much attention since epoch-making discoveries were made that particular trinucleotide repeats are expanded in the causal genes of human hereditary neurological disorders. For example, the CGG repeat is expanded in fragile X syndrome at the 5' untranslated region (UTR) of its causal gene. In myotonic dystrophy, it is the CTG repeat that is expanded at the 3' UTR of its causal gene. The CAG repeat was also found expanded in coding regions of the genes responsible for X-linked spinal and bulbar muscular atrophy, Huntington's disease, spinocerebellar ataxia, and other disorders. On the other hand, expansion of the GAA repeat was identified in the intron of the gene responsible for the Friedreich's ataxia. For these trinucleotide repeat diseases, the longer the trinucleotide expansion, the earlier the age of onset and the more severe the syndrome. Thus, these findings that showed the intriguing link between a particular trinucleotide expansion and its associated neurological disorders have led to a new field of intensive study. Active research addressing the underlying mechanisms for trinucleotide repeat diseases has employed various approaches ranging from DNA biochemistry to animal models for the diseases. In particular, animal models for the triplet repeat diseases have provided excellent resources not only for understanding the mechanisms but also for exploring therapeutic interventions. 342 pp. Englisch, Books<

2001, ISBN: 9781617374463

[ED: Taschenbuch], [PU: SPRINGER NATURE], Neuware - Trinucleotide repeats are relatively common in the human genome. These simple repeats have received much attention since epoch-making d… More...

[ED: Taschenbuch], [PU: SPRINGER NATURE], Neuware - Trinucleotide repeats are relatively common in the human genome. These simple repeats have received much attention since epoch-making discoveries were made that particular trinucleotide repeats are expanded in the causal genes of human hereditary neurological disorders. For example, the CGG repeat is expanded in fragile X syndrome at the 5' untranslated region (UTR) of its causal gene. In myotonic dystrophy, it is the CTG repeat that is expanded at the 3' UTR of its causal gene. The CAG repeat was also found expanded in coding regions of the genes responsible for X-linked spinal and bulbar muscular atrophy, Huntington's disease, spinocerebellar ataxia, and other disorders. On the other hand, expansion of the GAA repeat was identified in the intron of the gene responsible for the Friedreich's ataxia. For these trinucleotide repeat diseases, the longer the trinucleotide expansion, the earlier the age of onset and the more severe the syndrome. Thus, these findings that showed the intriguing link between a particular trinucleotide expansion and its associated neurological disorders have led to a new field of intensive study. Active research addressing the underlying mechanisms for trinucleotide repeat diseases has employed various approaches ranging from DNA biochemistry to animal models for the diseases. In particular, animal models for the triplet repeat diseases have provided excellent resources not only for understanding the mechanisms but also for exploring therapeutic interventions., DE, [SC: 2.70], Neuware, gewerbliches Angebot, 229x152x20 mm, 342, [GW: 522g], Banküberweisung, Offene Rechnung, Kreditkarte, PayPal, Offene Rechnung (Vorkasse vorbehalten), Internationaler Versand<

2010, ISBN: 1617374466

[EAN: 9781617374463], Neubuch, [SC: 0.0], [PU: SPRINGER NATURE], MEDICAL / NURSING; MICROBIOLOGY NATUROPATHY; NEUROLOGY; SCIENCE LIFE SCIENCES CELL BIOLOGY, Druck auf Anfrage Neuware - Pr… More...

[EAN: 9781617374463], Neubuch, [SC: 0.0], [PU: SPRINGER NATURE], MEDICAL / NURSING; MICROBIOLOGY NATUROPATHY; NEUROLOGY; SCIENCE LIFE SCIENCES CELL BIOLOGY, Druck auf Anfrage Neuware - Printed after ordering - Trinucleotide repeats are relatively common in the human genome. These simple repeats have received much attention since epoch-making discoveries were made that particular trinucleotide repeats are expanded in the causal genes of human hereditary neurological disorders. For example, the CGG repeat is expanded in fragile X syndrome at the 5' untranslated region (UTR) of its causal gene. In myotonic dystrophy, it is the CTG repeat that is expanded at the 3' UTR of its causal gene. The CAG repeat was also found expanded in coding regions of the genes responsible for X-linked spinal and bulbar muscular atrophy, Huntington's disease, spinocerebellar ataxia, and other disorders. On the other hand, expansion of the GAA repeat was identified in the intron of the gene responsible for the Friedreich's ataxia. For these trinucleotide repeat diseases, the longer the trinucleotide expansion, the earlier the age of onset and the more severe the syndrome. Thus, these findings that showed the intriguing link between a particular trinucleotide expansion and its associated neurological disorders have led to a new field of intensive study. Active research addressing the underlying mechanisms for trinucleotide repeat diseases has employed various approaches ranging from DNA biochemistry to animal models for the diseases. In particular, animal models for the triplet repeat diseases have provided excellent resources not only for understanding the mechanisms but also for exploring therapeutic interventions. 342 pp. Englisch, Books<

2010, ISBN: 1617374466

[EAN: 9781617374463], Neubuch, [SC: 0.0], [PU: SPRINGER NATURE], MEDICAL / NURSING; MICROBIOLOGY NATUROPATHY; NEUROLOGY; SCIENCE LIFE SCIENCES CELL BIOLOGY, Druck auf Anfrage Neuware -Tri… More...

[EAN: 9781617374463], Neubuch, [SC: 0.0], [PU: SPRINGER NATURE], MEDICAL / NURSING; MICROBIOLOGY NATUROPATHY; NEUROLOGY; SCIENCE LIFE SCIENCES CELL BIOLOGY, Druck auf Anfrage Neuware -Trinucleotide repeats are relatively common in the human genome. These simple repeats have received much attention since epoch-making discoveries were made that particular trinucleotide repeats are expanded in the causal genes of human hereditary neurological disorders. For example, the CGG repeat is expanded in fragile X syndrome at the 5' untranslated region (UTR) of its causal gene. In myotonic dystrophy, it is the CTG repeat that is expanded at the 3' UTR of its causal gene. The CAG repeat was also found expanded in coding regions of the genes responsible for X-linked spinal and bulbar muscular atrophy, Huntington's disease, spinocerebellar ataxia, and other disorders. On the other hand, expansion of the GAA repeat was identified in the intron of the gene responsible for the Friedreich's ataxia. For these trinucleotide repeat diseases, the longer the trinucleotide expansion, the earlier the age of onset and the more severe the syndrome. Thus, these findings that showed the intriguing link between a particular trinucleotide expansion and its associated neurological disorders have led to a new field of intensive study. Active research addressing the underlying mechanisms for trinucleotide repeat diseases has employed various approaches ranging from DNA biochemistry to animal models for the diseases. In particular, animal models for the triplet repeat diseases have provided excellent resources not only for understanding the mechanisms but also for exploring therapeutic interventions. 342 pp. Englisch, Books<

ISBN: 9781617374463

Trinucleotide repeats are relatively common in the human genome. These simple repeats have received much attention since epoch-making discoveries were made that particular trinucleotide r… More...

Trinucleotide repeats are relatively common in the human genome. These simple repeats have received much attention since epoch-making discoveries were made that particular trinucleotide repeats are expanded in the causal genes of human hereditary neurological disorders. For example, the CGG repeat is expanded in fragile X syndrome at the 5'' untranslated region (UTR) of its causal gene. In myotonic dystrophy, it is the CTG repeat that is expanded at the 3'' UTR of its causal gene. The CAG repeat was also found expanded in coding regions of the genes responsible for X-linked spinal and bulbar muscular atrophy, Huntington''s disease, spinocerebellar ataxia, and other disorders. On the other hand, expansion of the GAA repeat was identified in the intron of the gene responsible for the Friedreich''s ataxia. For these trinucleotide repeat diseases, the longer the trinucleotide expansion, the earlier the age of onset and the more severe the syndrome. Thus, these findings that showed the intriguing link between a particular trinucleotide expansion and its associated neurological disorders have led to a new field of intensive study. Active research addressing the underlying mechanisms for trinucleotide repeat diseases has employed various approaches ranging from DNA biochemistry to animal models for the diseases. In particular, animal models for the triplet repeat diseases have provided excellent resources not only for understanding the mechanisms but also for exploring therapeutic interventions. | Trinucleotide Repeat Protocols by Yoshinori KOHWI Paperback | Indigo Chapters Books > Science & Nature > Science > Life Sciences P10117, Yoshinori KOHWI<