ISBN: 9781588292438 - trinucleotide repeat protocols (methods in molecular biology, band 277) (8 Ergebnisse)

Zustand: New. pp. 356 52:B&W 6.14 x 9.21in or 234 x 156mm (Royal 8vo) Case Laminate on White w/Gloss Lam.

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Zustand: New. This is a Brand-new US Edition. This Item may be shipped from US or any other country as we have multiple locations worldwide.

Zustand: New. This is a Brand-new US Edition. This Item may be shipped from US or any other country as we have multiple locations worldwide.

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Gebunden. Zustand: New. 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 neurologic.

Zustand: New. Describes techniques for studying trinucleotide pathology at the molecular level. This book features protocols covering targets ranging from DNA and RNA, to proteins and whole animals. It utilizes techniques, including gel electrophoresis, quantitative RT-PCR, and immunological analysis, antibody usage and its applications. Series: Methods in Molecular Biology. Num Pages: 342 pages, biography. BIC Classification: PSAK. Category: (P) Professional & Vocational; (UP) Postgraduate, Research & Scholarly; (UU) Undergraduate. Dimension: 235 x 155 x 20. Weight in Grams: 690. . 2004. Hardback. . . . . Books ship from the US and Ireland.…

Buch. Zustand: Neu. 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. …