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Essay / Research Paper Abstract
A 3 page overview of the trinucleotide expansions within the huntingtin protein that result in the extension of polyQ-encoding repeats. Bibliography lists sources.
Page Count:
3 pages (~225 words per page)
File: AM2_PPhuntingtonMolStr.rtf
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Unformatted sample text from the term paper:
trinucleotide expansions within the huntingtin protein that result in the extension of polyQ-encoding repeats (Zhang, Smith, Meriin, et. al., 2005; Cattaneo, Zuccato and Tartari, 2005; Luthi-Carter, Strand, Hanson, et. al.,
2006). The gene includes the three nucleotides (cytosine (C), guanine (G), and adenine (A)) that form a CAG structure. This sequence is repeated over and over again in
Huntingtons Disease (Cattaneo, Zuccato and Tartari, 2005). The primary symptoms of Huntingtons disease include an impaired motor system, involuntary movements, and
impacted mental performance such as memory loss and personality changes (Cattaneo, Zuccato and Tartari, 2005). Huntingtons is typically fatal after fifteen to twenty years of mutation (Cattaneo, Zuccato and
Tartari, 2005). Cattaneo, Zuccato and Tartari (2005) observe twenty-eight putative consensus repeats in Drosophila melanogaster and thirty-seven in huntingtin. In
its unaltered form Hungtingtin is critical in embryogenesis and is found both inside the nervous system and outside it (Cattaneo, Zuccato and Tartari, 2005). The result of Huntingtons Disease is
selective neuronal death (Cattaneo, Zuccato and Tartari, 2005). With increased polyglutamine size there is a decreasing protein size and an increased propensity for apoptotic stress (Hackam, Singaraja, and Wellington,
et. al., 1998). In other words, the greater CAG length the shorter disease onset (Cattaneo, Zuccato and Tartari, 2005). Cattaneo, Zuccato and Tartari (2005) clarify:
"The disease-causing gene mutation consists of an expanded CAG tract (>35 repeats) at the 5 end, which is
translated into a corresponding poly- glutamine stretch (polyQ)" The gene products are unrelated with the
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