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Books on the topic 'Trinucleotides'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Richard, Guy-Franck, ed. Trinucleotide Repeats. Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4939-9784-8.

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2

Kohwi, Yoshinori. Trinucleotide Repeat Protocols. Humana Press, 2004. http://dx.doi.org/10.1385/1592598048.

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3

Kohwi, Yoshinori, and Cynthia T. McMurray, eds. Trinucleotide Repeat Protocols. Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-411-1.

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4

Kohwi, Yoshinori, and Cynthia T. McMurray. Trinucleotide repeat protocols. 2nd ed. Humana Press, 2013.

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5

Yoshinori, Kohwi, ed. Trinucleotide repeat protocols. Humana Press, 2004.

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6

Oostra, Ben A., ed. Trinucleotide Diseases and Instability. Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-540-69680-3.

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7

1946-, Oostra Ben A., ed. Trinucleotide diseases and instability. Springer, 1998.

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8

Oliver, Quarrell, ed. Juvenile Huntington's disease: (and other trinucleotide repeat disorders). Oxford University Press, 2009.

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9

Pinheiro, Philip Mark. A study of RNA trinucleotide repeats involved in myotonic dystrophy. University of Portsmouth, School of Biological Sciences, 1999.

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10

Montgomery, Samantha Erin. Structural characterization of slipped trinucleotide repeats and their processing in human cell extracts. National Library of Canada, 2002.

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11

R, Hayden Michael, and Rubinsztein D. C, eds. Analysis of triplet repeat disorders. Bios Scientific Publishers, 1998.

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12

Timchenko, Lubov T. Triple repeat diseases of the nervous system. Kluwer Academic/Plenum Publishers, 2002.

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13

Kohwi, Yoshinori. Trinucleotide Repeat Protocols. Humana Press, 2004.

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14

Kohwi, Yoshinori, and Cynthia T. McMurray. Trinucleotide Repeat Protocols. Humana Press, 2016.

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15

Kohwi, Yoshinori. Trinucleotide Repeat Protocols. Humana Press, 2010.

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16

Oostra, Ben A. Trinucleotide Diseases and Instability. Springer Berlin / Heidelberg, 2013.

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17

Oostra, Ben A. Trinucleotide Diseases and Instability. Springer London, Limited, 2013.

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18

Richard, Guy-Franck. Trinucleotide Repeats: Methods and Protocols. Springer New York, 2020.

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19

Richard, Guy-Franck. Trinucleotide Repeats: Methods and Protocols. Springer New York, 2019.

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20

Quarrell, Oliver W. J., Helen M. Brewer, Ferdinando Squitieri, Martha A. Nance, and Roger A. Barker. Juvenile Huntington's Disease: And Other Trinucleotide Repeat Disorders. Oxford University Press, Incorporated, 2009.

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21

Quarrell, Oliver W. J., and Helen M. Brewer. Juvenile Huntington's Disease: And Other Trinucleotide Repeat Disorders. Oxford University Press, 2009.

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22

Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Genetics. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0010.

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Chapter 10 covers the basic science and clinical topics relating to genetics which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers karyotype, mitosis, and meiosis, mechanisms of inheritance/disease transmission, mitochondrial disease, trinucleotide repeats and imprinting, investigative techniques in genetic medicine, Down syndrome, Klinefelter syndrome, Turner syndrome, neurofibromatosis, tuberous sclerosis, myotonic dystrophy, Friedreich ataxia, fragile X syndrome, Prader-Willi syndrome, Angelman syndrome, and Ehlers-Danlos syndrome.

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23

Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 52-Year-Old Female with Weakness and Droopy Eyelids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0024.

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Myotonic dystrophy type 1 affects multiple organ systems and is associated with cardiac, endocrine, and ophthalmological disorders. Executive dysfunction can lead to missed appointments and an apathetic attitude, causing patients to underestimate symptoms. The findings of both clinical and electrical myotonia should suggest myotonia congenita, DM1, or DM2. Myotonic dystrophy demonstrates anticipation, where the disease has an earlier onset and more severe course with subsequent generations due to increasing trinucleotide repeats. Therefore, the diagnosis can be heralded in an adult by his/her

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24

Zuccato, Chiara, and Elena Cattaneo. Normal Function of Huntingtin. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0011.

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Huntingtin (HTT) is the 3,144–amino acid protein product of the Huntington’s disease gene (HTT), which can be traced back through 800 million years of evolution. It carries a trinucleotide CAG repeat that encodes polyglutamine (polyQ) at an evolutionarily conserved NH2-terminal position in exon 1. This chapter discusses the discoveries that have mapped the evolutionary history of HTT and the CAG repeat and the critical role of the protein in development as well as its activities in the adult brain. During embryogenesis, HTT is critical for gastrulation, neurulation, and neurogenesis. In the ad

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25

Harper, Peter S. Huntington’s Disease in a Historical Context. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0001.

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Huntington’s disease (HD) provides a paradigm for advancement of our understanding of numerous inherited brain degenerations. The classic 1872 description by George Huntington led to its recognition worldwide. HD was one of the first clearly Mendelian disorders recognized, but also one closely linked to abuses of eugenics. It has provided a model for analyzing unusual genetic features, notably genetic anticipation, and for positional cloning of disease genes. The finding that its molecular basis is an unstable trinucleotide repeat expansion coding for polyglutamine has led to an increasing und

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