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Updated: Sep 28, 2026

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分子ピンチ CLR01によるハンティングチンエクソン-1 集積の抑制

Tobias Vöpel1, Kenny Bravo-Rodriguez2, Sumit Mittal2

  • 1Department of Physical Chemistry II, Ruhr-University Bochum , 44780 Bochum, Germany.

Journal of the American Chemical Society
|April 14, 2017
PubMed
まとめ

ハンチントンタンパク質 (htt) のN端の断片 (N17) は,ハンチントン病の結合の鍵です. 分子ピンチ CLR01はN17を標的とし,HTTの集積と毒性を抑制する.

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Huntington Disease l: Introduction01:21

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Huntington disease or HD is a progressive, fatal neurodegenerative disorder inherited in an autosomal dominant pattern.PathophysiologyIt is caused by expansion of the CAG trinucleotide repeat in the HTT gene on chromosome 4 (4p16.3), producing an abnormal huntingtin protein with an expanded polyglutamine tract. This misfolded protein disrupts cellular function, leading to neuronal death. Normal alleles have ≤26 repeats, 27–35 are intermediate (risk of expansion), 36–39 show reduced penetrance,...