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Key cellular pathogenic mechanisms in Huntington's disease (HD). Multiple cellular pathways have been implicated in the pathogenesis of HD. These mechanisms could be exclusive or, more likely, have a high degree of cross-talk. A: the mutation in huntingtin causes a conformational change of the protein that leads to partial unfolding or abnormal folding of the protein, which can be corrected by molecular chaperones. Full-length mutant huntingtin is cleaved by proteases in the cytoplasm. In an attempt to eliminate the toxic huntingtin, fragments are ubiquitinated and targeted to the proteasome for degradation. However, the proteasome becomes less efficient in HD. Induction of the proteasome activity as well as of autophagy protects against the toxic insults of mutant huntingtin proteins by enhancing its clearance. B: NH2-terminal fragments containing the polyQ strech accumulate in the cell cytoplasm and interact with several proteins causing impairment of calcium signaling and homeostasis (C) and mitochondrial dysfunction (D). E: NH2-terminal mutant huntingtin fragments translocate to the nucleus where they impair gene transcription or form intranuclear inclusions. F: the mutation in huntingtin alters vesicular transport and recycling. muHtt, mutant huntingtin.

[1]


Reference

  1. <pubmed>20664076</pubmed>


http://physrev.physiology.org/content/90/3/905.full

Image URL: http://physrev.physiology.org/content/90/3/905/F3.expansion.html


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Cite this page: Hill, M.A. (2024, June 17) Embryology Key cellular pathogenic mechanisms in HD.jpg. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/File:Key_cellular_pathogenic_mechanisms_in_HD.jpg

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