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2016 Fiscal Year Final Research Report

Elucidation of the vesicular trafficking mechanism for prion propagation on the basis of our previous findings of the disturbed vesicular trafficking in prion disease

Research Project

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Project/Area Number 26293212
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypePartial Multi-year Fund
Section一般
Research Field Neurology
Research InstitutionThe University of Tokushima

Principal Investigator

SAKAGUCHI Suehiro  徳島大学, 先端酵素学研究所, 教授 (60274635)

Co-Investigator(Kenkyū-buntansha) 矢野 雅司  徳島大学, 疾患酵素学研究センター, 技術員 (10531858)
千田 淳司  徳島大学, 疾患酵素学研究センター, 助教 (20437651)
原 英之  徳島大学, 疾患酵素学研究センター, 助教 (40469953)
Project Period (FY) 2014-04-01 – 2017-03-31
Keywordsプリオン / プリオン病 / ソーチリン / 蛋白質輸送 / 蛋白質分解 / ノックアウトマウス / 神経変性疾患
Outline of Final Research Achievements

We identified that sortilin promotes degradation of prions. Sortilin interacted with the normal and abnormal prion proteins and transported them to lysosomes for degradation. Downregulation of sortilin increased the abnormal prion protein in prion-infected cells. The normal prion protein was also increased by downregulation of sortilin in prion-uninfected cells. Interestingly, prion infection reduced sortilin by promoting lysosomal degradation of sortilin. Finally, we intracerebrally inoculated prions into sortilin-knockout (KO) and control wild-type (WT) mice. Sortilin-KO mice developed prion disease and died significantly earlier than WT mice. Sortilin-KO mice also accumulated the abnormal prion protein from the earlier stages of infection, compared to control WT mice. These results suggest that prions could propagate themselves through reducing sortilin.

Free Research Field

プリオン学

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Published: 2018-03-22  

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