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81244 |
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|a dc
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|a Shulman, J. M.
|e author
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|a Massachusetts Institute of Technology. Department of Biology
|e contributor
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|a Whitehead Institute for Biomedical Research
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|a Treusch, Sebastian
|e contributor
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|a Hamamichi, Shusei
|e contributor
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|a Goodman, Jessica L.
|e contributor
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|a Matlack, Kent E. S.
|e contributor
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|a Chung, Chee Yeun
|e contributor
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|a Baru, Valeriya
|e contributor
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|a Bevis, Brooke J.
|e contributor
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|a Valastyan, Julie Suzanne
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|a Han, Haesun
|e contributor
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|a Lindquist, Susan
|e contributor
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|a Parrado, A.
|e author
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|a Lindhagen-Persson, M.
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|a Reiman, E. M.
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|a Evans, D. A.
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|a Bennett, David A.
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|a Olofsson, A.
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|a De Jager, Philip L.
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|a Tanzi, R. E.
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|a Caldwell, Kim A.
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|a Caldwell, Guy A.
|e author
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|a Lindquist, Susan
|e author
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|a Treusch, Sebastian
|e author
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|a Hamamichi, Shusei
|e author
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| 700 |
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|a Goodman, Jessica L.
|e author
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| 700 |
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|a Matlack, Kent E. S.
|e author
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| 700 |
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|a Chung, Chee Yeun
|e author
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| 700 |
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|a Baru, Valeriya
|e author
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| 700 |
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|a Valastyan, Julie Suzanne
|e author
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| 700 |
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|a Han, Haesun
|e author
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| 700 |
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|a Lindquist, Susan
|e author
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| 700 |
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|a Bevis, Brooke J.
|e author
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|a Functional Links Between Aβ Toxicity, Endocytic Trafficking, and Alzheimer's Disease Risk Factors in Yeast
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|b American Association for the Advancement of Science (AAAS),
|c 2013-09-30T16:44:28Z.
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| 856 |
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|z Get fulltext
|u http://hdl.handle.net/1721.1/81244
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|a 2011 December 2 Author's Manuscript
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|a Aβ (beta-amyloid peptide) is an important contributor to Alzheimer's disease (AD). We modeled Aβ toxicity in yeast by directing the peptide to the secretory pathway. A genome-wide screen for toxicity modifiers identified the yeast homolog of phosphatidylinositol binding clathrin assembly protein (PICALM) and other endocytic factors connected to AD whose relationship to Aβ was previously unknown. The factors identified in yeast modified Aβ toxicity in glutamatergic neurons of Caenorhabditis elegans and in primary rat cortical neurons. In yeast, Aβ impaired the endocytic trafficking of a plasma membrane receptor, which was ameliorated by endocytic pathway factors identified in the yeast screen. Thus, links between Aβ, endocytosis, and human AD risk factors can be ascertained with yeast as a model system.
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|a Howard Hughes Medical Institute (Collaborative Innovation Award)
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|a National Institutes of Health (U.S.). Ruth L. Kirschstein National Research Service (Award Fellowship F32 NS067782-02)
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|a Cure Alzheimer's Fund
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|a National Institutes of Health (U.S.) (Grant K08AG034290)
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|a National Institutes of Health (U.S.) (Grant P30AG10161)
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|a National Institutes of Health (U.S.) (Grant R01AG15819)
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|a National Institutes of Health (U.S.) (Grant R01AG17917)
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|a en_US
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|a Article
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