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Paper Details

Soluble TREM2 inhibits secondary nucleation of Aβ fibrillization and enhances cellular uptake of fibrillar Aβ.
Proc Natl Acad Sci U S A
12
2022
A, AD, Alzheimer's disease, R47H, TREM2, Triggering receptor expressed on myeloid cells 2, WT sTREM2-A, amyloid plaques, fibrillar, human, human microglial and neuroglioma derived cell lines, immunoglobulin superfamily, microglial processes, neuroglioma, sTREM2, sTREM2 mutant, single
Alzheimer Disease, Amyloid, Amyloid beta-Peptides, Animals, Humans, Kinetics, Membrane Glycoproteins, Mice, Microglia, Mutation, Peptide Fragments, Plaque, Amyloid, Receptors, Immunologic, tau Proteins
Author NameAffiliation
Ketaki D BelsareDepartment of Pharmaceutical Chemistry, Cardiovascular Research Institute, University of California san francisco
Haifan WuDepartment of Pharmaceutical Chemistry, Cardiovascular Research Institute, University of California san francisco
Annalise BondInstitute for Neurodegenerative Diseases, University of California san francisco
Erika CastilloInstitute for Neurodegenerative Diseases, University of California san francisco
Ji JinDepartment of Pharmaceutical Chemistry, Cardiovascular Research Institute, University of California san francisco
Ji JinCollege of Life Sciences and Medicine, Zhejiang Sci-Tech University
Hyunil JoDepartment of Pharmaceutical Chemistry, Cardiovascular Research Institute, University of California san francisco
Addison E RoushDepartment of Pharmaceutical Chemistry, Cardiovascular Research Institute, University of California san francisco
Kala Bharath PillaQuantitative Biology Institute, University of California san francisco
Kala Bharath PillaDepartment of Pharmaceutical Chemistry, Quantitative Biology Institute, University of California san francisco
Andrej Sali (CM4AI)Quantitative Biology Institute, University of California san francisco
Andrej Sali (CM4AI)Department of Pharmaceutical Chemistry, Quantitative Biology Institute, University of California san francisco
Andrej Sali (CM4AI)Quantitative Biology Institute, University of California san francisco
Andrej Sali (CM4AI)Department of Pharmaceutical Chemistry, Quantitative Biology Institute, University of California san francisco
Carlo CondelloInstitute for Neurodegenerative Diseases, University of California san francisco
Carlo CondelloWeill Institute for Neurosciences, University of California san francisco
William F DeGradoDepartment of Pharmaceutical Chemistry, Cardiovascular Research Institute, University of California san francisco
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