Genome wide screening of genes involved in Abeta phagocytosis by CRISPR/Cas9 system
Project/Area Number |
16K18871
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Biological pharmacy
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Research Institution | The University of Tokyo |
Principal Investigator |
Hori Yukiko 東京大学, 大学院薬学系研究科(薬学部), 助教 (80610683)
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Project Period (FY) |
2016-04-01 – 2018-03-31
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Project Status |
Completed (Fiscal Year 2017)
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Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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Keywords | 脳神経疾患 / 神経科学 / アルツハイマー病 |
Outline of Final Research Achievements |
Alzheimer disease (AD) is a neurodegenerative disease characterized by the deposition of senile plaques, which are composed of amyloid β peptide (Aβ). As rate of Aβ clearance from the brain is impaired in sporadic AD cases, understanding the molecular mechanism of Aβ clearance is important. In this study, we have performed the genome-wide screening for Aβ uptake ability using CRISPR/Cas9 system, and established the validation method in Cas9 knockin mouse. Using these strategies, we have identified several genes and cell function involving Aβ uptake. Additionally, our data indicate that one of the known AD risk genes may exert effect by Aβ uptake pathway.
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Report
(3 results)
Research Products
(10 results)
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[Journal Article] Loss of kallikrein-related peptidase 7 exacerbates amyloid pathology in Alzheimer’s disease model mice2018
Author(s)
Kidana K, Tatebe T, Ito K, Hara N, Kakita A, Saito T, Takatori S, Ouchi Y, Ikeuchi T, Makino M, Saido TC, Akishita M, Iwatsubo T, Hori Y, Tomita T
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Journal Title
EMBO Molecular Medicine
Volume: 10
Issue: 3
DOI
Related Report
Peer Reviewed / Open Access
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