CRISPR/Cas9 介导的晚发性阿尔茨海默病风险变体 SHARPIN G186R 基因敲入细胞显示 NF-κB 通路减少，Aβ 分泌加速。

IF 2.6 3区生物学 Q2 GENETICS & HEREDITY

Journal of Human Genetics Pub Date : 2024-02-13 DOI:10.1038/s10038-024-01224-x

Yuya Asanomi, Tetsuaki Kimura, Nobuyoshi Shimoda, Daichi Shigemizu, Shumpei Niida, Kouichi Ozaki

引用次数: 0

摘要

本文章由计算机程序翻译，如有差异，请以英文原文为准。

CRISPR/Cas9-mediated knock-in cells of the late-onset Alzheimer’s disease-risk variant, SHARPIN G186R, reveal reduced NF-κB pathway and accelerated Aβ secretion

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CRISPR/Cas9-mediated knock-in cells of the late-onset Alzheimer’s disease-risk variant, SHARPIN G186R, reveal reduced NF-κB pathway and accelerated Aβ secretion

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来源期刊

Journal of Human Genetics 生物-遗传学

CiteScore

7.20

自引率

0.00%

发文量

101

审稿时长

4-8 weeks

期刊介绍： The Journal of Human Genetics is an international journal publishing articles on human genetics, including medical genetics and human genome analysis. It covers all aspects of human genetics, including molecular genetics, clinical genetics, behavioral genetics, immunogenetics, pharmacogenomics, population genetics, functional genomics, epigenetics, genetic counseling and gene therapy. Articles on the following areas are especially welcome: genetic factors of monogenic and complex disorders, genome-wide association studies, genetic epidemiology, cancer genetics, personal genomics, genotype-phenotype relationships and genome diversity.