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-Reference-Cited by-同舟云学术

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

Published:2024-02-13 Issue:5 Volume:69 Page:171-176
ISSN:1434-5161
Container-title:Journal of Human Genetics
language:en
Short-container-title:J Hum Genet

Author:

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

Funder

Japan Agency for Medical Research and Development

National Center for Geriatrics and Gerontology

Ministry of Health, Labour and Welfare

Hori Sciences and Arts Foundation

Chukyo Longevity Medical Research and Promotion Foundation

Japan Foundation for Aging and Health

Publisher

Springer Science and Business Media LLC

Link

https://www.nature.com/articles/s10038-024-01224-x.pdf

Reference41 articles.

1. Gatz M, Reynolds CA, Fratiglioni L, Johansson B, Mortimer JA, Berg S, et al. Role of genes and environments for explaining Alzheimer disease. Arch Gen Psychiatry. 2006;63:168.

2. Bellenguez C, Küçükali F, Jansen IE, Kleineidam L, Moreno-Grau S, Amin N, et al. New insights into the genetic etiology of Alzheimer’s disease and related dementias. Nat Genet. 2022;54:412–36.

3. Asanomi Y, Shigemizu D, Miyashita A, Mitsumori R, Mori T, Hara N, et al. A rare functional variant of SHARPIN attenuates the inflammatory response and associates with increased risk of late-onset Alzheimer’s disease. Mol Med. 2019;25:20.

4. Gerlach B, Cordier SM, Schmukle AC, Emmerich CH, Rieser E, Haas TL, et al. Linear ubiquitination prevents inflammation and regulates immune signalling. Nature. 2011;471:591–6.

5. Tokunaga F, Nakagawa T, Nakahara M, Saeki Y, Taniguchi M, Sakata S, et al. SHARPIN is a component of the NF-κB-activating linear ubiquitin chain assembly complex. Nature. 2011;471:633–6.