Regulation of USP25 by SP1 Associates with Amyloidogenesis

doi:10.3233/JAD-221184

科研成果详情

题名	Regulation of USP25 by SP1 Associates with Amyloidogenesis
作者	Li, Ran 1,2; Song, Beibei 3; Xu, Lu2; Zheng, Jiali2; Pan, Wenhao2; Cai, Fang 3; Wang, Juelu 3; Wu, Yili2,4; Song, Weihong1,2,3,4
发表日期	2023
发表期刊	Journal of Alzheimer's disease : JAD 影响因子和分区
语种	英语
原始文献类型	Journal Article
关键词	Amyloidogenesis Ubiquitin Specific Peptidase 25 gene regulation neuronal cell non-neuronal cell specificity protein 1
其他关键词	GENE-EXPRESSION ; TRANSCRIPTIONAL REGULATION ; MOUSE MODEL ; PROTEIN ; BINDING ; CHROMOSOME ; SECRETASE ; ENZYME ; BACE1
摘要	Trisomy 21, an extra copy of human chromosome 21 (HSA21), causes most Down's syndrome (DS) cases. Individuals with DS inevitably develop Alzheimer's disease (AD) neuropathological phenotypes after middle age including amyloid plaques and tau neurofibrillary tangles. Ubiquitin Specific Peptidase 25 (USP25), encoding by USP25 gene located on HSA21, is a deubiquitinating enzyme, which plays an important role in both DS and AD pathogenesis. However, the regulation of USP25 remains unclear., We aimed to determine the regulation of USP25 by specificity protein 1 (SP1) in neuronal cells and its potential role in amyloidogenesis., The transcription start site and promoter activity was identified by SMART-RACE and Dual-luciferase assay. Functional SP1-responsive elements were examined by EMSA. USP25 expression was examined by RT-PCR and immunoblotting. Student's t-test or one-way ANOVA were applied or statistical analysis., The transcription start site of human USP25 gene was identified. Three functional SP1 responsive elements in human USP25 gene were revealed. SP1 promotes USP25 transcription and subsequent USP25 protein expression, while SP1 inhibition significantly reduces USP25 expression in both non-neuronal and neuronal cells. Moreover, SP1 inhibition dramatically reduces amyloidogenesis., We demonstrates that transcription factor SP1 regulates USP25 gene expression, which associates with amyloidogenesis. It suggests that SP1 signaling may play an important role in USP25 regulation and contribute to USP25-mediated DS and AD pathogenesis.
资助项目	National Natural Science Foundation of China[81971019,82150710557,82293642];
出版者	IOS PRESS
ISSN	1387-2877
EISSN	1875-8908
卷号	92 期号:4 页码:1459-1472
DOI	10.3233/JAD-221184
页数	14
WOS类目	Neurosciences
WOS研究方向	Neurosciences & Neurology
WOS记录号	WOS:000971602900024
收录类别	PUBMED ; SCIE ; SCOPUS
URL	查看原文
PubMed ID	36938736
SCOPUSEID	2-s2.0-85153540624
通讯作者地址	[Wu, Yili]1Chashan District, Wenzhou, Zhejiang 325000, China ; [Song, Weihong]2Chashan District, Wenzhou, Zhejiang, China
Scopus学科分类	Neuroscience (all);Clinical Psychology;Geriatrics and Gerontology;Psychiatry and Mental Health
引用统计
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/174379
专题	第二临床医学院、附属第二医院、育英儿童医院附属第二医院精神医学学院卓越中心_老年研究院其他_附属康宁医院（温州市康宁医院）
通讯作者	Wu, Yili; Song, Weihong
作者单位	1.The Second Affiliated Hospital and Yuying Children's Hospital,Wenzhou Medical University,Zhejiang,Wenzhou,China; 2.Institute of Aging,Key Laboratory of Alzheimer's Disease of Zhejiang Province,Zhejiang Provincial Clinical Research Center for Mental Disorders,School of Mental Health and Kangning Hospital,Wenzhou Medical University,Zhejiang,Wenzhou,China; 3.Townsend Family Laboratories,Department of Psychiatry,Graduate Program in Neuroscience,The University of British Columbia,Vancouver,Canada; 4.Oujiang Laboratory Zhejiang Lab for Regenerative Medicine,Vision and Brain Health,Zhejiang,Wenzhou,China
第一作者单位	附属第二医院; 精神医学学院
第一作者的第一单位	附属第二医院
推荐引用方式 GB/T 7714	Li, Ran,Song, Beibei,Xu, Lu,et al. Regulation of USP25 by SP1 Associates with Amyloidogenesis[J]. Journal of Alzheimer's disease : JAD,2023,92(4):1459-1472.
APA	Li, Ran., Song, Beibei., Xu, Lu., Zheng, Jiali., Pan, Wenhao., ... & Song, Weihong. (2023). Regulation of USP25 by SP1 Associates with Amyloidogenesis. Journal of Alzheimer's disease : JAD, 92(4), 1459-1472.
MLA	Li, Ran,et al."Regulation of USP25 by SP1 Associates with Amyloidogenesis".Journal of Alzheimer's disease : JAD 92.4(2023):1459-1472.