دورية أكاديمية
أعرض في EDS

Moesin is an effector of tau-induced actin overstabilization, cell cycle activation, and neurotoxicity in Alzheimer's disease.

التفاصيل البيبلوغرافية
العنوان: Moesin is an effector of tau-induced actin overstabilization, cell cycle activation, and neurotoxicity in Alzheimer's disease.
المؤلفون: Beckmann A; Sam and Ann Barshop Institute for Longevity and Aging Studies, San Antonio, TX, USA.; Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, San Antonio, TX, USA.; Department of Cell Systems and Anatomy, San Antonio, TX, USA.; University of Texas Health San Antonio, San Antonio, TX, USA., Ramirez P; Sam and Ann Barshop Institute for Longevity and Aging Studies, San Antonio, TX, USA.; Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, San Antonio, TX, USA.; Department of Cell Systems and Anatomy, San Antonio, TX, USA.; University of Texas Health San Antonio, San Antonio, TX, USA., Gamez M; Sam and Ann Barshop Institute for Longevity and Aging Studies, San Antonio, TX, USA.; Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, San Antonio, TX, USA.; Department of Cell Systems and Anatomy, San Antonio, TX, USA.; University of Texas Health San Antonio, San Antonio, TX, USA., Gonzalez E; Sam and Ann Barshop Institute for Longevity and Aging Studies, San Antonio, TX, USA.; Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, San Antonio, TX, USA.; Department of Cell Systems and Anatomy, San Antonio, TX, USA.; University of Texas Health San Antonio, San Antonio, TX, USA., De Mange J; Sam and Ann Barshop Institute for Longevity and Aging Studies, San Antonio, TX, USA.; Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, San Antonio, TX, USA.; Department of Cell Systems and Anatomy, San Antonio, TX, USA.; University of Texas Health San Antonio, San Antonio, TX, USA., Bieniek KF; Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, San Antonio, TX, USA.; University of Texas Health San Antonio, San Antonio, TX, USA., Ray WJ; The Neurodegeneration Consortium, Therapeutics Discovery Division, University of Texas MD Anderson Cancer Center, Houston, TX, USA., Frost B; Sam and Ann Barshop Institute for Longevity and Aging Studies, San Antonio, TX, USA.; Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, San Antonio, TX, USA.; Department of Cell Systems and Anatomy, San Antonio, TX, USA.; University of Texas Health San Antonio, San Antonio, TX, USA.
المصدر: IScience [iScience] 2023 Feb 08; Vol. 26 (3), pp. 106152. Date of Electronic Publication: 2023 Feb 08 (Print Publication: 2023).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101724038 Publication Model: eCollection Cited Medium: Internet ISSN: 2589-0042 (Electronic) Linking ISSN: 25890042 NLM ISO Abbreviation: iScience Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [Cambridge, MA] : Cell Press, [2018]-
مستخلص: In Alzheimer's disease, neurons acquire phenotypes that are also present in various cancers, including aberrant activation of the cell cycle. Unlike cancer, cell cycle activation in post-mitotic neurons is sufficient to induce cell death. Multiple lines of evidence suggest that abortive cell cycle activation is a consequence of pathogenic forms of tau, a protein that drives neurodegeneration in Alzheimer's disease and related "tauopathies." Here we combine network analyses of human Alzheimer's disease and mouse models of Alzheimer's disease and primary tauopathy with studies in Drosophila to discover that pathogenic forms of tau drive cell cycle activation by disrupting a cellular program involved in cancer and the epithelial-mesenchymal transition (EMT). Moesin, an EMT driver, is elevated in cells harboring disease-associated phosphotau, over-stabilized actin, and ectopic cell cycle activation. We further find that genetic manipulation of Moesin mediates tau-induced neurodegeneration. Taken together, our study identifies novel parallels between tauopathy and cancer.
(© 2023 The Author(s).)
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معلومات مُعتمدة: T32 AG021890 United States AG NIA NIH HHS; P01 AG019316 United States AG NIA NIH HHS; R25 GM095480 United States GM NIGMS NIH HHS; R01 AG057896 United States AG NIA NIH HHS; F31 NS108657 United States NS NINDS NIH HHS; P30 CA054174 United States CA NCI NIH HHS; P40 OD018537 United States OD NIH HHS; P30 AG013319 United States AG NIA NIH HHS; P30 AG066546 United States AG NIA NIH HHS; U01 AG046139 United States AG NIA NIH HHS
فهرسة مساهمة: Keywords: Cellular physiology; Gene network; Pathophysiology
تواريخ الأحداث: Date Created: 20230307 Latest Revision: 20240501
رمز التحديث: 20240501
مُعرف محوري في PubMed: PMC9984563
DOI: 10.1016/j.isci.2023.106152
PMID: 36879821
قاعدة البيانات: MEDLINE
الوصف
تدمد:2589-0042
DOI:10.1016/j.isci.2023.106152