000141139 001__ 141139
000141139 005__ 20240321220929.0
000141139 0247_ $$2doi$$a10.2174/2211536607666180821162403
000141139 0247_ $$2pmid$$apmid:30147021
000141139 0247_ $$2ISSN$$a2211-5366
000141139 0247_ $$2ISSN$$a2211-5374
000141139 037__ $$aDZNE-2020-07461
000141139 041__ $$aEnglish
000141139 082__ $$a570
000141139 1001_ $$0P:(DE-2719)2421562$$aKrauß, Sybille$$b0$$eFirst author
000141139 245__ $$aUpregulation of miR-25 and miR-181 Family Members Correlates with Reduced Expression of ATXN3 in Lymphocytes from SCA3 Patients.
000141139 260__ $$aSharjah [u.a.]$$bBentham Science$$c2019
000141139 264_1 $$2Crossref$$3print$$bBentham Science Publishers Ltd.$$c2018-11-27
000141139 3367_ $$2DRIVER$$aarticle
000141139 3367_ $$2DataCite$$aOutput Types/Journal article
000141139 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1700147394_27198
000141139 3367_ $$2BibTeX$$aARTICLE
000141139 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000141139 3367_ $$00$$2EndNote$$aJournal Article
000141139 520__ $$aSpinocerebellar ataxia type 3 (SCA3), the most common spinocerebellar ataxia, is caused by a polyglutamine (polyQ) expansion in the protein ataxin-3 (ATXN3). Silencing the expression of polyQ-expanded ATXN3 rescues the cellular disease phenotype.This study investigated the differential expression of microRNAs (miRNAs), small noncoding RNAs targeting gene expression, in lymphoblastoid cells (LCs) from SCA3 patients and the capability of identified deregulated miRNAs to target and alter ATXN3 expression.MiRNA profiling was performed by microarray hybridization of total RNA from control and SCA3-LCs. The capability of the identified miRNAs and their target sites to suppress ATXN3 expression was analyzed using mutagenesis, reverse transcription PCR, immunoblotting, luciferase reporter assays, mimics and precursors of the identified miRNAs.SCA3-LCs showed significantly decreased expression levels of ATXN3 and a significant upregulation of the ATXN3-3'UTR targeting miRNAs, miR-32 and miR-181c and closely related members of the miR-25 and miR-181 family, respectively. MiR-32 and miR-181c effectively targeted the 3'UTR of ATXN3 and suppressed the expression of ATXN3.The simultaneous upregulation of closely related miRNAs targeting the 3'UTR of ATXN3 and the significantly reduced ATXN3 expression levels in SCA3-LCs suggests that miR-25 and miR-181 family members cooperatively bind to the 3'UTR to suppress the expression of ATXN3. The findings further suggest that the upregulation of miR-25 and miR-181 family members in SCA3- LCs reflects a cell type-specific, protective mechanism to diminish polyQ-mediated cytotoxic effects. Thus, miRNA mimics of miR-25 and miR-181 family members may prove useful for the treatment of SCA3.
000141139 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0
000141139 542__ $$2Crossref$$i2018-11-27$$uhttps://creativecommons.org/licenses/by/4.0/legalcode
000141139 588__ $$aDataset connected to CrossRef, PubMed,
000141139 650_7 $$2NLM Chemicals$$a3' Untranslated Regions
000141139 650_7 $$2NLM Chemicals$$aMIRN25 microRNA, human
000141139 650_7 $$2NLM Chemicals$$aMIrn181 microRNA, human
000141139 650_7 $$2NLM Chemicals$$aMicroRNAs
000141139 650_7 $$2NLM Chemicals$$aRepressor Proteins
000141139 650_7 $$0EC 3.4.19.12$$2NLM Chemicals$$aATXN3 protein, human
000141139 650_7 $$0EC 3.4.19.12$$2NLM Chemicals$$aAtaxin-3
000141139 650_2 $$2MeSH$$a3' Untranslated Regions
000141139 650_2 $$2MeSH$$aAtaxin-3: genetics
000141139 650_2 $$2MeSH$$aAtaxin-3: metabolism
000141139 650_2 $$2MeSH$$aHeLa Cells
000141139 650_2 $$2MeSH$$aHumans
000141139 650_2 $$2MeSH$$aLymphocytes: metabolism
000141139 650_2 $$2MeSH$$aMachado-Joseph Disease: genetics
000141139 650_2 $$2MeSH$$aMachado-Joseph Disease: metabolism
000141139 650_2 $$2MeSH$$aMicroRNAs: genetics
000141139 650_2 $$2MeSH$$aMicroRNAs: metabolism
000141139 650_2 $$2MeSH$$aRepressor Proteins: genetics
000141139 650_2 $$2MeSH$$aRepressor Proteins: metabolism
000141139 7001_ $$0P:(DE-2719)2809904$$aNalavade, Rohit$$b1
000141139 7001_ $$0P:(DE-2719)2662310$$aWeber, Stephanie$$b2
000141139 7001_ $$0P:(DE-HGF)0$$aCarter, Katlynn$$b3
000141139 7001_ $$0P:(DE-HGF)0$$aEvert, Bernd O$$b4
000141139 77318 $$2Crossref$$3journal-article$$a10.2174/2211536607666180821162403$$b : Bentham Science Publishers Ltd., 2018-11-27$$n1$$p76-85$$tMicroRNA$$v8$$x2211-5366$$y2018
000141139 773__ $$0PERI:(DE-600)2800970-8$$a10.2174/2211536607666180821162403$$gVol. 8, no. 1, p. 76 - 85$$n1$$p76-85$$q8:1<76 - 85$$tMicroRNA$$v8$$x2211-5366$$y2019
000141139 8564_ $$uhttps://pub.dzne.de/record/141139/files/DZNE-2020-07461_Restricted.pdf
000141139 8564_ $$uhttps://pub.dzne.de/record/141139/files/DZNE-2020-07461_Restricted.pdf?subformat=pdfa$$xpdfa
000141139 909CO $$ooai:pub.dzne.de:141139$$pVDB
000141139 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2421562$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b0$$kDZNE
000141139 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2809904$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b1$$kDZNE
000141139 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2662310$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b2$$kDZNE
000141139 9131_ $$0G:(DE-HGF)POF3-342$$1G:(DE-HGF)POF3-340$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lErkrankungen des Nervensystems$$vDisease Mechanisms and Model Systems$$x0
000141139 9141_ $$y2019
000141139 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2022-11-19
000141139 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2022-11-19
000141139 9201_ $$0I:(DE-2719)1011006$$kAG Krauß$$lRegulatory RNA-protein interaction in neurodegenerative diseases$$x0
000141139 980__ $$ajournal
000141139 980__ $$aVDB
000141139 980__ $$aI:(DE-2719)1011006
000141139 980__ $$aUNRESTRICTED
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