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000140673 0247_ $$2doi$$a10.1016/j.jmb.2019.01.019
000140673 0247_ $$2pmid$$apmid:30664869
000140673 0247_ $$2ISSN$$a0022-2836
000140673 0247_ $$2ISSN$$a1089-8638
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000140673 037__ $$aDZNE-2020-06995
000140673 041__ $$aEnglish
000140673 082__ $$a610
000140673 1001_ $$0P:(DE-2719)2421562$$aKrauss, Sybille$$b0$$eFirst author$$udzne
000140673 245__ $$aThe Role of MicroRNAs in Spinocerebellar Ataxia Type 3.
000140673 260__ $$aAmsterdam [u.a.]$$bElsevier$$c2019
000140673 264_1 $$2Crossref$$3print$$bElsevier BV$$c2019-04-01
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000140673 520__ $$aMore than 90% of the human genome are transcribed as non-coding RNAs. While it is still under debate if all these non-coding transcripts are functional, there is emerging evidence that RNA has several important functions in addition to coding for proteins. For example, microRNAs (miRNAs) are important regulatory RNAs that control gene expression in various biological processes and human diseases. In spinocerebellar ataxia type 3 (SCA3), a devastating neurodegenerative disease, miRNAs are involved in the disease process at different levels, including the deregulation of components of the general miRNA biogenesis machinery, as well as in the cell type-specific control of the expression of the SCA3 disease protein and other SCA3 disease-relevant proteins. However, it remains difficult to predict whether these changes are a cause or a consequence of the neurodegenerative process in SCA3. Further studies using standardized procedures for the analysis of miRNA expression and larger sample numbers are required to enhance our understanding of the miRNA-mediated processes involved in SCA3 disease and may enable the development of miRNA-based therapeutics. In this review, we summarize the findings of independent studies highlighting both the disease-related and cytoprotective roles of miRNAs that have been implicated so far in the disease process of SCA3.
000140673 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0
000140673 542__ $$2Crossref$$i2019-04-01$$uhttps://www.elsevier.com/tdm/userlicense/1.0/
000140673 542__ $$2Crossref$$i2019-01-30$$uhttp://creativecommons.org/licenses/by-nc-nd/4.0/
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000140673 650_2 $$2MeSH$$aAnimals
000140673 650_2 $$2MeSH$$aAtaxin-3: genetics
000140673 650_2 $$2MeSH$$aAtaxin-3: metabolism
000140673 650_2 $$2MeSH$$aBiomarkers: metabolism
000140673 650_2 $$2MeSH$$aBrain: metabolism
000140673 650_2 $$2MeSH$$aBrain: pathology
000140673 650_2 $$2MeSH$$aCell Line
000140673 650_2 $$2MeSH$$aDisease Models, Animal
000140673 650_2 $$2MeSH$$aDrosophila melanogaster: genetics
000140673 650_2 $$2MeSH$$aDrosophila melanogaster: metabolism
000140673 650_2 $$2MeSH$$aGene Expression Regulation
000140673 650_2 $$2MeSH$$aHumans
000140673 650_2 $$2MeSH$$aLymphocytes: metabolism
000140673 650_2 $$2MeSH$$aLymphocytes: pathology
000140673 650_2 $$2MeSH$$aMachado-Joseph Disease: genetics
000140673 650_2 $$2MeSH$$aMachado-Joseph Disease: metabolism
000140673 650_2 $$2MeSH$$aMachado-Joseph Disease: pathology
000140673 650_2 $$2MeSH$$aMachado-Joseph Disease: therapy
000140673 650_2 $$2MeSH$$aMice
000140673 650_2 $$2MeSH$$aMicroRNAs: genetics
000140673 650_2 $$2MeSH$$aMicroRNAs: metabolism
000140673 650_2 $$2MeSH$$aMolecular Targeted Therapy: methods
000140673 650_2 $$2MeSH$$aNeurons: metabolism
000140673 650_2 $$2MeSH$$aNeurons: pathology
000140673 650_2 $$2MeSH$$aRepressor Proteins: genetics
000140673 650_2 $$2MeSH$$aRepressor Proteins: metabolism
000140673 650_2 $$2MeSH$$aSignal Transduction
000140673 7001_ $$0P:(DE-HGF)0$$aEvert, Bernd O$$b1$$eCorresponding author
000140673 77318 $$2Crossref$$3journal-article$$a10.1016/j.jmb.2019.01.019$$b : Elsevier BV, 2019-04-01$$n9$$p1729-1742$$tJournal of Molecular Biology$$v431$$x0022-2836$$y2019
000140673 773__ $$0PERI:(DE-600)1355192-9$$a10.1016/j.jmb.2019.01.019$$gVol. 431, no. 9, p. 1729 - 1742$$n9$$p1729-1742$$q431:9<1729 - 1742$$tJournal of molecular biology$$v431$$x0022-2836$$y2019
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000140673 9141_ $$y2019
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000140673 9201_ $$0I:(DE-2719)1011006$$kAG Krauß ; AG Krauß$$lRegulatory RNA-protein interaction in neurodegenerative diseases$$x0
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