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001     140673
005     20240321220843.0
024 7 _ |a 10.1016/j.jmb.2019.01.019
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024 7 _ |a pmid:30664869
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024 7 _ |a 0022-2836
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024 7 _ |a 1089-8638
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037 _ _ |a DZNE-2020-06995
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Krauss, Sybille
|0 P:(DE-2719)2421562
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|e First author
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245 _ _ |a The Role of MicroRNAs in Spinocerebellar Ataxia Type 3.
260 _ _ |a Amsterdam [u.a.]
|c 2019
|b Elsevier
264 _ 1 |3 print
|2 Crossref
|b Elsevier BV
|c 2019-04-01
336 7 _ |a article
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a More 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.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
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542 _ _ |i 2019-04-01
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|u https://www.elsevier.com/tdm/userlicense/1.0/
542 _ _ |i 2019-01-30
|2 Crossref
|u http://creativecommons.org/licenses/by-nc-nd/4.0/
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Ataxin-3: genetics
|2 MeSH
650 _ 2 |a Ataxin-3: metabolism
|2 MeSH
650 _ 2 |a Biomarkers: metabolism
|2 MeSH
650 _ 2 |a Brain: metabolism
|2 MeSH
650 _ 2 |a Brain: pathology
|2 MeSH
650 _ 2 |a Cell Line
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Drosophila melanogaster: genetics
|2 MeSH
650 _ 2 |a Drosophila melanogaster: metabolism
|2 MeSH
650 _ 2 |a Gene Expression Regulation
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Lymphocytes: metabolism
|2 MeSH
650 _ 2 |a Lymphocytes: pathology
|2 MeSH
650 _ 2 |a Machado-Joseph Disease: genetics
|2 MeSH
650 _ 2 |a Machado-Joseph Disease: metabolism
|2 MeSH
650 _ 2 |a Machado-Joseph Disease: pathology
|2 MeSH
650 _ 2 |a Machado-Joseph Disease: therapy
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a MicroRNAs: genetics
|2 MeSH
650 _ 2 |a MicroRNAs: metabolism
|2 MeSH
650 _ 2 |a Molecular Targeted Therapy: methods
|2 MeSH
650 _ 2 |a Neurons: metabolism
|2 MeSH
650 _ 2 |a Neurons: pathology
|2 MeSH
650 _ 2 |a Repressor Proteins: genetics
|2 MeSH
650 _ 2 |a Repressor Proteins: metabolism
|2 MeSH
650 _ 2 |a Signal Transduction
|2 MeSH
700 1 _ |a Evert, Bernd O
|0 P:(DE-HGF)0
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|e Corresponding author
773 1 8 |a 10.1016/j.jmb.2019.01.019
|b : Elsevier BV, 2019-04-01
|n 9
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|t Journal of Molecular Biology
|v 431
|y 2019
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773 _ _ |a 10.1016/j.jmb.2019.01.019
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856 4 _ |y OpenAccess
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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913 1 _ |a DE-HGF
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914 1 _ |y 2019
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