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Intracellular localization and splicing regulation of FUS/TLS are variably affected by amyotrophic lateral sclerosis-linked mutations.
- Published in:
- Nucleic Acids Research, 2011, v. 39, n. 7, p. 2781, doi. 10.1093/nar/gkq1162
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- Article
MBNL and CELF proteins regulate alternative splicing of the skeletal muscle chloride channel CLCN1.
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- Nucleic Acids Research, 2009, v. 37, n. 19, p. 6477, doi. 10.1093/nar/gkp681
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- Article
FUS/TLS deficiency causes behavioral and pathological abnormalities distinct from amyotrophic lateral sclerosis.
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- Acta Neuropathologica Communications, 2015, v. 3, n. 1, p. 1, doi. 10.1186/s40478-015-0202-6
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- Article
FUS/TLS acts as an aggregation-dependent modifier of polyglutamine disease model mice.
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- Scientific Reports, 2016, p. 35236, doi. 10.1038/srep35236
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- Article
Mutant Huntingtin reduces HSP70 expression through the sequestration of NF-Y transcription factor.
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- EMBO Journal, 2008, v. 27, n. 6, p. 827, doi. 10.1038/emboj.2008.23
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- Article
Depletion of p62 reduces nuclear inclusions and paradoxically ameliorates disease phenotypes in Huntington’s model mice.
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- Human Molecular Genetics, 2015, v. 24, n. 4, p. 1092, doi. 10.1093/hmg/ddu522
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- Article
Nuclear localization of MBNL1: splicing-mediated autoregulation and repression of repeat-derived aberrant proteins.
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- Human Molecular Genetics, 2015, v. 24, n. 3, p. 740, doi. 10.1093/hmg/ddu492
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- Article
Blocking acid-sensing ion channel 1 alleviates Huntington's disease pathology via an ubiquitin-proteasome system-dependent mechanism.
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- Human Molecular Genetics, 2008, v. 17, n. 20, p. 3223, doi. 10.1093/hmg/ddn218
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- Article