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1
Large Polyglutamine Repeats Cause Muscle Degeneration in SCA17 Mice.
Cell Rep. 2015 Oct 6;13(1):196-208. doi: 10.1016/j.celrep.2015.08.060. Epub 2015 Sep 17.
2
Role of Mutant TBP in Regulation of Myogenesis on Muscle Satellite Cells.
Curr Med Sci. 2019 Oct;39(5):734-740. doi: 10.1007/s11596-019-2099-y. Epub 2019 Oct 14.
3
Transcriptional dysregulation of TrkA associates with neurodegeneration in spinocerebellar ataxia type 17.
Hum Mol Genet. 2009 Nov 1;18(21):4141-52. doi: 10.1093/hmg/ddp363. Epub 2009 Jul 30.
6
Molecular Mechanisms and Therapeutics for SCA17.
Neurotherapeutics. 2019 Oct;16(4):1097-1105. doi: 10.1007/s13311-019-00762-z.
7
Polyglutamine expansion reduces the association of TATA-binding protein with DNA and induces DNA binding-independent neurotoxicity.
J Biol Chem. 2008 Mar 28;283(13):8283-90. doi: 10.1074/jbc.M709674200. Epub 2008 Jan 24.
8
Deactivation of TBP contributes to SCA17 pathogenesis.
Hum Mol Genet. 2014 Dec 20;23(25):6878-93. doi: 10.1093/hmg/ddu410. Epub 2014 Aug 7.
10
Molecular investigation of TBP allele length: a SCA17 cellular model and population study.
Neurobiol Dis. 2003 Jun;13(1):37-45. doi: 10.1016/s0969-9961(03)00014-7.

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Molecular Mechanisms of Spinocerebellar Ataxia Type 17.
Mol Neurobiol. 2025 May;62(5):5720-5729. doi: 10.1007/s12035-024-04645-z. Epub 2024 Nov 30.
2
The role(s) of NF-Y in development and differentiation.
Cell Death Differ. 2025 Feb;32(2):195-206. doi: 10.1038/s41418-024-01388-1. Epub 2024 Sep 26.
4
Advances in Nucleotide Repeat Expansion Diseases: Transcription Gets in Phase.
Cells. 2023 Mar 7;12(6):826. doi: 10.3390/cells12060826.
5
LncRNA-TBP mediates TATA-binding protein recruitment to regulate myogenesis and induce slow-twitch myofibers.
Cell Commun Signal. 2023 Jan 12;21(1):7. doi: 10.1186/s12964-022-01001-3.
6
A survey of protein interactions and posttranslational modifications that influence the polyglutamine diseases.
Front Mol Neurosci. 2022 Sep 14;15:974167. doi: 10.3389/fnmol.2022.974167. eCollection 2022.
7
Skeletal Muscle Pathogenesis in Polyglutamine Diseases.
Cells. 2022 Jul 3;11(13):2105. doi: 10.3390/cells11132105.
8
Consensus Paper: Strengths and Weaknesses of Animal Models of Spinocerebellar Ataxias and Their Clinical Implications.
Cerebellum. 2022 Jun;21(3):452-481. doi: 10.1007/s12311-021-01311-1. Epub 2021 Aug 10.
9
Polyglutamine diseases: looking beyond the neurodegenerative universe.
Neural Regen Res. 2021 Jun;16(6):1186-1187. doi: 10.4103/1673-5374.300434.
10
The Gene-Regulatory Footprint of Aging Highlights Conserved Central Regulators.
Cell Rep. 2020 Sep 29;32(13):108203. doi: 10.1016/j.celrep.2020.108203.

本文引用的文献

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HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy.
PLoS Genet. 2015 Mar 6;11(3):e1005021. doi: 10.1371/journal.pgen.1005021. eCollection 2015 Mar.
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Peripheral androgen receptor gene suppression rescues disease in mouse models of spinal and bulbar muscular atrophy.
Cell Rep. 2014 May 8;7(3):774-84. doi: 10.1016/j.celrep.2014.02.008. Epub 2014 Apr 16.
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Repeat-associated non-ATG (RAN) translation in neurological disease.
Hum Mol Genet. 2013 Oct 15;22(R1):R45-51. doi: 10.1093/hmg/ddt371. Epub 2013 Aug 4.
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Automated home cage assessment shows behavioral changes in a transgenic mouse model of spinocerebellar ataxia type 17.
Behav Brain Res. 2013 Aug 1;250:157-65. doi: 10.1016/j.bbr.2013.04.042. Epub 2013 May 7.
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Neuroprotective effects of granulocyte-colony stimulating factor in a novel transgenic mouse model of SCA17.
J Neurochem. 2011 Jul;118(2):288-303. doi: 10.1111/j.1471-4159.2011.07304.x. Epub 2011 Jun 2.
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CLOCK and BMAL1 regulate MyoD and are necessary for maintenance of skeletal muscle phenotype and function.
Proc Natl Acad Sci U S A. 2010 Nov 2;107(44):19090-5. doi: 10.1073/pnas.1014523107. Epub 2010 Oct 18.

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