Correction: Corrigendum: Motivational, proteostatic and transcriptional deficits precede synapse loss, gliosis and neurodegeneration in the B6.HttQ111/+ model of Huntington’s disease

Bragg, Robert M.; Coffey, Sydney R.; Weston, Rory M.; Ament, Seth A.; Cantle, Jeffrey P.; Minnig, Shawn; Funk, Cory C.; Shuttleworth, Dominic D.; Woods, Emily; Sullivan, Bonnie; Jones, Lindsey; Glickenhaus, Anne; Anderson, John S.; Anderson, Michael D.; Dunnett, Stephen B.; Wheeler, Vanessa C.; MacDonald, Marcy E.; Brooks, Simon Philip; Price, Nathan D.; Carroll, Jeffrey B.

doi:10.1038/srep44960

Sci Rep

2017

DOI: 10.1038/srep44960

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Correction: Corrigendum: Motivational, proteostatic and transcriptional deficits precede synapse loss, gliosis and neurodegeneration in the B6.HttQ111/+ model of Huntington’s disease

Robert M. Bragg¹,

Sydney R. Coffey²,

Rory M. Weston³

et al.

Abstract: Scientific Reports 7: Article number: 41570; published online: 08 February 2017; updated: 28 March 2017 This Article contains a typographical error in the Methods section, under the subheading “Library construction, RNA Sequencing and RNASeq analysis”, where: “The fastq files were aligned using the default parameters of SNAPR50 (https://github.

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Huntingtin lowering reduces somatic instability at CAG-expanded loci

Coffey

Andrew

Ging

et al. 2020

Preprint

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Expanded trinucleotide repeats cause many human diseases, including Huntington’s disease (HD). Recent studies indicate that somatic instability of these repeats contributes to pathogenesis in several expansion disorders. We find that lowering huntingtin protein (HTT) levels reduces somatic instability of both the Htt and Atxn2 CAG tracts in knockin mouse models, and the HTT CAG tract in human iPSC-derived neurons, revealing an unexpected role for HTT in regulating somatic instability.

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Huntingtin lowering reduces somatic instability at CAG-expanded loci

Coffey

Andrew

Ging

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

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Correction: Corrigendum: Motivational, proteostatic and transcriptional deficits precede synapse loss, gliosis and neurodegeneration in the B6.HttQ111/+ model of Huntington’s disease

Cited by 1 publication

References 0 publications

Huntingtin lowering reduces somatic instability at CAG-expanded loci

Huntingtin lowering reduces somatic instability at CAG-expanded loci

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