Gillian P. Bates
UCL Queen Square Institute Of Neurology
London, ENG, United Kingdom
London, ENG, United Kingdom
Last Updated: 09/26/2026
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Found 94 publications
Blocking somatic repeat expansion and lowering huntingtin by RNAi synergize to attenuate Huntington's disease pathogenesis in mice.
Journal: Science translational medicine
Published: August 12, 2026
Selective targeting of mutant huntingtin intron 1 improves rescue provided by antisense oligonucleotides in Huntington's disease mice.
Journal: Science translational medicine
Published: March 18, 2026
Lowering the HTT1a transcript as an effective therapy for Huntington's disease in a knockin mouse model.
Journal: Science translational medicine
Published: March 18, 2026
Enhancing the detection of HTT1a with neoepitope antibodies in mouse models of Huntington's disease.
Enhancing the detection of HTT1a with neoepitope antibodies in mouse models of Huntington's disease.
Journal: Brain communications
Published: February 10, 2026
Molecular features of a Huntington's disease knock-in minipig.
Journal: Disease models & mechanisms
Published: December 17, 2025
Nuclear RNA clusters are dynamic structural entities in Huntington's disease.
Journal: Communications biology
Published: November 17, 2025
The HTT1a protein initiates HTT aggregation in a knock-in mouse model of Huntington's disease.
Journal: Brain : a journal of neurology
Published: September 19, 2025
Human-specific sequence features in HTT exon 1 promote toxic misprocessing via splicing factor SRSF7.
Journal: Nature communications
Published: August 14, 2025
Blocking somatic repeat expansion and lowering huntingtin via RNA interference synergize to prevent Huntington's disease pathogenesis in mice.
Journal: bioRxiv : the preprint server for biology
Published: July 16, 2025
Somatic CAG-repeat expansion drives neuronal loss in Huntington's disease.
Journal: Neuron
Published: January 03, 2025
Last Updated: 09/26/2026