Jeffrey B. Carroll
Affiliations: | 2004-2010 | University of British Columbia, Vancouver, Vancouver, BC, Canada |
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Parents
Sign in to add mentor| Michael R. Hayden | grad student | 2004-2010 | Western Washington University |
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Publications
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| Greco TM, Secker C, Ramos ES, et al. (2022) Dynamics of huntingtin protein interactions in the striatum identifies candidate modifiers of Huntington disease. Cell Systems |
| Malaiya S, Cortes-Gutierrez M, Herb BR, et al. (2021) Single-Nucleus RNA-Seq Reveals Dysregulation of Striatal Cell Identity Due to Huntington's Disease Mutations. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience |
| Minikel EV, Zhao HT, Le J, et al. (2020) Prion protein lowering is a disease-modifying therapy across prion disease stages, strains and endpoints. Nucleic Acids Research |
| Raymond GJ, Zhao HT, Race B, et al. (2019) Antisense oligonucleotides extend survival of prion-infected mice. Jci Insight. 5 |
| Ament SA, Pearl JR, Cantle JP, et al. (2018) Transcriptional regulatory networks underlying gene expression changes in Huntington's disease. Molecular Systems Biology. 14: e7435 |
| Kovalenko M, Milnerwood A, Giordano J, et al. (2018) HttQ111/+ Huntington's Disease Knock-in Mice Exhibit Brain Region-Specific Morphological Changes and Synaptic Dysfunction. Journal of Huntington's Disease. 7: 17-33 |
| Minnig S, Bragg RM, Tiwana HS, et al. (2018) Early Detection of Apathetic Phenotypes in Huntington's Disease Knock-in Mice Using Open Source Tools. Scientific Reports. 8: 2304 |
| Coffey SR, Bragg RM, Minnig S, et al. (2017) Peripheral huntingtin silencing does not ameliorate central signs of disease in the B6.HttQ111/+ mouse model of Huntington's disease. Plos One. 12: e0175968 |
| Ament SA, Pearl JR, Grindeland A, et al. (2017) High resolution time-course mapping of early transcriptomic, molecular and cellular phenotypes in Huntington's disease CAG knock-in mice across multiple genetic backgrounds. Human Molecular Genetics |
| Bragg RM, Coffey SR, Weston RM, et al. (2017) Motivational, proteostatic and transcriptional deficits precede synapse loss, gliosis and neurodegeneration in the B6.Htt(Q111/+) model of Huntington's disease. Scientific Reports. 7: 41570 |