日期:
2020 年 — 2026 年
2020
2021
2022
2023
2024
2025
2026
影响因子:

Atrophin-1 antisense oligonucleotide provides robust protection from pathology in a fully humanized DRPLA model.

Atrophin-1 反义寡核苷酸在完全人源化的 DRPLA 模型中提供了强大的病理保护作用。

Smith Velvet L, Gidi Bereket Z, Bragg Robert M, Cantle Jeffrey P, Ben-Varon Aliza, Noble Briana, Prades Silvia, Compton Andrea, Greenfield Julie, Korecka Joanna A, Gemos Anya, Yu Timothy, Khurana Vikram, Kordasiewicz Holly B, Zhao Hien T, Barker-Haliski Melissa, Child Daniel D, Carroll Jeffrey B

Huntingtin knockdown dysregulates autophagic degradation of Apolipoprotein E.

亨廷顿蛋白敲低会扰乱载脂蛋白 E 的自噬降解。

Fote Gianna M, McClure Nicolette R, Bragg Robert M, McKnight Jharrayne, Thompson Leslie M, Carroll Jeffrey B, Steffan Joan S

Suppression of Huntington's Disease Somatic Instability by Transcriptional Repression and Direct CAG Repeat Binding.

通过转录抑制和直接 CAG 重复序列结合抑制亨廷顿病体细胞不稳定性。

Mathews Ella W, Coffey Sydney R, Gärtner Annette, Belgrad Jillian, Bragg Robert M, O'Reilly Daniel, Cantle Jeffrey P, McHugh Cassandra, Summers Ashley, Fentz Joachim, Schwagarus Tom, Cornelius Antje, Lingos Ioannis, Burch Zoe, Kovalenko Marina, Andrew Marissa A, Bennett C Frank, Kordasiewicz Holly B, Marchionini Deanna M, Wilkinson Hilary, Vogt Thomas F, Beuzer Paolo, Pinto Ricardo M, Khvorova Anastasia, Howland David, Wheeler Vanessa C, Carroll Jeffrey B

Altered huntingtin-chromatin interactions predict transcriptional and epigenetic changes in Huntington's disease.

亨廷顿蛋白-染色质相互作用的改变可预测亨廷顿病中的转录和表观遗传变化

Pearl Jocelynn R, Shetty Amol C, Cantle Jeffrey P, Bergey Dani E, Bragg Robert M, Coffey Sydney R, Kordasiewicz Holly B, Hood Leroy E, Price Nathan D, Ament Seth A, Carroll Jeffrey B

Hereditary spastic paraplegia with thin corpus callosum and SPG11 mutation: A neuropathological evaluation.

胼胝体变薄伴 SPG11 基因突变的遗传性痉挛性截瘫:神经病理学评估

Scherpelz Kathryn P, Yoda Rebecca A, Jayadev Suman, Davis Marie Y, Hincks Joshua C, Liachko Nicole F, Bragg Robert M, Cochoit Alexa, MacDonald Christine L, Keene C Dirk, Bird Thomas D, Latimer Caitlin S

Corrigendum: Motivational, proteostatic and transcriptional deficits precede synapse loss, gliosis and neurodegeneration in the B6.Htt(Q111/+) model of Huntington's disease

更正:在亨廷顿病B6.Htt(Q111/+)模型中,动机、蛋白质稳态和转录缺陷先于突触丢失、胶质增生和神经退行性变发生。

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 L; Sullivan, Bonnie R; Jones, Lindsey; Glickenhaus, Anne; Anderson, John S; Anderson, Michael D; Dunnett, Stephen B; Wheeler, Vanessa C; MacDonald, Marcy E; Brooks, Simon P; Price, Nathan D; Carroll, Jeffrey B

Peripheral huntingtin silencing does not ameliorate central signs of disease in the B6.HttQ111/+ mouse model of Huntington's disease

在亨廷顿病B6.HttQ111/+小鼠模型中,外周亨廷顿蛋白沉默并不能改善中枢疾病症状。

Coffey, Sydney R; Bragg, Robert M; Minnig, Shawn; Ament, Seth A; Cantle, Jeffrey P; Glickenhaus, Anne; Shelnut, Daniel; Carrillo, José M; Shuttleworth, Dominic D; Rodier, Julie-Anne; Noguchi, Kimihiro; Bennett, C Frank; Price, Nathan D; Kordasiewicz, Holly B; Carroll, Jeffrey B