Expression profile analysis in cells overexpressing <scp>DRPLA cDNA</scp> to explore the roles of <scp>DRPLAp</scp> as a transcriptional coregulator-Reference-Cited by-同舟云学术

Expression profile analysis in cells overexpressing DRPLA cDNA to explore the roles of DRPLAp as a transcriptional coregulator

Published:2022-05-11 Issue:4 Volume:10 Page:210-217
ISSN:2049-4173
Container-title:Neurology and Clinical Neuroscience
language:en
Short-container-title:Neurology & Clinical Neurosc

Author:

Hatano Keiko¹²^ORCID,Date Hidetoshi¹³,Ishiura Hiroyuki¹^ORCID,Matsukawa Takashi¹⁴,Tanaka Masaki¹⁵,Mitsui Jun¹⁴,Goto Jun¹⁶,Yoshimura Jun⁷,Doi Koichiro⁷⁸,Morishita Shinichi⁷,Tsuji Shoji⁴⁵

Affiliation:

1. Department of Neurology Graduate School of Medicine The University of Tokyo Tokyo Japan

2. Department of Neurology Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology Tokyo Japan

3. Department of Neurology National Center of Neurology and Psychiatry Tokyo Japan

4. Department of Molecular Neurology The University of Tokyo Tokyo Japan

5. Institute of Medical Genomics International University of Health and Welfare Chiba Japan

6. Department of Neurology International University of Health and Welfare Ichikawa Hospital Chiba Japan

7. Department of Computational Biology Graduate School of Frontier Sciences The University of Tokyo Chiba Japan

8. Department of Bionics Program Tokyo University of Technology Tokyo Japan

Funder

Japan Agency for Medical Research and Development

Publisher

Wiley

Subject

Neurology (clinical),Neurology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1111/ncn3.12607

Reference28 articles.

1. Unstable expansion of CAG repeat in hereditary dentatorubral–pallidoluysian atrophy (DRPLA)

2. Dentatorubral and pallidoluysian atrophy expansion of an unstable CAG trinucleotide on chromosome 12p

3. Androgen receptor gene mutations in X-linked spinal and bulbar muscular atrophy

4. A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes

5. Expansion of an unstable trinucleotide CAG repeat in spinocerebellar ataxia type 1