TAF15 and Transportin 1 in Intranuclear Inclusions of Neuronal Intranuclear Inclusion Disease
- PMID: 40404483
- DOI: 10.1111/nan.70021
TAF15 and Transportin 1 in Intranuclear Inclusions of Neuronal Intranuclear Inclusion Disease
Keywords: FTLD‐FUS; TAF15; intranuclear inclusion; neuronal intranuclear inclusion disease; transportin 1.
References
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    - M. Neumann, E. Bentmann, D. Dormann, et al., “FET Proteins TAF15 and EWS Are Selective Markers That Distinguish FTLD With FUS Pathology From Amyotrophic Lateral Sclerosis With FUS Mutations,” Brain 134 (2011): 2595–2609.
 
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    - J. Brelstaff, T. Lashley, J. L. Holton, et al., “Transportin1: A Marker of FTLD‐FUS,” Acta Neuropathologica 122 (2011): 591–600.
 
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    - S. Tetter, D. Arseni, A. G. Murzin, et al., “TAF15 Amyloid Filaments in Frontotemporal Lobar Degeneration,” Nature 625 (2024): 345–351.
 
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    - J. Sone, K. Mori, T. Inagaki, et al., “Clinicopathological Features of Adult‐Onset Neuronal Intranuclear Inclusion Disease,” Brain 139 (2016): 3170–3186.
 
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    - H. Ishiura, S. Shibata, J. Yoshimura, et al., “Noncoding CGG Repeat Expansions in Neuronal Intranuclear Inclusion Disease, Oculopharyngodistal Myopathy and an Overlapping Disease,” Nature Genetics 51 (2019): 1222–1232.
 
Grants and funding
- Grants-in-Aid from the Research Committee of CNS Degenerative Diseases, Research on Policy Planning and Evaluation for Rare and Intractable Diseases, Health, Labour and Welfare Sciences Research Grants, the Ministry of Health, Labour and Welfare, Japan
- 24K10654/Japan Society for the Promotion of Science
- 23K06802/Japan Society for the Promotion of Science
- 23K24209/Japan Society for the Promotion of Science
- JP23wm0425019/The Collaborative Research Project of the Brain Research Institute, Niigata University, Japan Agency for Medical Research and Development
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