TAF15 and Transportin 1 in Intranuclear Inclusions of Neuronal Intranuclear Inclusion Disease

All authors have no competing interests to report. TL is a member of the editorial board of Neuropathology and Applied Neurobiology. The Editors of Neuropathology and Applied Neurobiology are committed to peer-review integrity and upholding the highest standards of review. As such, this article was peer-reviewed by independent, anonymous expert referees, and the authors had no role in either the editorial decision or the handling of the paper. The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions. TABLE S1 The proportion of TAF15- or transportin 1-positive intranuclear inclusions relative to the total number of p62-positive intranuclear inclusions. FIGURE S1 Specificity of an antibody against the fused in sarcoma homologue TATA-binding protein-associated with factor 15 (TAF15). (a) An antibody-absorption test [the anti-TAF15 antibody (EPR9197(B); ab134916, Abcam, Cambridge, UK): human TAF15 recombinant protein (H00008148-P02, Abnova, Taipei City, Taiwan = 1: 20] demonstrating no immunoreactivity for TAF15 in intranuclear inclusions of neuronal intranuclear inclusion body disease (arrowhead). (b,c) No immunoreactivity observed with a rabbit (b, arrowhead) or mouse (c, arrowhead) secondary antibody alone. Bar = 10 μm. FIGURE S2 Double immunofluorescence analysis with antibodies against the fused in sarcoma homologue TATA-binding protein-associated with factor 15 (TAF15) and p62 in intranuclear inclusions of spinocerebellar ataxia (SCA) 1, SCA3, and Huntington’s disease (HD). (a–i) No co-localisation of p62 and TAF15 in intranuclear inclusions (white arrowheads) of SCA1, SCA3, and HD. p62 (a,d,g) and TAF15 (b,e,h). Bars = 10 μm. FIGURE S3 Double immunofluorescence analysis with antibodies against transportin 1 and p62 in intranuclear inclusions of spinocerebellar ataxia (SCA) 1, SCA3, and Huntington’s disease (HD). (a–i) No co-localisation of p62 and transportin 1 in intranuclear inclusions (white arrowheads) of SCA1, SCA3, and HD. p62 (a,d,g) and transportin 1 (b,e,h). Bars = 10 μm. FIGURE S4 Double immunofluorescence analysis with antibodies against Ewing’s sarcoma (EWS) and p62 in intranuclear inclusions of spinocerebellar ataxia (SCA) 1, SCA3, and Huntington’s disease (HD). (a–i) No co-localisation of p62 and EWS in intranuclear inclusions (white arrowheads) of SCA1, SCA3, and HD. p62 (a,d,g) and EWS (b,e,h). Bars = 10 μm. Data S1 Supporting information. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

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Journal
Neuropathology and Applied Neurobiology
Published
2025-05-22
DOI
https://doi.org/10.1111/nan.70021
Primary Topic
Amyotrophic Lateral Sclerosis Research
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article
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0.00

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article

TAF15 and Transportin 1 in Intranuclear Inclusions of Neuronal Intranuclear Inclusion Disease

Akiyoshi Kakita, Thomas T. Warner, Mari Tada, Mari Yoshida et al.
Neuropathology and Applied Neurobiology
Amyotrophic Lateral Sclerosis Research
article

TAF15 and Transportin 1 in Intranuclear Inclusions of Neuronal Intranuclear Inclusion Disease

Akiyoshi Kakita, Thomas T. Warner, Mari Tada, Mari Yoshida, Yutaka Inoue, Tammaryn Lashley, Yasuo Miki, Fumiaki Mori, Koichi Wakabayashi
article en

Abstract

All authors have no competing interests to report. TL is a member of the editorial board of Neuropathology and Applied Neurobiology. The Editors of Neuropathology and Applied Neurobiology are committed to peer-review integrity and upholding the highest standards of review. As such, this article was peer-reviewed by independent, anonymous expert referees, and the authors had no role in either the editorial decision or the handling of the paper. The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions. TABLE S1 The proportion of TAF15- or transportin 1-positive intranuclear inclusions relative to the total number of p62-positive intranuclear inclusions. FIGURE S1 Specificity of an antibody against the fused in sarcoma homologue TATA-binding protein-associated with factor 15 (TAF15). (a) An antibody-absorption test [the anti-TAF15 antibody (EPR9197(B); ab134916, Abcam, Cambridge, UK): human TAF15 recombinant protein (H00008148-P02, Abnova, Taipei City, Taiwan = 1: 20] demonstrating no immunoreactivity for TAF15 in intranuclear inclusions of neuronal intranuclear inclusion body disease (arrowhead). (b,c) No immunoreactivity observed with a rabbit (b, arrowhead) or mouse (c, arrowhead) secondary antibody alone. Bar = 10 μm. FIGURE S2 Double immunofluorescence analysis with antibodies against the fused in sarcoma homologue TATA-binding protein-associated with factor 15 (TAF15) and p62 in intranuclear inclusions of spinocerebellar ataxia (SCA) 1, SCA3, and Huntington’s disease (HD). (a–i) No co-localisation of p62 and TAF15 in intranuclear inclusions (white arrowheads) of SCA1, SCA3, and HD. p62 (a,d,g) and TAF15 (b,e,h). Bars = 10 μm. FIGURE S3 Double immunofluorescence analysis with antibodies against transportin 1 and p62 in intranuclear inclusions of spinocerebellar ataxia (SCA) 1, SCA3, and Huntington’s disease (HD). (a–i) No co-localisation of p62 and transportin 1 in intranuclear inclusions (white arrowheads) of SCA1, SCA3, and HD. p62 (a,d,g) and transportin 1 (b,e,h). Bars = 10 μm. FIGURE S4 Double immunofluorescence analysis with antibodies against Ewing’s sarcoma (EWS) and p62 in intranuclear inclusions of spinocerebellar ataxia (SCA) 1, SCA3, and Huntington’s disease (HD). (a–i) No co-localisation of p62 and EWS in intranuclear inclusions (white arrowheads) of SCA1, SCA3, and HD. p62 (a,d,g) and EWS (b,e,h). Bars = 10 μm. Data S1 Supporting information. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

Neuropathology and Applied NeurobiologyVol. 51(3)
Hirosaki University (JP), Aichi Medical University (JP), National Hospital for Neurology and Neurosurgery (GB), University College London (GB), Niigata University (JP)
Japan Society for the Promotion of Science
Reduced inequalities
Openalex Percentile: Top 81%
Amyotrophic Lateral Sclerosis Research
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