uN2CpolyG-mediated p65 nuclear sequestration suppresses the NF-κB-NLRP3 pathway in neuronal intranuclear inclusion disease
This study revealed that uN2CpolyG directly interacts with and sequesters p65, thereby inhibiting the NF-κB-NLRP3 pathway and impairing autophagy. This mechanism highlights a novel therapeutic target for NIID and provides potentially broader insights into similar mechanisms in other neurodegenerative diseases characterized by misfolded protein aggregates.
Authors
- Wen‐Quan Zou (ORCID: https://orcid.org/0000-0001-8062-0370)
- Kaiyan Jiang
- Yusen Qiu
- Daojun Hong (ORCID: https://orcid.org/0000-0003-1380-3534)
- Dandan Tan (ORCID: https://orcid.org/0000-0001-5216-6393)
- Jianwen Deng (ORCID: https://orcid.org/0000-0003-1206-1778)
- Ying Xiong (ORCID: https://orcid.org/0009-0002-3581-2845)
- Min Zhu (ORCID: https://orcid.org/0000-0002-8417-9698)
- Yu Shen
- Zhaoxia Wang
- Po-Feng Huang
Institutions
- Nanchang University (CN)
- Peking University (CN)
- Jiangxi Provincial Academy of Medical Sciences (CN)
- First Affiliated Hospital of Jiangxi Medical College (CN)
- Peking University First Hospital (CN)
- First Affiliated Hospital of Nanchang University (CN)
Publication Details
- Journal
- Cell Communication and Signaling
- Published
- 2025-02-07
- DOI
- https://doi.org/10.1186/s12964-025-02079-1
- Citations
- 1
- Primary Topic
- RNA regulation and disease
- Type
- article
- Field-Weighted Citation Impact
- 0.81
Funders
- National Natural Science Foundation of China
- Natural Science Foundation of Jiangxi Province
- Recruitment Program of Global Experts