Death-associated protein kinase 1-dependent SENP1 degradation increases tau SUMOylation and leads to cognitive dysfunction in a mouse model for tauopathy
DAPK1-mediated SENP1 phosphorylation and degradation promote tau SUMOylation, exacerbating tau pathology and cognitive dysfunction in tauopathy. Our findings highlight the DAPK1-SENP1-tau SUMOylation axis as a critical regulator of tau homeostasis, and establish DAPK1 inhibition as a promising therapeutic strategy for AD and related tauopathies.
Authors
- Renxuan Chen
- Xindong Shui
- Z Wang (ORCID: https://orcid.org/0000-0002-1331-4207)
- Gamin Kim (ORCID: https://orcid.org/0000-0001-8504-7921)
- Jinfeng Wu (ORCID: https://orcid.org/0000-0002-6930-5465)
- Ruomeng Li (ORCID: https://orcid.org/0000-0002-7278-1585)
- Ling Zhang (ORCID: https://orcid.org/0000-0002-2964-7436)
- Tao Zhang (ORCID: https://orcid.org/0000-0002-8157-7674)
- Ying Zhou (ORCID: https://orcid.org/0000-0003-3607-8216)
- Long Wang (ORCID: https://orcid.org/0000-0002-2733-7370)
- Mi Zhang (ORCID: https://orcid.org/0000-0002-9780-136X)
- Tae Ho Lee (ORCID: https://orcid.org/0000-0001-5968-1478)
- Xiaoqing Zheng
- Yameng Zheng
- Jungho Kim (ORCID: https://orcid.org/0009-0001-6113-6484)
- Dongmei Chen
- Leilei Peng
Institutions
- Fujian Medical University (CN)
- Sogang University (KR)
Publication Details
- Journal
- Molecular Neurodegeneration
- Published
- 2025-11-21
- DOI
- https://doi.org/10.1186/s13024-025-00911-3
- Citations
- 1
- Primary Topic
- Ubiquitin and proteasome pathways
- Type
- article
- Field-Weighted Citation Impact
- 0.81