SIK2-mediated phosphorylation of GABARAPL2 facilitates autophagosome–lysosome fusion and rescues neurodegeneration in an Alzheimer’s disease model
These findings establish the SIK2-GABARAPL2 axis as a novel signaling cascade governing autophagic flux through lysosomal fusion competence. Dysfunction in this axis contributes to Aβ deposition in AD, offering new insights into the pathogenic mechanisms underlying autophagosome-lysosome fusion in AD and highlighting its potential as a therapeutic target.
Authors
- Xiaoman Dai (ORCID: https://orcid.org/0000-0003-3409-5936)
- Yufei Huang (ORCID: https://orcid.org/0000-0001-5141-5941)
- Tianqing Han
- Ziling Ye (ORCID: https://orcid.org/0009-0005-0436-5925)
- Chen Wang (ORCID: https://orcid.org/0000-0003-2931-7856)
- Jing Zhang (ORCID: https://orcid.org/0000-0001-9940-8572)
- Yun Chen (ORCID: https://orcid.org/0000-0002-3130-8118)
- Xiaochun Chen (ORCID: https://orcid.org/0000-0001-6619-0175)
- Xin Wu (ORCID: https://orcid.org/0000-0002-3170-0312)
- Weijie Gao (ORCID: https://orcid.org/0009-0008-9025-267X)
Institutions
- Fujian Medical University (CN)
- Union Hospital (CN)
Publication Details
- Journal
- Translational Neurodegeneration
- Published
- 2025-10-23
- DOI
- https://doi.org/10.1186/s40035-025-00514-4
- Citations
- 2
- Primary Topic
- Autophagy in Disease and Therapy
- Type
- article
- Field-Weighted Citation Impact
- 2.71
Funders
- National Natural Science Foundation of China
- Fujian Medical University