KCC2 inhibition and neuronal hyperexcitability promote extrinsic apoptosis dependent upon C1q
These results strongly support the hypothesis that the KCC2/C1q protein complex plays a critical role in the apoptotic process that occurs following loss of KCC2 function.
Authors
- Joshua L. Smalley (ORCID: https://orcid.org/0000-0002-7437-6655)
- Stephen J. Moss (ORCID: https://orcid.org/0000-0002-5150-8926)
- Catherine Choi (ORCID: https://orcid.org/0000-0002-3215-9601)
- Christopher E. Bope
- Jacob S. Dengler
- Jinglin Ji
Institutions
- Tufts University (US)
Publication Details
- Journal
- Frontiers in Molecular Neuroscience
- Published
- 2025-08-18
- DOI
- https://doi.org/10.3389/fnmol.2025.1645428
- Primary Topic
- Complement system in diseases
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Institutes of Health
- National Institute of Mental Health