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.

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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

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article

KCC2 inhibition and neuronal hyperexcitability promote extrinsic apoptosis dependent upon C1q

Joshua L. Smalley, Stephen J. Moss, Catherine Choi, Christopher E. Bope et al.
Frontiers in Molecular Neuroscience
Complement system in diseases
article

KCC2 inhibition and neuronal hyperexcitability promote extrinsic apoptosis dependent upon C1q

Joshua L. Smalley, Stephen J. Moss, Catherine Choi, Christopher E. Bope, Jacob S. Dengler, Jinglin Ji
article en

Abstract

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.

Frontiers in Molecular NeuroscienceVol. 18
Tufts University (US)
National Institutes of Health, National Institute of Mental Health
Openalex Percentile: Top 77%
Complement system in diseases
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