ArticleFrontiers in molecular neuroscience2025
KCC2 inhibition and neuronal hyperexcitability promote extrinsic apoptosis dependent upon C1q.
Article in Frontiers in molecular neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Synaptic vs. Non-Synaptic Glycine Receptors: Physiological Role and Implications in Alzheimer's Disease Pathology.International journal of molecular sciences · 2026Review
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6 authors.
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Abstract
Introduction: The potassium chloride co-transporter 2 (KCC2) is the principal Cl Methods: Here, we studied apoptotic induction in models of KCC2 loss of function and demonstrated the importance of C1q in this process using a constitutive C1qKO mouse model. We characterized the activation of different apoptotic pathways by measuring caspase 8 and caspase 9 cleavage as markers of extrinsic and intrinsic apoptosis, respectively. Results: This study demonstrates Discussion: 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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