ArticleEMBO molecular medicine2011
A CAG repeat polymorphism of KCNN3 predicts SK3 channel function and cognitive performance in schizophrenia.
Article in EMBO molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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42 citing papers in PubMed, 68 citations in OpenAlex.
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- Spatial transcriptomics reveals the distinct organization of mouse prefrontal cortex and neuronal subtypes regulating chronic pain.Nature neuroscience · 2023Article
- Domesticated HERV-W env contributes to the activation of the small conductance CaVirologica Sinica · 2023Article
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- Revisiting tandem repeats in psychiatric disorders from perspectives of genetics, physiology, and brain evolution.Molecular psychiatry · 2022Review
- L1 Retrotransposons: A Potential Endogenous Regulator for Schizophrenia.Frontiers in genetics · 2022Review
- Targets and regulation of microRNA-652-3p in homoeostasis and disease.Journal of molecular medicine (Berlin, Germany) · 2021Review
- PKA and Ube3a regulate SK2 channel trafficking to promote synaptic plasticity in hippocampus: Implications for Angelman Syndrome.Scientific reports · 2020Article
- SAP97 rs3915512 Polymorphism Affects the Neurocognition of Schizophrenic Patients: A Genetic Neuroimaging Study.Frontiers in genetics · 2020Article
- Age-dependent neuroprotective effect of an SK3 channel agonist on excitotoxity to dopaminergic neurons in organotypic culture.PloS one · 2020Article
- Gain-of-Function Mutations in KCNN3 Encoding the Small-Conductance CaAmerican journal of human genetics · 2019Article
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Authors and funding
20 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
KCNN3, encoding the small conductance calcium-activated potassium channel SK3, harbours a polymorphic CAG repeat in the amino-terminal coding region with yet unproven function. Hypothesizing that KCNN3 genotypes do not influence susceptibility to schizophrenia but modify its phenotype, we explored their contribution to specific schizophrenic symptoms. Using the Göttingen Research Association for Schizophrenia (GRAS) data collection of schizophrenic patients (n = 1074), we performed a phenotype-based genetic association study (PGAS) of KCNN3. We show that long CAG repeats in the schizophrenic sample are specifically associated with better performance in higher cognitive tasks, comprising the capacity to discriminate, select and execute (p < 0.0001). Long repeats reduce SK3 channel function, as we demonstrate by patch-clamping of transfected HEK293 cells. In contrast, modelling the opposite in mice, i.e. KCNN3 overexpression/channel hyperfunction, leads to selective deficits in higher brain functions comparable to those influenced by SK3 conductance in humans. To conclude, KCNN3 genotypes modify cognitive performance, shown here in a large sample of schizophrenic patients. Reduction of SK3 function may constitute a pharmacological target to improve cognition in schizophrenia and other conditions with cognitive impairment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.