ArticleHuman molecular genetics2013
Behavioural and functional characterization of Kv10.1 (Eag1) knockout mice.
Article in Human molecular genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Intellectual Disability and Potassium Channelopathies: A Systematic Review.Frontiers in genetics · 2020Pooled it
- New insights into the physiological, pathological and pharmacological roles of voltage‑gated potassium channel Kv10.1 in cancer (Review).International journal of oncology · 2026Review
- Amitriptyline inhibits EAG1 channels by binding to their PAS domains and exerts EAG1-dependent anti-tumorigenic effects.Cancer gene therapy · 2026Article
- The molecular basis of KCNH1-related epileptic encephalopathy and the challenge of developing targeted therapeutics.Brain : a journal of neurology · 2026Review
- Adam, amigo, brain, and K channel.Biophysical reviews · 2023Review
- The mechanism study ofTranslational cancer research · 2022Article
- Voltage-Gated Potassium Channels Beyond the Action Potential.Bioelectricity · 2022Article
- Genetic architecture and phenotypic landscape of deafness and onychodystrophy syndromes.Human genetics · 2022Review
- Bioelectric Dysregulation in Cancer Initiation, Promotion, and Progression.Frontiers in oncology · 2022Review
- Gating and regulation of KCNH (ERG, EAG, and ELK) channels by intracellular domains.Channels (Austin, Tex.) · 2020Review
- Eag1 Gene and Protein Expression in Human Retinoblastoma Tumors and its Regulation by pRb in HeLa Cells.Genes · 2020Article
- Monoclonal Antibodies Targeting Ion Channels and Their Therapeutic Potential.Frontiers in pharmacology · 2019Review
- Regulation of Eag by CaJournal of neurophysiology · 2018Article
- Ether-à-go-go KThe Journal of physiology · 2018Review
- Knockout Mice for Dyslexia Susceptibility Gene Homologs KIAA0319 and KIAA0319L have Unaffected Neuronal Migration but Display Abnormal Auditory Processing.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- Normal radial migration and lamination are maintained in dyslexia-susceptibility candidate gene homolog Kiaa0319 knockout mice.Brain structure & function · 2017Article
- Eag1 KOxidative medicine and cellular longevity · 2017Review
- Suppression of the Eag1 potassium channel sensitizes glioblastoma cells to injury caused by temozolomide.Oncology letters · 2016Article
- Cyclic expression of the voltage-gated potassium channel KV10.1 promotes disassembly of the primary cilium.EMBO reports · 2016Article
- Kv10.1 K(+) channel: from physiology to cancer.Pflugers Archiv : European journal of physiology · 2016Review
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 5 countries.
Funding
Abstract
Kv10.1 (Eag1), member of the Kv10 family of voltage-gated potassium channels, is preferentially expressed in adult brain. The aim of the present study was to unravel the functional role of Kv10.1 in the brain by generating knockout mice, where the voltage sensor and pore region of Kv10.1 were removed to render non-functional proteins through deletion of exon 7 of the KCNH1 gene using the '3 Lox P strategy'. Kv10.1-deficient mice show no obvious alterations during embryogenesis and develop normally to adulthood; cortex, hippocampus and cerebellum appear anatomically normal. Other tests, including general health screen, sensorimotor functioning and gating, anxiety, social behaviour, learning and memory did not show any functional aberrations in Kv10.1 null mice. Kv10.1 null mice display mild hyperactivity and longer-lasting haloperidol-induced catalepsy, but there was no difference between genotypes in amphetamine sensitization and withdrawal, reactivity to apomorphine and haloperidol in the prepulse inhibition tests or to antidepressants in the haloperidol-induced catalepsy. Furthermore, electrical properties of Kv10.1 in cerebellar Purkinje cells did not show any difference between genotypes. Bearing in mind that Kv10.1 is overexpressed in over 70% of all human tumours and that its inhibition leads to a reduced tumour cell proliferation, the fact that deletion of Kv10.1 does not show a marked phenotype is a prerequisite for utilizing Kv10.1 blocking and/or reduction techniques, such as siRNA, to treat cancer.
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Registered trials
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.