ArticleBMC neuroscience2005
A truncated Kv1.1 protein in the brain of the megencephaly mouse: expression and interaction.
Article in BMC neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Novel Genetic Variants Expand the Functional, Molecular, and Pathological Diversity ofInternational journal of molecular sciences · 2023Review
- Identification of key potassium channel genes of temporal lobe epilepsy by bioinformatics analyses and experimental verification.Frontiers in neurology · 2023Article
- Clinical Spectrum ofInternational journal of molecular sciences · 2020Review
- Spontaneous seizures in Kcna1-null mice lacking voltage-gated Kv1.1 channels activate Fos expression in select limbic circuits.Journal of neurochemistry · 2015Article
- Kv1.1-dependent control of hippocampal neuron number as revealed by mosaic analysis with double markers.The Journal of physiology · 2012Article
- Evidence for presence and functional effects of Kv1.1 channels in β-cells: general survey and results from mceph/mceph mice.PloS one · 2011Article
- Cerebrovascular responses in mice deficient in the potassium channel, TREK-1.American journal of physiology. Regulatory, integrative and comparative physiology · 2010Article
- Shaker and Shal mediate transient calcium-independent potassium current in a Drosophila flight motoneuron.Journal of neurophysiology · 2009Article
- Structural consequences of Kcna1 gene deletion and transfer in the mouse hippocampus.Epilepsia · 2007Article
- Kv1.1 null mice have enlarged hippocampus and ventral cortex.BMC neuroscience · 2007Article
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9 authors.
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Abstract
backgroundThe megencephaly mouse, mceph/mceph, is epileptic and displays a dramatically increased brain volume and neuronal count. The responsible mutation was recently revealed to be an eleven base pair deletion, leading to a frame shift, in the gene encoding the potassium channel Kv1.1. The predicted MCEPH protein is truncated at amino acid 230 out of 495. Truncated proteins are usually not expressed since nonsense mRNAs are most often degraded. However, high Kv1.1 mRNA levels in mceph/mceph brain indicated that it escaped this control mechanism. Therefore, we hypothesized that the truncated Kv1.1 would be expressed and dysregulate other Kv1 subunits in the mceph/mceph mice.
resultsWe found that the MCEPH protein is expressed in the brain of mceph/mceph mice. MCEPH was found to lack mature (Golgi) glycosylation, but to be core glycosylated and trapped in the endoplasmic reticulum (ER). Interactions between MCEPH and other Kv1 subunits were studied in cell culture, Xenopus oocytes and the brain. MCEPH can form tetramers with Kv1.1 in cell culture and has a dominant negative effect on Kv1.2 and Kv1.3 currents in oocytes. However, it does not retain Kv1.2 in the ER of neurons.
conclusionThe megencephaly mice express a truncated Kv1.1 in the brain, and constitute a unique tool to study Kv1.1 trafficking relevant for understanding epilepsy, ataxia and pathologic brain overgrowth.
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