2013
DOI: 10.1093/hmg/ddt076
|View full text |Cite
|
Sign up to set email alerts
|

Behavioural and functional characterization of Kv10.1 (Eag1) knockout mice

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… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

5
43
0
2

Year Published

2013
2013
2021
2021

Publication Types

Select...
7
2

Relationship

1
8

Authors

Journals

citations
Cited by 53 publications
(50 citation statements)
references
References 59 publications
5
43
0
2
Order By: Relevance
“…Considering the high redundancy of ion transport mechanisms in neurons, the strict control of excitatory neuron output exerted by inhibitory feedback, and the effective blood-brain barrier mechanisms, the CNS networks appear to be considerably robust to pharmacological perturbation. For example, it has been recently observed that knocking out Kv10.1, whose expression is largely restricted to the CNS in healthy individuals, produces mild phenotypic consequences (Ufartes et al, 2013). In agreement with these notions, one of the most serious problems encountered in epilepsy treatment is not excessive neuronal network silencing, but quite the opposite, i.e.…”
Section: Targeting Ion Channels In Oncology: Pros and Consmentioning
confidence: 86%
“…Considering the high redundancy of ion transport mechanisms in neurons, the strict control of excitatory neuron output exerted by inhibitory feedback, and the effective blood-brain barrier mechanisms, the CNS networks appear to be considerably robust to pharmacological perturbation. For example, it has been recently observed that knocking out Kv10.1, whose expression is largely restricted to the CNS in healthy individuals, produces mild phenotypic consequences (Ufartes et al, 2013). In agreement with these notions, one of the most serious problems encountered in epilepsy treatment is not excessive neuronal network silencing, but quite the opposite, i.e.…”
Section: Targeting Ion Channels In Oncology: Pros and Consmentioning
confidence: 86%
“…Both mammalian Eag orthologs have been genetically associated with neuronal excitability control (Ufartes et al, 2013;Yang et al, 2013), but the cellular mechanisms have not been explored. As cnidocytes are a cnidarian-specific cell type believed to be derived from a neuronal cell type (Pantin, 1942), it is tempting to speculate that ancestral Eag subfamily channels regulated subthreshold excitability of neurons.…”
Section: Research Articlementioning
confidence: 99%
“…For instance, knockout of the EAG family K + channel Kv12.2 in mice reduces subthreshold K + current and lowers action potential threshold in hippocampal pyramidal neurons (Zhang et al, 2010). Both knockout of Kv12.2 (Elk2) in mice and a gain-of-function mutation in Kv10.2 (Eag2) in humans cause seizures (Yang et al, 2013;Zhang et al, 2010), and knockout of Eag1 in mouse causes generalized hyperexcitability (Ufartes et al, 2013). Similarly, pharmacologic block of Erg (Eag-related gene) channels enhances the excitability of neurons in several brain regions (Hardman and Forsythe, 2009;Hirdes et al, 2009;Hirdes et al, 2005;Ji et al, 2012;Niculescu et al, 2013).…”
Section: Introductionmentioning
confidence: 99%
“…In normal tissues, KCNH1 is mainly expressed in the brain (Pardo et al 1999, Hemmerlein et al 2006. Interestingly, Kcnh1 knockout mice have been produced, but the animals did not show any major abnormality at the CNS level (Ufartes et al 2013). It is also known that ion channels have several non-conducting functions including interactions with other proteins like enzymes or cytoskeleton proteins (Kaczmarek 2006).…”
Section: Discussionmentioning
confidence: 99%