ArticlePloS one2012
14-3-3θ is a binding partner of rat Eag1 potassium channels.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- SIRT4 as a novel interactor and candidate suppressor of C-RAF kinase in MAPK signaling.Life science alliance · 2024Article
- 14-3-3 proteins regulate cullin 7-mediated Eag1 degradation.Cell & bioscience · 2023Article
- Identification of HCN1 as a 14-3-3 client.PloS one · 2022Article
- 14-3-3γ, a novel regulator of the large-conductance CaAmerican journal of physiology. Renal physiology · 2020Article
- Eag1 KOxidative medicine and cellular longevity · 2017Review
- Structure of the voltage-gated K⁺ channel Eag1 reveals an alternative voltage sensing mechanism.Science (New York, N.Y.) · 2016Article
- Kv10.1 K(+) channel: from physiology to cancer.Pflugers Archiv : European journal of physiology · 2016Review
- Ca(2+)-binding protein centrin 4 is a novel binding partner of rat Eag1 K(+) channels.FEBS open bio · 2016Article
- Alternatively Spliced Isoforms of KV10.1 Potassium Channels Modulate Channel Properties and Can Activate Cyclin-dependent Kinase in Xenopus Oocytes.The Journal of biological chemistry · 2015Article
- Increased 14-3-3 phosphorylation observed in Parkinson's disease reduces neuroprotective potential of 14-3-3 proteins.Neurobiology of disease · 2015Article
- The punctate localization of rat Eag1 K+ channels is conferred by the proximal post-CNBHD region.BMC neuroscience · 2014Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ether-à-go-go (Eag) potassium (K(+)) channel belongs to the superfamily of voltage-gated K(+) channel. In mammals, the expression of Eag channels is neuron-specific but their neurophysiological role remains obscure. We have applied the yeast two-hybrid screening system to identify rat Eag1 (rEag1)-interacting proteins from a rat brain cDNA library. One of the clones we identified was 14-3-3θ, which belongs to a family of small acidic protein abundantly expressed in the brain. Data from in vitro yeast two-hybrid and GST pull-down assays suggested that the direct association with 14-3-3θ was mediated by both the N- and the C-termini of rEag1. Co-precipitation of the two proteins was confirmed in both heterologous HEK293T cells and native hippocampal neurons. Electrophysiological studies showed that over-expression of 14-3-3θ led to a sizable suppression of rEag1 K(+) currents with no apparent alteration of the steady-state voltage dependence and gating kinetics. Furthermore, co-expression with 14-3-3θ failed to affect the total protein level, membrane trafficking, and single channel conductance of rEag1, implying that 14-3-3θ binding may render a fraction of the channel locked in a non-conducting state. Together these data suggest that 14-3-3θ is a binding partner of rEag1 and may modulate the functional expression of the K(+) channel in neurons.
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