https://scholars.lib.ntu.edu.tw/handle/123456789/416270
Title: | 14-3-3θ is a binding partner of rat Eag1 potassium channels | Authors: | Hsu, Po-Hao SHI-CHUEN MIAW Chuang, Chau-Ching Chang, Pei-Yu Fu, Ssu-Ju Jow, Guey-Mei Chiu, Mei-Miao Jeng, Chung-Jiuan |
Issue Date: | 2012 | Publisher: | PUBLIC LIBRARY SCIENCE | Journal Volume: | 7 | Journal Issue: | 7 | Source: | PloS one | 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. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84864098814&doi=10.1371%2fjournal.pone.0041203&partnerID=40&md5=be82d3ab73081591794e4312397d4957 https://scholars.lib.ntu.edu.tw/handle/123456789/416270 |
ISSN: | 1932-6203 | DOI: | 10.1371/journal.pone.0041203 |
Appears in Collections: | 免疫學研究所 |
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