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Cdo Regulates Surface Expression of Kir2.1 K+ Channel in Myoblast Differentiationopen access

Authors
Leem, Young-EunJeong, Hyeon-JuKim, Hyun-JiKoh, JewooKang, KyeongJinBae, Gyu-UnCho, HanaKang, Jong-Sun
Issue Date
Jul-2016
Publisher
PUBLIC LIBRARY SCIENCE
Citation
PLOS ONE, v.11, no.7, pp 1 - 14
Pages
14
Journal Title
PLOS ONE
Volume
11
Number
7
Start Page
1
End Page
14
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/9729
DOI
10.1371/journal.pone.0158707
ISSN
1932-6203
Abstract
A potassium channel Kir2.1-associated membrane hyperpolarization is required for myogenic differentiation. However the molecular regulatory mechanisms modulating Kir2.1 channel activities in early stage of myogenesis are largely unknown. A cell surface protein, Cdo functions as a component of multiprotein cell surface complexes to promote myogenesis. In this study, we report that Cdo forms a complex with Kir2.1 during myogenic differentiation, and is required for the channel activity by enhancing the surface expression of Kir2.1 in the early stage of differentiation. The expression of a constitutively active form of the upstream kinase for p38MAPK, MKK6(EE) can restore Kir2.1 activities in Cdo-depleted C2C12 cells, while the treatment with a p38MAPK inhibitor, SB203580 exhibits a similar effect of Cdo depletion on Kir2.1 surface expression. Furthermore, Cdo(-/-) primary myoblasts, which display a defective differentiation program, exhibit a defective Kir2.1 activity. Taken together, our results suggest that a promyogenic Cdo signaling is critical for Kir2.1 activities in the induction of myogenic differentiation.
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