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Title: ERK5 phosphorylates Kv4.2 and inhibits inactivation of the A-type current in PC12 cells
Authors: Kashino, Yurina
Obara, Yutaro
Okamoto, Yosuke
Saneyoshi, Takeo
Hayashi, Yasunori  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-7560-3004 (unconfirmed)
Ishii, Kuniaki
Author's alias: 實吉, 岳郎
林, 康紀
Keywords: Extracellular signal-regulated kinase 5 (ERK5)
Kv4.2
PC12 cells
Issue Date: Jul-2018
Publisher: MDPI AG
Journal title: International Journal of Molecular Sciences
Volume: 19
Issue: 7
Thesis number: 2008
Abstract: Extracellular signal-regulated kinase 5 (ERK5) regulates diverse physiological responses such as proliferation, differentiation, and gene expression. Previously, we demonstrated that ERK5 is essential for neurite outgrowth and catecholamine biosynthesis in PC12 cells and sympathetic neurons. However, it remains unclear how ERK5 regulates the activity of ion channels, which are important for membrane excitability. Thus, we examined the effect of ERK5 on the ion channel activity in the PC12 cells that overexpress both ERK5 and the constitutively active MEK5 mutant. The gene and protein expression levels of voltage-dependent Ca²⁺ and K⁺ channels were determined by RT-qPCR or Western blotting. The A-type K⁺ current was recorded using the whole-cell patch clamp method. In these ERK5-activated cells, the gene expression levels of voltage-dependent L- and P/Q-type Ca²⁺ channels did not alter, but the N-type Ca²⁺ channel was slightly reduced. In contrast, those of Kv4.2 and Kv4.3, which are components of the A-type current, were significantly enhanced. Unexpectedly, the protein levels of Kv4.2 were not elevated by ERK5 activation, but the phosphorylation levels were increased by ERK5 activation. By electrophysiological analysis, the inactivation time constant of the A-type current was prolonged by ERK5 activation, without changes in the peak current. Taken together, ERK5 inhibits an inactivation of the A-type current by phosphorylation of Kv4.2, which may contribute to the neuronal differentiation process.
Rights: © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
URI: http://hdl.handle.net/2433/236577
DOI(Published Version): 10.3390/ijms19072008
PubMed ID: 29996472
Appears in Collections:Journal Articles

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