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Article

Tyrosine Phosphorylation of the Kv2.1 Channel Contributes to Injury in Brain Ischemia

1
Department of Physiology, College of Medicine, Kyung Hee University, Seoul 02447, Korea
2
Department of Anatomy & Neurobiology, College of Medicine, Kyung Hee University, Seoul 02447, Korea
3
Department of Pathology, College of Medicine, Kyung Hee University, Seoul 02447, Korea
4
KHU-KIST Department of Converging Science and Technology, Kyung Hee University, Seoul 02447, Korea
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(24), 9538; https://doi.org/10.3390/ijms21249538
Received: 18 November 2020 / Revised: 11 December 2020 / Accepted: 12 December 2020 / Published: 15 December 2020
(This article belongs to the Special Issue Ion Channel and Ion-Related Signaling 2020)
In brain ischemia, oxidative stress induces neuronal apoptosis, which is mediated by increased activity of the voltage-gated K+ channel Kv2.1 and results in an efflux of intracellular K+. The molecular mechanisms underlying the regulation of Kv2.1 and its activity during brain ischemia are not yet fully understood. Here this study provides evidence that oxidant-induced apoptosis resulting from brain ischemia promotes rapid tyrosine phosphorylation of Kv2.1. When the tyrosine phosphorylation sites Y124, Y686, and Y810 on the Kv2.1 channel are mutated to non-phosphorylatable residues, PARP-1 cleavage levels decrease, indicating suppression of neuronal cell death. The tyrosine residue Y810 on Kv2.1 was a major phosphorylation site. In fact, cells mutated Y810 were more viable in our study than were wild-type cells, suggesting an important role for this site during ischemic neuronal injury. In an animal model, tyrosine phosphorylation of Kv2.1 increased after ischemic brain injury, with an observable sustained increase for at least 2 h after reperfusion. These results demonstrate that tyrosine phosphorylation of the Kv2.1 channel in the brain may play a critical role in regulating neuronal ischemia and is therefore a potential therapeutic target in patients with brain ischemia. View Full-Text
Keywords: Kv2.1; tyrosine phosphorylation; brain ischemia; oxidative stress Kv2.1; tyrosine phosphorylation; brain ischemia; oxidative stress
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MDPI and ACS Style

Song, M.-Y.; Hwang, J.Y.; Bae, E.J.; Kim, S.; Kang, H.-M.; Kim, Y.J.; Park, C.; Park, K.-S. Tyrosine Phosphorylation of the Kv2.1 Channel Contributes to Injury in Brain Ischemia. Int. J. Mol. Sci. 2020, 21, 9538. https://doi.org/10.3390/ijms21249538

AMA Style

Song M-Y, Hwang JY, Bae EJ, Kim S, Kang H-M, Kim YJ, Park C, Park K-S. Tyrosine Phosphorylation of the Kv2.1 Channel Contributes to Injury in Brain Ischemia. International Journal of Molecular Sciences. 2020; 21(24):9538. https://doi.org/10.3390/ijms21249538

Chicago/Turabian Style

Song, Min-Young, Ji Y. Hwang, Eun J. Bae, Saesbyeol Kim, Hye-Min Kang, Yong J. Kim, Chan Park, and Kang-Sik Park. 2020. "Tyrosine Phosphorylation of the Kv2.1 Channel Contributes to Injury in Brain Ischemia" International Journal of Molecular Sciences 21, no. 24: 9538. https://doi.org/10.3390/ijms21249538

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