Startseite The role of non-receptor protein tyrosine kinases in the excitotoxicity induced by the overactivation of NMDA receptors
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The role of non-receptor protein tyrosine kinases in the excitotoxicity induced by the overactivation of NMDA receptors

  • Yongjun Sun , You Chen , Liying Zhan , Linan Zhang , Jie Hu und Zibin Gao EMAIL logo
Veröffentlicht/Copyright: 5. November 2015
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Abstract

Protein tyrosine phosphorylation is one of the primary modes of regulation of N-methyl-d-aspartate (NMDA) receptors. The non-receptor tyrosine kinases are one of the two types of protein tyrosine kinases that are involved in this process. The overactivation of NMDA receptors is a primary reason for neuron death following cerebral ischemia. Many studies have illustrated the important role of non-receptor tyrosine kinases in ischemia insults. This review introduces the roles of Src, Fyn, focal adhesion kinase, and proline-rich tyrosine kinase 2 in the excitotoxicity induced by the overactivation of NMDA receptors following cerebral ischemia.


Corresponding author: Zibin Gao, Department of Pharmacy, Hebei University of Science and Technology, Yuhua East Road 70, Shijiazhuang 050018, P.R. China, e-mail: ; Hebei Research Center of Pharmaceutical and Chemical Engineering, Hebei University of Science and Technology, Shijiazhuang 050018, P.R. China; and State Key Laboratory Breeding Base – Hebei Province Key Laboratory of Molecular Chemistry for Drugs, Shijiazhuang 050018, P.R. China

Acknowledgments

The authors acknowledge support from the Natural Science Foundation of China (NSFC 81200886, NSFC 81402886), the Natural Science Foundation of Hebei Province (H2014208004), the Science and Technology Project of Hebei Province (13397703D), the Key Basic Research Program of the Application Foundation Research Project of Hebei Province (14967719D, 15962704D), the State Key Laboratory Breeding Base–Hebei Key Laboratory of Molecular Chemistry for Drug, and Hebei Research Center of Pharmaceutical and Chemical Engineering.

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Received: 2015-7-30
Accepted: 2015-9-17
Published Online: 2015-11-5
Published in Print: 2016-4-1

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