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Li-hong Sun


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Journal of Zhejiang University SCIENCE B 2016 Vol.17 No.10 P.733-741


Research progress of the role and mechanism of extracellular signal-regulated protein kinase 5 (ERK5) pathway in pathological pain

Author(s):  Li-na Yu, Li-hong Sun, Min Wang, Min Yan

Affiliation(s):  Department of Anesthesiology, the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China; more

Corresponding email(s):   zryanmin@zju.edu.cn

Key Words:  Extracellular signal-regulated protein kinase 5 (ERK5), Pain, Cyclic adenosine monophosphate (cAMP)-response element-binding protein (CREB), N-methyl-D-aspartate (NMDA), Nerve growth factor (NGF), Brain-derived neurotrophic factor (BDNF)

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Li-na Yu, Li-hong Sun, Min Wang, Min Yan. Research progress of the role and mechanism of extracellular signal-regulated protein kinase 5 (ERK5) pathway in pathological pain[J]. Journal of Zhejiang University Science B, 2016, 17(10): 733-741.

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journal="Journal of Zhejiang University Science B",
publisher="Zhejiang University Press & Springer",

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%A Min Yan
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%DOI 10.1631/jzus.B1600188

T1 - Research progress of the role and mechanism of extracellular signal-regulated protein kinase 5 (ERK5) pathway in pathological pain
A1 - Li-na Yu
A1 - Li-hong Sun
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J0 - Journal of Zhejiang University Science B
VL - 17
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%@ 1673-1581
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PB - Zhejiang University Press & Springer
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DOI - 10.1631/jzus.B1600188

extracellular signal-regulated protein kinase 5 (ERK5), also known as big mitogen-activated protein kinase 1 (MAPK1), is an important member of ERK family, which is a subfamily of the large MAPK family. ERK5 is expressed in many tissues, including the dorsal root ganglion (DRG) neurons and the spinal cord. In this review, we focus on elaborating ERK5-associated pathway in pathological pain, in which the ERK5/CREB (cyclic adenosine monophosphate (cAMP)-response element-binding protein) pathway plays a crucial role in the transduction of pain signal and contributes to pain hypersensitivity. ERK5 activation in the spinal dorsal horn occurs mainly in microglia. The activation of ERK5 can be mediated by N-methyl-D-aspartate (NMDA) receptors. We also elaborate the relationship between ERK5 activation and nerve growth factor-tyrosine kinase A (NGF-TrkA), and the connection between ERK5 activation and brain-derived neurotrophic factor (BDNF) in pathological pain in detail.



Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article


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