JNK in spinal cord facilitates bone cancer pain in rats through modulation of CXCL1.

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2016 nî lūn-bûn

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2016年の論文

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2016年論文

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2016年論文

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2016年論文

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2016年論文

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2016年論文

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2016年论文

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2016年论文

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2016年论文

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JNK in spinal cord facilitates bone cancer pain in rats through modulation of CXCL1.

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JNK in spinal cord facilitates bone cancer pain in rats through modulation of CXCL1.

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JNK in spinal cord facilitates bone cancer pain in rats through modulation of CXCL1.

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P1476

JNK in spinal cord facilitates bone cancer pain in rats through modulation of CXCL1.

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P2093

Rui-guang Zhang

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Ting-ting Du

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Zhong-liang Wang

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P2860

Chemokines and the pathophysiology of neuropathic pain

NF-kappaB mediated enhancement of potassium currents by the chemokine CXCL1/growth related oncogene in small diameter rat sensory neurons

A new and sensitive method for measuring thermal nociception in cutaneous hyperalgesia

Selective inhibition of JNK with a peptide inhibitor attenuates pain hypersensitivity and tumor growth in a mouse skin cancer pain model

The c-Jun N-terminal kinase 1 (JNK1) in spinal astrocytes is required for the maintenance of bilateral mechanical allodynia under a persistent inflammatory pain condition

β2- and β3-adrenergic receptors drive COMT-dependent pain by increasing production of nitric oxide and cytokines

Uses for JNK: the many and varied substrates of the c-Jun N-terminal kinases.

Increased function of the TRPV1 channel in small sensory neurons after local inflammation or in vitro exposure to the pro-inflammatory cytokine GRO/KC.

Activation of c-jun N-terminal kinase in spinal cord contributes to breast cancer induced bone pain in rats.

TNF-α induces CXCL1 chemokine expression and release in human vascular endothelial cells in vitro via two distinct signaling pathways.

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scholarly article

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10.1007/S11596-016-1547-1

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2016-02-03T00:00:00Z

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1038545037

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