Differential activation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (

来源 :中国神经科学学会第四次会员代表大会暨第七届全国学术会议(The 7th Biennial Meeting and the | 被引量 : 0次 | 上传用户:muyanger280
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  Recent advances have given us a much more detailed understanding of the roles played by MAPKs in the pathophysiogenesis of clinically-relevant pathological pain.The MAPK family has three major members,extracellular signal-regulated kinase (ERK),p38 and c-Jun N-terminal kinase (JNK),representing three different signal transduction pathways.Compared with the enormous amounts of literature reporting activation and involvement of ERK,p38 or JNK in the process of inflammatory of neuropathic pain,fewer study has been performed to investigate possible regional differences in activation of different MAPK isoforms following peripheral noxious stimulation.Recently,our lab has conducted series of preliminary work to address this issue using Western blot technique in the bee venom tonical pain model.
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