申请人:The Regents of the University of California
公开号:US20030008807A1
公开(公告)日:2003-01-09
This invention pertains to the discovery of a novel pathway that mediates hyperalgesia, neuropathic pain, and inflammatory pain. This pathway is a third independent pathway that involves activation of extracellular signal-regulated kinases (ERKs) 1 and 2. The pathway comprises a Ras-MEK-ERK1/2 cascade that acts independent of PKA or PKC&egr; as a novel signaling pathway for the production of inflammatory (and neuropathic) pain. This pathway presents numerous targets for a new class of analgesic agents.
本发明涉及一种介导痛觉减退、神经性疼痛和炎症性疼痛的新型途径的发现。这条途径是第三条独立的途径,涉及细胞外信号调节激酶(ERK)1 和 2 的激活。该通路由 Ras-MEK-ERK1/2 级联组成,其作用独立于 PKA 或 PKC&egr,是产生炎性(和神经性)疼痛的新型信号通路。这一途径为新型镇痛剂提供了众多靶点。