Redox-dependent activation of protein kinase G1α contributes to transient receptor potential cation channel subfamily V member 1-mediated acute nociceptive pain behavior.

蛋白激酶 G1α 的氧化还原依赖性激活有助于瞬时受体电位阳离子通道亚家族 V 成员 1 介导的急性伤害性疼痛行为