机译:p10,p35的N末端域,可防止CDK5 / p25诱导的神经毒性
Department of Molecular, Cellular and Developmental Biology and the Neuroscience Research Institute and University of California, Santa Barbara, CA 93106;
Howard Hughes Medical Institute,University of California at San Diego, La Jolla, CA 92093,Department of Medicine, University of California at San Diego, La Jolla, CA 92093;
Department of Psychological and Brain Sciences and the Neuroscience Research Institute, University of California, Santa Barbara, CA 93106;
Department of Molecular, Cellular and Developmental Biology and the Neuroscience Research Institute and University of California, Santa Barbara, CA 93106;
alzheimer's disease; anti-death;
机译:Munc 18(p67)与p35的p10结构域的相互作用可保护体内Cdk5 / p35活性免受TFP5(一种源自p35的肽)的抑制
机译:Munc 18(p67)与p35的p10结构域的相互作用可保护体内Cdk5 / p35活性免受TFP5(一种源自p35的肽)的抑制
机译:将p10鉴定为由神经元Cdk5激活剂的蛋白水解裂解产生的神经毒性产物。
机译:皮质激素释放因子受体N-末端结构域的三维结构:寿司结构域和B1蛋白偶联受体的B1系列
机译:cAMP和多胺通过激活ed5A调节的p35表达的增加来激活Cdk5,从而克服了MAG的抑制作用。
机译:p10p35的N末端域可防止CDK5 / p25诱导的神经毒性
机译:P10,P35的N-末端结构域,可防止CDK5 / P25诱导的神经毒性