机译:蛋白激酶Akt的小分子诱导的胞质活化可挽救缺血引起的神经元死亡
Department of Pathology, Harvard Medical School, Dana-Farber/Harvard Cancer Center, Boston, MA 02115, Department of Laboratory Medicine, Children's Hospital Boston, Boston, MA 02115, Environmental Health Sciences Program, Yale University School of Public Health, New Haven, CT 06520;
Department of Pathology, Harvard Medical School, Dana-Farber/Harvard Cancer Center, Boston, MA 02115, Department of Laboratory Medicine, Children's Hospital Boston, Boston, MA 02115;
Department of Pathology, Harvard Medical School, Dana-Farber/Harvard Cancer Center, Boston, MA 02115, Department of Laboratory Medicine, Children's Hospital Boston, Boston, MA 02115;
Department of Neurology, Tokai University School of Medicine, Isehara 259-1193, Japan;
Department of Neurology, Tokai University School of Medicine, Isehara 259-1193, Japan;
Division of Molecular and Vascular Medicine, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA 02115;
Department of Biology, Boston University, Boston, MA 02215;
Division of Molecular and Vascular Medicine, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA 02115;
Department of Pathology, Harvard Medical School, Dana-Farber/Harvard Cancer Center, Boston, MA 02115, Department of Laboratory Medicine, Children's Hospital Boston, Boston, MA 02115;
Department of Pathology, Harvard Medical School, Dana-Farber/Harvard Cancer Center, Boston, MA 02115, Department of Laboratory Medicine, Children's Hospital Boston, Boston, MA 02115;
Department of Pathology, Harvard Medical School, Dana-Farber/Harvard Cancer Center, Boston, MA 02115, Department of Laboratory Medicine, Children's Hospital Boston, Boston, MA 02115;
Department of Biology, Boston University, Boston, MA 02215;
Division of Molecular and Vascular Medicine, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA 02115;
Department of Pathology, Harvard Medical School, Dana-Farber/Harvard Cancer Center, Boston, MA 02115, Department of Laboratory Medicine, Children's Hospital Boston, Boston, MA 02115;
drug discovery; cell signaling;
机译:活化转录因子3的表达通过促进热休克蛋白27的表达和Akt活化来防止c-Jun N末端激酶诱导的神经元死亡。
机译:小胶质细胞释放由有丝分裂原激活的蛋白激酶,磷脂酰肌醇-3-激酶/ Akt和δ-Notch信号级联反应介导的神经元增殖激活剂。
机译:Akt-磷酸化的丝裂剂激活激酶激活死亡结构域蛋白(MADD)通过阻断与死亡受体4的Fas相关的死亡结构域(FADD)结合来抑制血迹诱导的细胞凋亡
机译:血管平滑肌细胞氧化应激激活丝裂剂活化蛋白激酶和蛋白激酶B / Akt信号传导:血管病理生理学中的参与
机译:促分裂原激活蛋白激酶激活蛋白激酶2在调节p38促分裂原激活蛋白激酶诱导的环氧合酶2和心力衰竭中的作用。
机译:蛋白激酶Akt的小分子诱导的胞质活化可挽救缺血引起的神经元死亡
机译:应激活化蛋白激酶p38和JNK在神经细胞死亡中的调节和作用
机译:调节神经元存活和死亡的蛋白激酶途径