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机译:ATP13A2 / PARK9通过新型PI(3,5)P2介导的脚手架功能来调节内皮/溶酶体货物分选和蛋白质ostasis
Univ Leuven KU Leuven Lab Cell Death Res &
Therapy Dept Cellular &
Mol Med Campus Gasthuisberg O;
Univ Leuven KU Leuven Lab Cellular Transport Syst Dept Cellular &
Mol Med Campus Gasthuisberg O;
Univ Leuven KU Leuven Lab Cell Death Res &
Therapy Dept Cellular &
Mol Med Campus Gasthuisberg O;
Univ Leuven KU Leuven Lab Cellular Transport Syst Dept Cellular &
Mol Med Campus Gasthuisberg O;
Univ Leuven KU Leuven Lab Cellular Transport Syst Dept Cellular &
Mol Med Campus Gasthuisberg O;
Univ Leuven KU Leuven Res Grp Neurobiol &
Gene Therapy Dept Neurosci B-3000 Leuven Belgium;
Univ Antwerp Mol Neurogen Grp VIB Ctr Mol Neurol B-2610 Antwerp Belgium;
Univ Leuven KU Leuven Res Grp Neurobiol &
Gene Therapy Dept Neurosci B-3000 Leuven Belgium;
Univ Leuven KU Leuven Lab Cellular Transport Syst Dept Cellular &
Mol Med Campus Gasthuisberg O;
Univ Leuven KU Leuven Lab Cell Death Res &
Therapy Dept Cellular &
Mol Med Campus Gasthuisberg O;
机译:ATP13A2 / PARK9通过新型PI(3,5)P2介导的脚手架功能来调节内皮/溶酶体货物分选和蛋白质ostasis
机译:P型ATPase ATP13A2 / PARK9功能的丧失导致一般的溶酶体缺乏症并导致帕金森氏病神经变性
机译:神经变性溶酶体功能障碍:ATP13A2 / PARK9的作用
机译:保守的卷曲卷蛋白CCCP1和内体复合物耳朵调节密集芯囊泡货物分类
机译:P型ATPase ATP13A2 / PARK9功能的丧失导致一般的溶酶体缺乏症并导致帕金森氏病神经变性
机译:Zn2 + Dyshomeostasis因损失ATP13A2 / Park9导致溶酶体功能障碍和α-突触核蛋白积累