TY - JOUR AU - Welsbie, Derek S. AU - Ziogas, Nikolaos K. AU - Xu, Leyan AU - Kim, Byung-Jin AU - Ge, Yusong AU - Patel, Amit K. AU - Ryu, Jiwon AU - Lehar, Mohamed AU - Alexandris, Athanasios S. AU - Stewart, Nicholas AU - Zack, Donald J. AU - Koliatsos, Vassilis E. PY - 2019 DA - 2019/11/27 TI - Targeted disruption of dual leucine zipper kinase and leucine zipper kinase promotes neuronal survival in a model of diffuse traumatic brain injury JO - Molecular Neurodegeneration SP - 44 VL - 14 IS - 1 AB - Traumatic brain injury (TBI) is a major cause of CNS neurodegeneration and has no disease-altering therapies. It is commonly associated with a specific type of biomechanical disruption of the axon called traumatic axonal injury (TAI), which often leads to axonal and sometimes perikaryal degeneration of CNS neurons. We have previously used genome-scale, arrayed RNA interference-based screens in primary mouse retinal ganglion cells (RGCs) to identify a pair of related kinases, dual leucine zipper kinase (DLK) and leucine zipper kinase (LZK) that are key mediators of cell death in response to simple axotomy. Moreover, we showed that DLK and LZK are the major upstream triggers for JUN N-terminal kinase (JNK) signaling following total axonal transection. However, the degree to which DLK/LZK are involved in TAI/TBI is unknown. SN - 1750-1326 UR - https://doi.org/10.1186/s13024-019-0345-1 DO - 10.1186/s13024-019-0345-1 ID - Welsbie2019 ER -