Volume 7 Issue 9
Sep.  2016
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Zhi-Dong Liu, Su Zhang, Jian-Jin Hao, Tao-Rong Xie, Jian-Sheng Kang. Cellular model of neuronal atrophy induced by DYNC1I1 deficiency reveals protective roles of RAS-RAF-MEK signaling[J]. Protein&Cell, 2016, 7(9): 638-650. doi: 10.1007/s13238-016-0301-6
Citation: Zhi-Dong Liu, Su Zhang, Jian-Jin Hao, Tao-Rong Xie, Jian-Sheng Kang. Cellular model of neuronal atrophy induced by DYNC1I1 deficiency reveals protective roles of RAS-RAF-MEK signaling[J]. Protein&Cell, 2016, 7(9): 638-650. doi: 10.1007/s13238-016-0301-6

Cellular model of neuronal atrophy induced by DYNC1I1 deficiency reveals protective roles of RAS-RAF-MEK signaling

doi: 10.1007/s13238-016-0301-6
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This work was supported by the National Natural Science Foundation of China (Grant No. 31171369), and partially supported by the National Basic Research Program (973 Program) (Nos. 2011CB910903 and 2010CB912001), Chinese Academy of Sciences (Hundred Talents Program and 2009OHTP10).

  • Received Date: 2016-06-17
  • Rev Recd Date: 2016-07-07
  • Neuronal atrophy is a common pathological feature occurred in aging and neurodegenerative diseases. A variety of abnormalities including motor protein malfunction and mitochondrial dysfunction contribute to the loss of neuronal architecture; however, less is known about the intracellular signaling pathways that can protect against or delay this pathogenic process. Here, we show that the DYNC1I1 deficiency, a neuron-specific dynein intermediate chain, causes neuronal atrophy in primary hippocampal neurons. With this cellular model, we are able to find that activation of RAS-RAF-MEK signaling protects against neuronal atrophy induced by DYNC1I1 deficiency, which relies on MEK-dependent autophagy in neuron. Moreover, we further reveal that BRAF also protects against neuronal atrophy induced by mitochondrial impairment. These findings demonstrate protective roles of the RAS-RAF-MEK axis against neuronal atrophy, and imply a new therapeutic target for clinical intervention.
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