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Publication : Mst-1 deficiency promotes post-traumatic spinal motor neuron survival via enhancement of autophagy flux.

First Author  Zhang M Year  2017
Journal  J Neurochem Volume  143
Issue  2 Pages  244-256
PubMed ID  28833175 Mgi Jnum  J:246433
Mgi Id  MGI:5916445 Doi  10.1111/jnc.14154
Citation  Zhang M, et al. (2017) Mst-1 deficiency promotes post-traumatic spinal motor neuron survival via enhancement of autophagy flux. J Neurochem 143(2):244-256
abstractText  The mammalian Ste20-like kinase 1 (Mst-1) is a serine-threonine kinase and a component of the Hippo tumor suppressor pathway, which reacts to pathologically relevant stress and regulates cell death. However, little is known about its role in spinal cord injury. Here, we found that p-Mst-1, the activated form of Mst-1, was induced in the post-traumatic spinal motor neurons. In vivo evidence demonstrated that Mst-1 deficiency promoted post-traumatic spinal motor neuron survival, Basso mouse scale scores, and synapse survival. Moreover, we found that autophagosome formation and autolysosome degradation enhanced by Mst-1 deficiency were crucial to attenuate the death of injured spinal motor neurons. Taken together, our findings demonstrate that Mst-1 deficiency promotes post-traumatic spinal motor neuron survival via enhancement of autophagy flux.
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