THESIS
2020
ix leaves, 31 pages : illustrations (some color) ; 30 cm
Abstract
DLK is a MAPKKK family protein and plays an important role in axon injury response.
It is retrogradely transported to neuron soma after injury and leads to both cell death
and axon regeneration. However, the mechanism of cell fate decision induced by DLK
is unknown. It is meaningful to understand the mechanism so that manipulation DLK
could potentially improve neuronal survival as well as axon regeneration after injury.
In this study, two CNS axon injury model, optic nerve crush and pre-OPN crush were
applied to explore the role of DLK in RGC response to optic nerve injury. Pre-OPN
crush showed less cell loss and DLK activation was weaker compared with optic nerve
crush. Both virus and small molecule were utilized to modify the activation of DLK
pathway to understand whether ac...[
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DLK is a MAPKKK family protein and plays an important role in axon injury response.
It is retrogradely transported to neuron soma after injury and leads to both cell death
and axon regeneration. However, the mechanism of cell fate decision induced by DLK
is unknown. It is meaningful to understand the mechanism so that manipulation DLK
could potentially improve neuronal survival as well as axon regeneration after injury.
In this study, two CNS axon injury model, optic nerve crush and pre-OPN crush were
applied to explore the role of DLK in RGC response to optic nerve injury. Pre-OPN
crush showed less cell loss and DLK activation was weaker compared with optic nerve
crush. Both virus and small molecule were utilized to modify the activation of DLK
pathway to understand whether activation time or extent is important for different
response. Further experiments could be done in this field to find a method to improve
axon regeneration while keep RGCs survive, which is a potential direction for therapy discovery.
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