English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Spinal cord injury entails a high risk of major disability, but there is still no effective treatment for this condition. This study aims to explore the neuronal apoptosis after spinal cord injury, which is a key component of secondary injury processes, and plays a critical role in the development of neurological dysfunction. We studied the expression of the E3 ubiquitin ligase Triad1 and its interaction with p53 in the spinal cord after a spinal cord contusion injury in rats. We explored the regulation function of Triad1 to the neuronal apoptosis through p53-caspase3 pathway in primary neurons. Triad1 was markedly up-regulated in the grey matter one day after injury, and the distribution and time point of Triad1 expression correlated with the presence of apoptotic neurons. Co-immunoprecipitation experiments further demonstrated that Triad1 interacted with p53 after spinal cord injury. Specific siRNA and overexpression plasmids for Triad1 were transfected into primary neurons, and the expression of both p53 and caspase3 was altered following the change of Triad1. These findings indicate that Triad1 is involved in regulating the pathological process of neuronal apoptosis mediated by p53-caspase3 pathway after spinal cord injury.

E3 ubiquitin ligase Triad1 promotes neuronal apoptosis by regulating the p53-caspase3 pathway after spinal cord injury