Raf-1 Kinase Inhibitory Protein (RKIP) Promotes Retinal Ganglion Cell Survival and Axonal Regeneration Following Optic Nerve Crush
Journal of Molecular Neuroscience, ISSN: 1559-1166, Vol: 57, Issue: 2, Page: 243-248
2015
- 16Citations
- 6Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations16
- Citation Indexes16
- 16
- CrossRef3
- Captures6
- Readers6
Article Description
Raf-1 kinase inhibitory protein (RKIP), a member of the phosphatidylethanolamine-binding protein (PEBP) family, plays an important role in neuronal apoptosis and cognitive deficits associated with neurodegenerative diseases. However, the biological function of RKIP in the retina is still unclear. Therefore, in the present study, we investigated the expression of RKIP in mouse retina following optic nerve crush (ONC) and evaluated the effects of RKIP on retinal ganglion cells (RGCs) apoptosis and axonal regeneration after ONC. Our results showed that the expression of RKIP was markedly decreased in the injured retina. Overexpression of RKIP inhibits RGC apoptosis and promotes axonal regeneration after ONC. Furthermore, overexpression of RKIP significantly increased the phosphorylation in extracellular signal-related kinase (ERK)1/2 and AKT in the injured retina. Taken together, these results suggest that RKIP promotes RGCs survival and axonal regeneration following ONC through promoting the ERK signaling pathway, implying that RKIP may serve as a potential molecular target for the treatment of glaucoma.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84942081586&origin=inward; http://dx.doi.org/10.1007/s12031-015-0612-8; http://www.ncbi.nlm.nih.gov/pubmed/26160696; http://link.springer.com/10.1007/s12031-015-0612-8; https://dx.doi.org/10.1007/s12031-015-0612-8; https://link.springer.com/article/10.1007/s12031-015-0612-8
Springer Science and Business Media LLC
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