Inhibition of UHRF1 Improves Motor Function in Mice with Spinal Cord Injury
Cellular and Molecular Neurobiology, ISSN: 1573-6830, Vol: 44, Issue: 1, Page: 39
2024
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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.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
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Article Description
Spinal-cord injury (SCI) is a severe condition that can lead to limb paralysis and motor dysfunction, and its pathogenesis is not fully understood. The objective of this study was to characterize the differential gene expression and molecular mechanisms in the spinal cord of mice three days after spinal cord injury. By analyzing RNA sequencing data, we identified differentially expressed genes and discovered that the immune system and various metabolic processes play crucial roles in SCI. Additionally, we identified UHRF1 as a key gene that plays a significant role in SCI and found that SCI can be improved by suppressing UHRF1. These findings provide important insights into the molecular mechanisms of SCI and identify potential therapeutic targets that could greatly contribute to the development of new treatment strategies for SCI. Graphical Abstract: Downregulation of UHRF1 promotes the recovery of motor function in mice with spinal cord injury. By analyzing the RNA sequencing results of mice with spinal cord injury for 3 days and selecting UHRF1 for experimental validation, the study found that inhibiting UHRF1 can promote motor function recovery. (Figure presented.)
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85191081687&origin=inward; http://dx.doi.org/10.1007/s10571-024-01474-5; http://www.ncbi.nlm.nih.gov/pubmed/38649645; https://link.springer.com/10.1007/s10571-024-01474-5; https://dx.doi.org/10.1007/s10571-024-01474-5; https://link.springer.com/article/10.1007/s10571-024-01474-5
Springer Science and Business Media LLC
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