ArticleJournal of neurotrauma2013
Changes in the GEF-H1 pathways after traumatic brain injury.
Article in Journal of neurotrauma, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- White matter injury after brain ischemia.Experimental neurology · 2026Review
- Cerebrospinal fluid purinomics as a biomarker approach to predict outcome after severe traumatic brain injury.Journal of neurochemistry · 2022Article
- Review
- RhoA-ROCK Inhibition Reverses Synaptic Remodeling and Motor and Cognitive Deficits Caused by Traumatic Brain Injury.Scientific reports · 2017Article
- Pathophysiology Associated with Traumatic Brain Injury: Current Treatments and Potential Novel Therapeutics.Cellular and molecular neurobiology · 2017Review
- Upregulation of the GEF-H1 pathway after transient cerebral ischemia.Experimental neurology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Brains undergo significant remodeling after traumatic brain injury (TBI). The Rho guanine triphosphate (GTP)ase pathways control brain remodeling during development and under pathological conditions. How the Rho GTPase pathways are regulated in the brain after TBI remains largely unknown, however. This study used the rat fluid percussion injury model to investigate changes in the Rho GTPase pathways after TBI. The results showed that TBI leads to activation and translocation of RhoA and Rac1 proteins from cytosolic fraction to the membrane fraction after injury. Consistently, the Rho guanine nucleotide exchange factors GEF-H1 and Cool-2/αPix are significantly activated by dephosphorylation and accumulation in the cytosolic fractions during the post-TBI phase. Because the Rho GTPase pathways are key regulators of brain remodeling, these results depict regulatory mechanisms of the Rho GTPase pathways after TBI, and pave the way for the study of therapeutic agents targeting the Rho GTPase pathways for functional recovery after TBI.
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Registered trials
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