ArticleJournal of molecular neuroscience : MN2013
Upregulation of CRM1 relates to neuronal apoptosis after traumatic brain injury in adult rats.
Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- CRM-1 Aggravates Stroke Injury by Promoting BANF1-Mediated Unfolded Protein Response Through Inducing Nuclear Export of ALKBH5.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Trait - driven analysis of the 2p15p16.1 microdeletion syndrome suggests a complex pattern of interactions between candidate genes.Genes & genomics · 2023Article
- An update to the CRM1 cargo/NES database NESdb.Molecular biology of the cell · 2021Article
- PKCε phosphorylation regulates the mitochondrial translocation of ATF2 in ischemia-induced neurodegeneration.BMC neuroscience · 2018Article
- Karyopherin α-3 is a key protein in the pathogenesis of spinocerebellar ataxia type 3 controlling the nuclear localization of ataxin-3.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- A Nuclear Attack on Traumatic Brain Injury: Sequestration of Cell Death in the Nucleus.CNS neuroscience & therapeutics · 2016Article
- Intracellular Protein Shuttling: A Mechanism Relevant for Myelin Repair in Multiple Sclerosis?International journal of molecular sciences · 2015Review
- Nuclear export inhibitors avert progression in preclinical models of inflammatory demyelination.Nature neuroscience · 2015Article
- The expression changes of myelin and lymphocyte protein (MAL) following optic nerve crush in adult rats retinal ganglion cells.Journal of molecular neuroscience : MN · 2014Article
- Linking traumatic brain injury to chronic traumatic encephalopathy: identification of potential mechanisms leading to neurofibrillary tangle development.Journal of neurotrauma · 2014Review
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Authors and funding
7 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) initiates a complex series of neurochemical and signaling changes that leads to neuronal dysfunction and over-reactive astrocytes. There is increasing evidence that CRM1 mediated P27(Kip1), which is a potent inhibitor of G1 cyclin-dependent kinases complexes, nuclear export-dependent or -independent Jab1/CSN5, and cytoplasmic degradation in cells. Up to now, the function of CRM1 in central nervous system (CNS) is still with limited acquaintance. In our study, to investigate whether CRM1 is involved in CNS lesion, we performed a TBI model in adult rats. Western blot and RT-PCR analysis revealed that the level of protein and mRNA of CRM1 increased in ipsilateral brain cortex in comparison to the contralateral. Immunohistochemistry and immunofluorescence double labeling indicated that CRM1 was shutting into nucleus around the wound, and increased CRM1 co-localized with P27(Kip1). Terminal deoxynucleotidyl transferase deoxy-UTP-nick end labeling (TUNEL) staining suggested that CRM1 was involved in neuronal apoptosis after brain injury. We also investigated co-localization of CRM1 and active-caspase-3 in the ipsilateral brain cortex. In addition, the expression patterns of Bax and active-caspase-3 were parallel with that of CRM1. Based on our data, we suggested that CRM1 might play an important role in neuronal apoptosis following TBI, and might provide a basis for the further study on its role in regulating the expression of P27(Kip1) and cell cycle re-entry in TBI.
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