ArticleJournal of molecular histology2013
Up-regulation of ski-interacting protein in rat brain cortex after traumatic brain injury.
Article in Journal of molecular histology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- Running out the clock: Circadian rhythm dysfunction in cognitive disease.International review of neurobiology · 2026Review
- Regeneration in the nervous system with erythropoietin.Frontiers in bioscience (Landmark edition) · 2016Review
- Up-regulation of SKIP relates to retinal ganglion cells apoptosis after optic nerve crush in vivo.Journal of molecular histology · 2014Article
- Expression and prognostic role of SKIP in human breast carcinoma.Journal of molecular histology · 2014Article
- SCY1-like 1 binding protein 1 (SCYL1-bp1) interacts with p53-induced RING H2 protein (Pirh2) after traumatic brain injury in rats.Journal of molecular histology · 2013Article
- Phosphorylated retinoblastoma protein (p-Rb) is involved in neuronal apoptosis after traumatic brain injury in adult rats.Journal of molecular histology · 2013Article
- Increased expression of actin filament-stabilizing protein tropomyosin after rat traumatic brain injury.Journal of molecular histology · 2013Article
- Dynamic change of SGK expression and its role in neuron apoptosis after traumatic brain injury.International journal of clinical and experimental pathology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SKIP (Ski-interacting protein), is part of nuclear regulatory complexes and interacts with factors involved in preinitiation, splicing and polyadenylation, potentiates the activity of important transcription factors, involved in an increasing number of signaling cascades. However, its distribution and function in the central nervous system remains poorly understood. In this study, western blot analysis, RT-PCR and immunohistochemistry showed a significant up-regulation of SKIP in ipsilateral peritrauma cortex compared with the sham group. Immunofluorescent labeling indicated that SKIP was localized striking in the neurons, but not astrocytes and oligodendrocytes; co-localization of SKIP and active caspase-3 and PCNA in the ipsilateral cortex. In addition, the expression patterns of active caspase-3 and PCNA were parallel with that of SKIP. Based on our data, we speculated that SKIP might play an important role in neuronal apoptosis following TBI; and might provide a basis for the further study on its role in cell cycle re-entry in traumatic brain injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.