ArticleNeurochemical research2011
Activation of STAT1 in neurons following spinal cord injury in mice.
Article in Neurochemical research, 2011. 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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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Tofacitinib Promotes Functional Recovery after Spinal Cord Injury by Regulating Microglial Polarization via JAK/STAT Signaling Pathway.International journal of biological sciences · 2023Article
- Weighted gene co-expression network analysis reveals that CXCL10, IRF7, MX1, RSAD2, and STAT1 are related to the chronic stage of spinal cord injury.Annals of translational medicine · 2021Article
- Organophosphate pesticide chlorpyrifos impairs STAT1 signaling to induce dopaminergic neurotoxicity: Implications for mitochondria mediated oxidative stress signaling events.Neurobiology of disease · 2018Article
- Transcription factor networks involved in cell death in the dorsal root ganglia following peripheral nerve injury.Neural regeneration research · 2018Article
- microRNA dysregulation in polyglutamine toxicity of TATA-box binding protein is mediated through STAT1 in mouse neuronal cells.Journal of neuroinflammation · 2017Article
- Rapid Regulation of Depression-Associated Genes in a New Mouse Model Mimicking Interferon-α-Related Depression in Hepatitis C Virus Infection.Molecular neurobiology · 2015Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The signal transducer and activator of transcription 1 (STAT1) has been reported to be associated with neuronal cell death after cerebral ischemia. On the contrary, STAT3 has been revealed to regulate cell survival. We examined the chronological alteration and cellular localization of phosphorylated (p)-JAK1, p-STAT1 and p-STAT3 following mild spinal cord injury (SCI) in mice. Western blot analysis indicated that JAK1 is significantly phosphorylated, accompanied by the phosphorylation of STAT1 at Tyr(701) within a similar timeframe. Immunofluorescence staining indicated that signal transduction of STAT3 is introduced into the nucleus of the neurons within the anterior horns; however, in mirror sections, that of STAT1 is limited to the cytoplasm. These findings suggest that STAT3 signal is predominantly transduced into the nucleus and plays a stronger role in neuronal survival than STAT1. Modulation of the functional balance between STAT1 and STAT3 might determine the survival or death of neurons after SCI.
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