Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
The interferon regulatory factor (IRF) family was first discovered as a set of transcriptional regulators of the type I interferon system in 1988. In mammals, the IRF family includes nine members that play important roles in the immune system, oncogenesis, and apoptosis. However, the distribution and the function of IRF6 in the central nervous system are limited. In this study, we established an adult rat traumatic brain injury (TBI) model. Compared to the sham brain cortex, Western blot and immunohistochemistry showed significant upregulation of IRF6 in the ipsilateral brain cortex after TBI. Immunofluorescence double-labeling showed that IRF6 completely co-localized with neurons, not astrocytes or oligodendrocytes. Furthermore, we detected that the neuronal apoptosis marker active caspase-3 co-localized with IRF6 in neurons. Additionally, IRF6 knockdown in PC12 cells in vitro resulted in a decrease in active caspase-3 expression and an increase in Bcl-2 and p-Akt expression. We conclude that IRF6 might promote neuronal apoptosis by inhibiting Akt phosphorylation after TBI.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11482416 | PMC |
| http://dx.doi.org/10.1007/s10571-015-0217-3 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
5-HMF plays an intervention role in ischemic stroke by regulating GluR2 to improve mitochondrial function and promote angiogenesis.
Biochem Biophys Rep
December 2025
Henan University of Chinese Medicine, Zhengzhou, 450046, China.
Introduction: 5-Hydroxymethyl furfural (5-HMF) is a furan compound with a molecular formula of CHO. Studies have found that 5-HMF has many pharmacological effects, such as improving hemorheology, anti-inflammatory, antioxidant activity and anti-myocardial ischemia. Identifying the preventive effect of 5-HMF against ischemic stroke and its possible mechanism was the aim of this investigation.
View Article and Find Full Text PDFNovel small molecule derivatives improve survivability in the cellular model of Huntington's disease improving mitochondrial fusion.
RSC Med Chem
August 2025
Department of Biological Science, Birla Institute of Technology and Science, Pilani Hyderabad Campus, Jawahar Nagar, Kapra Mandal, Medchal District Telangana 500078 India
Mitochondrial dysfunction is one of the primary cellular conditions involved in developing Huntington's disease (HD) pathophysiology. The accumulation of mutant huntingtin protein with abnormal PolyQ repeats resulted in the death of striatal neurons with enhanced mitochondrial fragmentation. In search of neuroprotective molecules against HD conditions, we synthesized a set of isoxazole-based small molecules to screen their suitability as beneficial chemicals improving mitochondrial health.
View Article and Find Full Text PDFNucling, a stress-inducible protein associated with apoptosomes, is important for microglial polarization/activation in the brain neuroinflamation.
J Biochem
September 2025
Division of Enzyme Pathophysiology, Institute for Enzyme Research, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Microglia, the central nervous system's resident macrophages, are critical for immune defense, protecting neurons during infection. Their role in postnatal brain development, particularly after injury, remains unclear. Nucling, a protein up-regulated during cardiac muscle differentiation, regulates NF-κB, influencing apoptosis and cell proliferation.
View Article and Find Full Text PDFCETN3 deficiency induces microcephaly by disrupting neural stem/progenitor cell fate through impaired centrosome assembly and RNA splicing.
EMBO Mol Med
September 2025
Institute for Regenerative Medicine, Medical Innovation Center and State Key Laboratory of Cardiovascular Diseases, Shanghai East Hospital, National Stem Cell Translational Resource Center & Ministry of Education Stem Cell Resource Center, Frontier Science Center for Stem Cell Research, School of Li
Primary microcephaly, a rare congenital condition characterized by reduced brain size, occurs due to impaired neurogenesis during brain development. Through whole-exome sequencing, we identified compound heterozygous loss-of-function mutations in CENTRIN 3 (CETN3) in a 5-year-old patient with primary microcephaly. As CETN3 has not been previously linked to microcephaly, we investigated its potential function in neurodevelopment in human pluripotent stem cell-derived cerebral organoids.
View Article and Find Full Text PDFCell death in multiple sclerosis.
Cell Death Differ
September 2025
Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system (CNS) characterized by inflammatory demyelination and progressive neurodegeneration. Although current disease-modifying therapies modulate peripheral autoimmune responses, they are insufficient to fully prevent tissue specific neuroinflammation and long-term neuronal and oligodendrocyte loss. Growing evidence implicates various regulated cell death (RCD) pathways, including apoptosis, necroptosis, pyroptosis, and ferroptosis, not only as downstream consequences of chronic inflammation, but also as active drivers of demyelination, axonal injury, and glial dysfunction in MS.
View Article and Find Full Text PDF