Jurkat cells, a human T lymphocyte line that can be induced to synthesize and secrete interleukin 2, contain a factor that binds interleukin 2 mRNA. Binding can be demonstrated by formation of a complex detectable by gel electrophoresis. The binding is sequence specific and occurs in the 3'-non-coding region, within 160 nt of the end of the coding region, at or near a site on the mRNA that is rich in A and U residues. However, it appears not to be due to known AU binding factors. The factor is protease sensitive and binds non-covalently to interleukin 2 mRNA. It behaves like a protein of molecular weight 50 000-60 000 after UV-induced cross-linking to the mRNA. Preparations of the binding factor also protect interleukin 2 mRNA against degradation by a recently described RNasin-resistant endoribonuclease activity in Jurkat cells. Protection occurs under the same conditions required to generate the gel-retarded complex.
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http://dx.doi.org/10.1093/nar/24.5.970 | DOI Listing |
Scand J Immunol
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Institute of Chemical Biology and Fundamental Medicine SB RAS, Novosibirsk, Russia.
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Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea; BK21 Plus KNU Biomedical Convergence Program, Department of Biomedical Science, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea; Brain Science & Engineering Institute, Kyungpook National University, Daegu, Republic of Korea. Electronic address:
Microglia-mediated neuroinflammation has been implicated in the neuropathology of traumatic brain injuries (TBI). Recently, the expression of interleukin-2-inducible T-cell kinase (ITK) has been detected in brain microglia, regulating their inflammatory activities. However, the role of microglial ITK in TBI has not been investigated.
View Article and Find Full Text PDFSci Rep
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Department of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
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Department of Pediatric Surgery, Children's Hospital of Fudan University, Shanghai Key Laboratory of Birth Defect, and Key Laboratory of Neonatal Disease, Ministry of Health, Shanghai 201102, China. Electronic address:
The imbalance between Tregs and proinflammatory Th17 cells in children with biliary atresia (BA) causes immune damage to cholangiocytes. Dimethyl fumarate (DMF), an immunomodulatory drug, regulates the Treg/Th17 balance in diseases like multiple sclerosis (MS). This study explores DMF's effect on Treg/Th17 balance in BA and its potential mechanism.
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January 2025
Department of Pathology and Laboratory Medicine, Medical University of South Carolina, 173 Ashley Ave, Charleston, SC, 29425, USA.
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