ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2022
[TRAF6 promotes
Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Ag85B-induced M1 Macrophage Polarization via the TLR4/TRAF6/NF-κB Axis Leading to Bronchial Epithelial Cell Damage and TH17/Treg Imbalance.Current molecular medicine · 2025Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the role of tumor necrosis factor receptor-associated factor 6 (TRAF6) in regulating
methodsThe expression of TRAF6 in peripheral blood samples of 50 patients with active tuberculosis (TB) and 50 healthy individuals were detected using quantitative real-time PCR (qPCR). RAW264.7 macrophages were infected with BCG at different MOI and for different lengths of time, and the changes in expressions of Caspase 3 and TRAF6 were detected with Western blotting and qPCR. In a RAW264.7 cell model of BCG infection with TRAF6 knockdown established using RNA interference technique, the bacterial load was measured and cell apoptotic rate and mitochondrial membrane potential (MMP) were determined with flow cytometry. The expression levels of TRAF6, Caspase 3, PARP, BAX and Bcl-2 in the cells were detected using Western blotting, and the expressions of TRAF6 and Caspase 3 were also examined with immunofluorescence assay.
resultsThe expression of TRAF6 was significantly upregulated in the peripheral blood of patients with active TB as compared with healthy subjects (
conclusionTRAF6 promotes BCG-induced macrophage apoptosis by regulating the intrinsic apoptosis pathway.
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Registered trials
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