ArticleFree radical biology & medicine2013
TIFA upregulation after hypoxia-reoxygenation is TLR4- and MyD88-dependent and associated with HMGB1 upregulation and release.
Article in Free radical biology & medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- TIFA: a signaling hub linking inflammation, innate immunity, and human disease.Frontiers in immunology · 2026Review
- High-Voltage Electrostatic Field Hydrogel Microsphere 3D Culture System Improves Viability and Liver-like Properties of HepG2 Cells.International journal of molecular sciences · 2024Article
- TIFA promotes colorectal cancer cell proliferation in an RSK- and PRAS40-dependent manner.Cancer science · 2022Article
- Identification of the correlations between interleukin-27 (IL-27) and immune-inflammatory imbalance in preterm birth.Bioengineered · 2021Article
- Citrobacter rodentium induces rapid and unique metabolic and inflammatory responses in mice suffering from severe disease.Cellular microbiology · 2020Article
- Dibromoacetic Acid Induced Hepatotoxicity in Mice through Oxidative Stress and Toll-Like Receptor 4 Signaling Pathway Activation.Oxidative medicine and cellular longevity · 2019Article
- High-Mobility Group Box-1 and Liver Disease.Hepatology communications · 2018Review
- Complement Activation in Liver Transplantation: Role of Donor Macrosteatosis and Implications in Delayed Graft Function.International journal of molecular sciences · 2018Review
- GW4064 attenuates lipopolysaccharide‑induced hepatic inflammation and apoptosis through inhibition of the Toll‑like receptor 4‑mediated p38 mitogen‑activated protein kinase signaling pathway in mice.International journal of molecular medicine · 2018Article
- Article
- Analyses of caspase-1-regulated transcriptomes in various tissues lead to identification of novel IL-1β-, IL-18- and sirtuin-1-independent pathways.Journal of hematology & oncology · 2017Article
- Protective Effects of Dioscin against Lipopolysaccharide-Induced Acute Lung Injury through Inhibition of Oxidative Stress and Inflammation.Frontiers in pharmacology · 2017Article
- IL-17 induces MIP-1α expression in primary mouse astrocytes via TRPC channel.Inflammopharmacology · 2016Article
- Article
- Role of high-mobility group box 1 in methamphetamine-induced activation and migration of astrocytes.Journal of neuroinflammation · 2015Article
- Regulatory effects of AT₁R-TRAF6-MAPKs signaling on proliferation of intermittent hypoxia-induced human umbilical vein endothelial cells.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2015Article
- TIFA suppresses hepatocellular carcinoma progression via MALT1-dependent and -independent signaling pathways.Signal transduction and targeted therapyArticle
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
TRAF-interacting protein with a forkhead-associated domain (TIFA) is a tumor necrosis factor receptor-associated factor 6 (TRAF6) binding protein that mediates IL-1 signaling. We recently reported that TIFA mRNA is significantly upregulated early in the liver after trauma and hemorrhagic shock. In this study, we sought to characterize the upregulation of TIFA by hypoxia-reoxygenation and investigate its role in hypoxia-induced signaling. TIFA expression was detected by qRT-PCR and Western blotting in both mouse hemorrhagic shock with resuscitation (HS-R) and hepatocytes exposed to hypoxia-reoxygenation. Involvement of TLR4 and MyD88 was assessed using cells from TLR4(-/-) and MyD88(-/-) mice. The interaction of TIFA with TRAF6 and IRAK-1 was investigated using coimmunoprecipitation in vitro. RNAi was performed to knock down the endogenous expression of the TIFA gene in hepatocytes. High-mobility-group box 1 protein (HMGB1) expression was detected by Western blotting and ELISA, and the activation of NF-κB and MAPK was measured with EMSA and Western blotting. The results showed that TIFA expression was upregulated after HS-R in vivo and hypoxia-reoxygenation in vitro. Further analysis revealed that hypoxia-reoxygenation-induced upregulation of TIFA was TLR4- and MyD88-dependent. Moreover, TIFA was found to associate with TRAF6 constitutively, whereas its association with IRAK-1 was seen only after hypoxia-reoxygenation. Suppression of TIFA by siRNA reduced NF-κB activation and HMGB1 upregulation and release after hypoxia-reoxygenation. Taken together, these data suggest that TIFA is involved in the regulation of cell signaling in hypoxia-reoxygenation. The increase in TIFA level appears to be a feed-forward mechanism involved in TLR4/MyD88-dependent signaling, leading to NF-κB activation and HMGB1 release.
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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.