ArticleCell death & disease2015
Socs1 and Socs3 degrades Traf6 via polyubiquitination in LPS-induced acute necrotizing pancreatitis.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- TRAF6, a gga-miR-7b Target, PromotesBiomolecules · 2026Article
- Tumor necrosis factor-α promotes abnormal glucose metabolism after acute pancreatitis by inducing islet β-cell apoptosisWorld journal of gastroenterology · 2025Article
- Whole exome sequencing reveals aniMetaOmics · 2025Article
- FTO O-GlcNAcylation promotes TRIM21-mediated FTO ubiquitination degradation to sustain the negative feedback control of macrophage inflammation.Frontiers in immunology · 2025Article
- Toll-like receptor 4 in pancreatic damage and immune infiltration in acute pancreatitis.Frontiers in immunology · 2024Review
- Tumor Necrosis Factor Receptor-Associated Factor 6 and Human Cancer: A Systematic Review of Mechanistic Insights, Functional Roles, and Therapeutic Potential.Journal of Cancer · 2024Review
- Extracellular Vesicles-mediated recombinant IL-10 protects against ascending infection-associated preterm birth by reducing fetal inflammatory response.Frontiers in immunology · 2023Article
- Nanoparticle encapsulated CQ/TAM combination harmonizes with MSCs in arresting progression of severity in AP mice through iNOS (IDO) signaling.Materials today. Bio · 2022Article
- Identification of novel immune-related targets mediating disease progression in acute pancreatitis.Frontiers in cellular and infection microbiology · 2022Article
- NDevelopmental cell · 2020Article
- Article
- A hMTR4-PDIA3P1-miR-125/124-TRAF6 Regulatory Axis and Its Function in NF kappa B Signaling and Chemoresistance.Hepatology (Baltimore, Md.) · 2020Article
- SOCS Proteins Participate in the Regulation of Innate Immune Response Caused by Viruses.Frontiers in immunology · 2020Review
- Roles of TRAFs in Ischemia-Reperfusion Injury.Frontiers in cell and developmental biology · 2020Review
- Therapeutic Implication of SOCS1 Modulation in the Treatment of Autoimmunity and Cancer.Frontiers in pharmacology · 2019Review
- Macrophage/microglial Ezh2 facilitates autoimmune inflammation through inhibition of Socs3.The Journal of experimental medicine · 2018Article
- Clinical and functional significance of STEAP4-splice variant in CD14Clinical and experimental immunology · 2018Article
- TRAF molecules in inflammation and inflammatory diseases.Current pharmacology reports · 2018Article
- Blockade of high-mobility group box 1 attenuates intestinal mucosal barrier dysfunction in experimental acute pancreatitis.Scientific reports · 2017Article
- The loss-of-function mutations and down-regulated expression of ASB3 gene promote the growth and metastasis of colorectal cancer cells.Chinese journal of cancer · 2017Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mechanisms involved in inflammatory development during acute pancreatitis (AP) are largely vague, especially in the transformation of acute edematous pancreatitis (AEP) into acute necrotizing pancreatitis (ANP). This current study aims to investigate the functions of Traf6 in different AP models in vitro and in vivo, and to identify the possible regulatory mechanism in the progression of inflammation from mild to severe. Our data revealed that the level of Traf6 expression was significantly increased in the mild AP induced by caerulein, and the upregulation of Traf6 played a protective role in acinar cells against caerulein-induced apoptosis. In contrast, only Traf6 protein but not mRNA was downregulated in the severe ANP induced by combination treatment of caerulein and LPS. Mechanistic studies showed that LPS upregulated the levels of Socs1 and Socs3 expressions in acinar cells, Socs1 and Socs3 interacted Traf6 directly and degraded Traf6 protein via polyubiquitination, thereby counteracted the protective function of Traf6. In vivo study further showed that combination treatment of caerulein and LPS failed to induce an ANP model in the TLR4 knockout mice, and the level of Traf6 expression in the pancreatic tissues remained the same as that from the acute edematous pancreatitis (AEP) mouse. Taken together, our study reveals that Traf6 functioned as a protective factor in the progression of AP, and LPS-induced Socs1 and Socs3 exacerbate mild AP to severe AP, which provides evidence for developing a new therapeutic target to combat AP.
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