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these data demonstrate that miR-130b represses vascular inflammation via targeting Tpl2
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Results show that the binding of miR-589-5p to the MAP3K8 3'-UTR inhibits MAP3K8 expression and suppresses CD90+ cancer stem cells characteristics in hepatocellular carcinoma.
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RelAp43 interacts with the p105-ABIN2-TPL2 complex and we observe a strong perturbation of this complex in presence of M protein.
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miRNA-509-3p mimics or inhibitor transfection tests in KGN cells further confirmed that miRNA-509-3p improved oestradiol (E2) secretion by inhibiting the expression of MAP3K8
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role of p105/Tpl2 signaling in lung homeostasis
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rs1042058 GG Crohn's disease -risk polymorphism in TPL2 results in a gain-of-function by increasing TPL2 expression and signalling, thereby amplifying Pattern recognition receptor -initiated outcomes.
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MAP3K8 is a direct target of miR-144-3p, and miR-144-3p downregulation is a factor in renal cell carcinoma progression through potentiation of MAP3K8 expression.
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Taken together, these results suggest that Cot kinase might play a critical role in Helicobacter pylori type IV secretion apparatus-dependent early IL-8 secretion and CagA-dependent late IL-8 secretion as an alternative signaling molecule in the Erk pathway.
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Studies indicate that Tpl2, a MAP3K, participates in a broad range of cancer-related signaling pathways and induces tumorigenesis and progression of many cancers.
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the results of the present study demonstrated that the miR-509-3p RCC suppressor was a significant regulator of the MAP3K8 oncogene, suggesting that it may have a potential therapeutic role in the treatment of renal cell carcinoma
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findings provide a novel perspective on the role of the IL-33/ST2/COT signaling pathway in supporting cancer-associated inflammation in the tumor microenvironment
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structurally versatile active site significantly impacts the design of potent, low molecular weight COT kinase inhibitors
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TPL2 mediates the phosphorylation of a fraction of nucleophosmin at threonine 199, an event required for its proteasomal degradation and maintenance of steady-state nucleophosmin levels.
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MAP3K8 and miR-17-5p expression were inversely correlated with treatment response
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COT interacts with and phosphorylates Pin1 on Ser16. Consequently, Pin1 Ser16 phosphorylation by COT increases cyclin D1 abundance and enhances tumorigenecity of MCF7 cells.
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Aberrant expression of A-, B-, and C-RAF, and COT is frequent in PTC; increased expression of COT is correlated with recurrence of PTC.
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Tpl2 overexpression and downregulation showed significant stimulatory and inhibitory effects on tumorigenic and metastatic potential of ADI PC cells.
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Following epithelial injury, intestinal myofibroblasts sense innate or inflammatory signals and activate, via Tpl2, the cyclooxygenase-2 (Cox-2)-prostaglandin E2 (PGE2) pathway, which are essential for the epithelial homeostatic response.
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High MAP3K8 expression affects obesity-induced adipose tissue inflammation without systemic effects.
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Tpl2 regulates various inflammatory pathways by activating the ERK mediated MAP kinase pathway in innate immune cells such as macrophages and dendritic cells in humans but not in mice.