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these data demonstrate that miR-130b represses vascular inflammation via targeting Tpl2
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.
RelAp43 interacts with the p105-ABIN2-TPL2 complex and we observe a strong perturbation of this complex in presence of M protein.
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
role of p105/Tpl2 signaling in lung homeostasis
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.
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.
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.
Studies indicate that Tpl2, a MAP3K, participates in a broad range of cancer-related signaling pathways and induces tumorigenesis and progression of many cancers.
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
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
structurally versatile active site significantly impacts the design of potent, low molecular weight COT kinase inhibitors
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.
MAP3K8 and miR-17-5p expression were inversely correlated with treatment response
COT interacts with and phosphorylates Pin1 on Ser16. Consequently, Pin1 Ser16 phosphorylation by COT increases cyclin D1 abundance and enhances tumorigenecity of MCF7 cells.
Aberrant expression of A-, B-, and C-RAF, and COT is frequent in PTC; increased expression of COT is correlated with recurrence of PTC.
Tpl2 overexpression and downregulation showed significant stimulatory and inhibitory effects on tumorigenic and metastatic potential of ADI PC cells.
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.
High MAP3K8 expression affects obesity-induced adipose tissue inflammation without systemic effects.
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.
Map3k8 activity controls the massive production of neutrophils in LPS-induced emergency granulopoiesis. Map3k8 regulates LPS-induced G-CSF production, which upregulates C/EBPbeta expression in immature neutrophils to trigger their amplification.
Describe spontaneous S. xylosus infection in a genetically modified murine model. S. xylosus infection in Rag1-/-Tpl2-/- mice correlated with disseminated bacteria and elevated numbers of circulating monocytes.
study to determine whether Tpl2 influences the immune response generated to the extracellular bacterium Citrobacter rodentium, which induces a mixed Th1 and Th17 response; findings confirm the importance of Tpl2 in driving the development of the proinflammatory Th1 lineage as well as promoting IL-17A expression and neutrophil recruitment during infection with extracellular bacteria
TPL-2-regulated Ccl24 in CD11c+CD11b+ cells prevents accelerated type-2 mediated immunity to H. polygyrus.
this study shows that TPL-2 deficiency leads to severe house duct mite-induced airway allergy, when compared with wild-type mice
The kinase TPL2 activates ERK and p38 signaling to promote neutrophilic inflammation
TPL2 kinase is a crucial signaling factor in iNKT cells and major mediator of hepatic inflammation.
Taken together this study identified that TPL-2 regulated TH2-mediated inflammation by supporting lipolysis and M2 macrophage activation, preventing TH2 cell expansion and downstream immunopathology and fibrosis.
Map3k8 decreases apoptosis of monocytes and enhances CCR2 expression on Ly6C(high)CD11c(low) monocytes of atherosclerotic ApoE(-/-) mice fed an high fat diet.
results demonstrate that Tpl2 promotes inflammation in part by constraining FoxP3 expression and Treg immunosuppressive functions.
Tpl2 plays a significant role in promoting HCC development by its pro-inflammatory effect, which suggested that Tpl2 could be a molecular target for HCC prevention.
Tpl2 null mice displayed low COX-2 mRNA induction in adipose tissue.
The stimulating effect of estradiol on progesterone synthesis relies on the estrogen no-classical protein-coupled receptor 30, and MAP3K8.
these findings establish an essential role for Tpl2 in antiviral host defense mechanisms.
Tpl2 promotes Th1, but not Th17, differentiation in a T cell transfer model of colitis.
Tpl2 is an essential regulator of reactive oxygen species production during TLR3/9 signaling.
This study demonstrates a Tpl2-dependent mechanism for macrophage expression of select chemokine receptors.
This gene is an oncogene that encodes a member of the serine/threonine protein kinase family. The encoded protein localizes to the cytoplasm and can activate both the MAP kinase and JNK kinase pathways. This protein was shown to activate IkappaB kinases, and thus induce the nuclear production of NF-kappaB. This protein was also found to promote the production of TNF-alpha and IL-2 during T lymphocyte activation. This gene may also utilize a downstream in-frame translation start codon, and thus produce an isoform containing a shorter N-terminus. The shorter isoform has been shown to display weaker transforming activity. Alternate splicing results in multiple transcript variants that encode the same protein.
mitogen-activated protein kinase kinase kinase 8
, Ewing sarcoma transformant
, cot (cancer Osaka thyroid) oncogene
, proto-oncogene c-Cot
, proto-oncogene serine/threoine protein kinase
, tumor progression locus 2
, COT proto-oncogene serine/threonine-protein kinase
, cancer Osaka thyroid oncogene
, cancer Osaka thyroid, oncogene
, mitogen activated protein kinase kinase kinase 8
, serine/threonine-protein kinase cot
, serine/threonine kinase (Tpl-2)