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Results show that the binding of miR (show MLXIP Proteins)-589-5p to the MAP3K8 3'-UTR inhibits MAP3K8 expression and suppresses CD90 (show THY1 Proteins)+ 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 (show CDH13 Proteins)/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 (show MLXIP Proteins)-144-3p, and miR (show MLXIP Proteins)-144-3p downregulation is a factor in renal cell carcinoma (show MOK Proteins) 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 (show IL8 Proteins) secretion and CagA (show S100A8 Proteins)-dependent late IL-8 (show IL8 Proteins) secretion as an alternative signaling molecule in the Erk (show EPHB2 Proteins) 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 (show MLXIP Proteins)-509-3p RCC (show XRCC1 Proteins) suppressor was a significant regulator of the MAP3K8 oncogene (show RAB1A Proteins), suggesting that it may have a potential therapeutic role in the treatment of renal cell carcinoma (show MOK Proteins)
findings provide a novel perspective on the role of the IL-33 (show IL33 Proteins)/ST2 (show SULT2A1 Proteins)/COT signaling pathway in supporting cancer-associated inflammation in the tumor microenvironment
study to determine whether Tpl2 influences the immune response generated to the extracellular bacterium Citrobacter rodentium, which induces a mixed Th1 (show HAND1 Proteins) and Th17 response; findings confirm the importance of Tpl2 in driving the development of the proinflammatory Th1 (show HAND1 Proteins) lineage as well as promoting IL-17A (show IL17A Proteins) expression and neutrophil recruitment during infection with extracellular bacteria
TPL-2-regulated Ccl24 (show CCL24 Proteins) in CD11c (show ITGAX Proteins)+CD11b (show ITGAM Proteins)+ cells prevents accelerated type-2 mediated immunity to H. polygyrus.
role of p105 (show NEDD9 Proteins)/Tpl2 signaling in lung homeostasis
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 (show EPHB2 Proteins) and p38 (show CRK Proteins) 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 (show CCR2 Proteins) expression on Ly6C(high)CD11c (show ITGAX Proteins)(low) monocytes of atherosclerotic ApoE (show APOE Proteins)(-/-) mice fed an high fat diet.
results demonstrate that Tpl2 promotes inflammation in part by constraining FoxP3 (show FOXP3 Proteins) expression and Treg immunosuppressive functions.
Tpl2 plays a significant role in promoting HCC (show FAM126A Proteins) development by its pro-inflammatory effect, which suggested that Tpl2 could be a molecular target for HCC (show FAM126A Proteins) prevention.
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)