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USP8 interacted with transforming growth factorbetaactivated kinase1 (TAK1) and deubiquitinated the K63linked ubiquitination of TAK1.
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This study revealed that the recurrent deletion of MAP3K7/CASP8AP2 is associated with SIL-TAL1 fusions and a mature immunophenotype, but not with response to treatment and risk of relapse in pediatric T-cell acute lymphoblastic leukemia
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De novo splicing variant in MAP3K7 was identified in a patient with cardiospondylocarpofacial syndrome with features of hereditary connective tissue disorder.
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TAK1 plays a central role in promoting triple-negative breast cancer cell adaptation to the lung microenvironment by facilitating positive feedback signaling mediated by P38.
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In brief, TAK1 can function as direct AMPK upstream kinase in specific contexts and in response to a subset of TAK1 activating stimuli. Further research is needed to define the intricate signals that are conditional for TAK1 to phosphorylate and activate AMPKalpha at T172. [review]
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The expression of IL-6 gene and protein was significantly induced by IL-17F. IL-17F activated TAK1 and NF-kappaB in airway smooth muscle cells.
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overexpression of miR-20a reduced colony formation and tumor growth. Furthermore, the data revealed that the function of miR-20a was probably exerted via targeting the TAK1 expression. Overexpression of miR-20a sensitizes the osteosarcoma cells to chemotherapeutic drugs.
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TGFbeta and IL1beta signaling interact at the SMAD2/3 level in human primary MSC. Down-stream TGFbeta target genes were repressed by IL1beta independent of C-terminal SMAD2 phosphorylation. We demonstrate that SMAD2/3 linker modifications are required for this interplay and identified TAK1 as a crucial mediator of IL1beta-induced TGFbeta signal modulation.
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increased TAK1 expression may be involved in the progression of gastric cancer.
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miR-146a, serving as a tumor suppressor, may significantly promote GC cell apoptosis by inhibition of the NF-kappaB signaling pathway via targeting TAK1.
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In conclusion, for the first time, we report that TRADD, TRAF2, RIP1 and TAK1 play a role in the regulating TNF-alpha signalling in human myometrium. These findings are of significance given the central role of TNF-alpha in the processes of human labour and delivery.
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Rab1 is regulated by the host in a similar fashion, and that the innate immunity kinase TAK1 and Legionella effectors compete to regulate Rab1 by switch II modifications during infection.
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nMet accelerated HCC tumorigenesis and metastasis via the activation of TAK1/NF-kappaB pathway.
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TAK1 protein expression increased in cartilage tissue from spinal tuberculosis patients.
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TAK1 regulates Nrf2 through modulation of Keap-p62/SQSTM1 interaction. This regulation is important for homeostatic antioxidant protection in the intestinal epithelium.
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Overexpression of TAK1 was strongly associated with positive lymph node metastasis in pancreatic ductal adenocarcinoma.
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dysregulation of the TAK1 complex produces a close phenocopy of Frontometaphyseal Dysplasia caused by FLNA mutations; furthermore, the pathogenesis of some of the filaminopathies caused by FLNA mutations might be mediated by misregulation of signaling coordinated through the TAK1 signaling complex
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although TAK1 is located at the crossroad of inflammation, immunity, and cancer, this study reports MAP3K7 mutations in a developmental disorder affecting mainly cartilage, bone, and heart
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This study suggests that aberrant activity of TAK1 impairs autophagy and subsequently leads to alterations in the vitality of retinal pigment epithelial cells.
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TAK1 may be an important factor involved in the pathogenesis of thyroid cancer, and targeted down-regulation of TAK1 may improve the prognosis of patients with thyroid cancer.
