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Human Polyclonal MAP3K7 Primary Antibody für WB - ABIN541242
Irie, Muta, Takeshige: TAK1 mediates an activation signal from toll-like receptor(s) to nuclear factor-kappaB in lipopolysaccharide-stimulated macrophages. in FEBS letters 2000
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Human Polyclonal MAP3K7 Primary Antibody für DB, ELISA - ABIN537666
Ono, Ohtomo, Ninomiya-Tsuji, Tsuchiya: A dominant negative TAK1 inhibits cellular fibrotic responses induced by TGF-beta. in Biochemical and biophysical research communications 2003
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Human Polyclonal MAP3K7 Primary Antibody für DB, ELISA - ABIN537667
Sakurai, Suzuki, Kawasaki, Nakano, Okazaki, Chino, Doi, Saiki: Tumor necrosis factor-alpha-induced IKK phosphorylation of NF-kappaB p65 on serine 536 is mediated through the TRAF2, TRAF5, and TAK1 signaling pathway. in The Journal of biological chemistry 2003
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Human Polyclonal MAP3K7 Primary Antibody für IHC (p), ELISA - ABIN543284
Cheung, Campbell, Nebreda, Cohen: Feedback control of the protein kinase TAK1 by SAPK2a/p38alpha. in The EMBO journal 2003
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Human Polyclonal MAP3K7 Primary Antibody für DB - ABIN389721
Huang, Chiang, Hung, Hou: Targeting of TGF-β-activated protein kinase 1 inhibits chemokine (C-C motif) receptor 7 expression, tumor growth and metastasis in breast cancer. in Oncotarget 2015
USP8 interacted with transforming growth factorbetaactivated kinase1 (TAK1) and deubiquitinated the K63linked ubiquitination of TAK1.
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
De novo splicing variant in MAP3K7 was identified in a patient with cardiospondylocarpofacial syndrome with features of hereditary connective tissue disorder.
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.
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]
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.
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.
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.
increased TAK1 expression may be involved in the progression of gastric cancer.
miR-146a, serving as a tumor suppressor, may significantly promote GC cell apoptosis by inhibition of the NF-kappaB signaling pathway via targeting TAK1.
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.
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.
nMet accelerated HCC tumorigenesis and metastasis via the activation of TAK1/NF-kappaB pathway.
TAK1 protein expression increased in cartilage tissue from spinal tuberculosis patients.
TAK1 regulates Nrf2 through modulation of Keap-p62/SQSTM1 interaction. This regulation is important for homeostatic antioxidant protection in the intestinal epithelium.
Overexpression of TAK1 was strongly associated with positive lymph node metastasis in pancreatic ductal adenocarcinoma.
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
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
This study suggests that aberrant activity of TAK1 impairs autophagy and subsequently leads to alterations in the vitality of retinal pigment epithelial cells.
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.
TAK1 directly interacts with and phosphorylates alphaTAT1 at Ser237 to critically enhance its catalytic activity. Also TAK1 selectively inhibits AKT to suppress mitogenic and metabolism-related pathways through microtubules-based mechanisms in culture and in vivo.
TAK1 inhibits HBV primarily at viral transcription level through activation of MAPK-JNK pathway.
we generated the transgenic mouse line with deletion of Tak1 and gain of function of Bmpr1a. This compound mutation leads to more severe craniofacial deformities than each single mutation.
Protein expression, processing and secretion occurred abnormally in transgenic mice overexpressing caMAP3K7. The overexpression of caMAP3K7 had a profound effect on enamel structure by disrupting the orderly growth of enamel prisms.
Data indicate TNF receptor associated factor 6 (TRAF6) as an essential molecular switch leading to cardiac hypertrophy in a transforming growth factor beta-activated kinase 1 (TAK1), -dependent manner.
It is a key regulator of the toll-like receptor signaling pathway.
The conversion of Tak1-B to Tak1-A consistently led to significant accumulation of lipids in cultured AML12cells, as well as the dysregulation of several lipid metabolism-related genes in mouse liver. Different functional properties of the two isoforms may explain the conflicting functions previously reported for Tak1.
demonstrate the efficiency of ad--siRNA-TAK1 in controlling joint inflammation of Collagen-Induced Arthritis, which is associated with the suppression of the expression of pro-inflammatory cytokines and JNK activation.
These data, in addition to the fact that Map3k7 is upregulated in the sinus venous-the source of cells for the SAN-suggest that Map3k7 may be an endogenous regulator of the SAN fate
These results present a novel in vivo function, the negative role of TAK1 in marginal zone B-cell development that is likely associated with NF-kappaB2 activation.
Tnfr1 deletion partially restored thymic and lung macrophages.
TAK1 is required for PPARgamma transactivation and promotes PPARgamma transcriptional activity synergistically with TAK1 binding protein 1 (TAB1).
inhibition of TAK1 triggered two caspase 8 activation pathways through the induction of RIP1-FADD-caspase 8 complex as well as FLIP cleavage/degradation.
Transforming growth factor-beta activated kinase 1 (TAK1) regulation of sterol-regulatory element-binding proteins (SREBPs) critically contributes to the maintenance of liver homeostasis to prevent steatosis, which is a potentially important mechanism to prevent hepatocellular carcinoma (HCC) development.
Mekk1 (encoded by Map3k1) signaling activates Mapks to regulate Cdkn1b (encoding p27(Kip1)) expression and p27(Kip1)-dependent proliferative expansion in response to antigen.
TRADD knockout blunts pressure overload-induced cardiac hypertrophy through mediating TAK1/p38 MAPK but not AKT phosphorylation
this study demonstrates a pivotal role of TAK1 in dendritic cells in controlling trichloroethylene-induced contact hypersensitivity response and suggests that targeting TAK1 function in DCs may be a viable approach to preventing and treating TCE-related occupational health hazards
The E3 ligase TRIM8 is a potent regulator that exacerbates steatohepatitis and metabolic disorders dependent on its binding and ubiquitinating capacity on transforming growth factor-beta-activated kinase 1.
Angiotensin-II up-regulates the Ampkalpha1 isoform in renal tissue. Ampkalpha1 participates in renal Tak1 activation and Tak1-dependent signaling induced by angiotensin-II.
The protein encoded by this gene is a member of the serine/threonine protein kinase family. This kinase mediates the signaling transduction induced by TGF beta and morphogenetic protein (BMP), and controls a variety of cell functions including transcription regulation and apoptosis. In response to IL-1, this protein forms a kinase complex including TRAF6, MAP3K7P1/TAB1 and MAP3K7P2/TAB2\; this complex is required for the activation of nuclear factor kappa B. This kinase can also activate MAPK8/JNK, MAP2K4/MKK4, and thus plays a role in the cell response to environmental stresses. Four alternatively spliced transcript variants encoding distinct isoforms have been reported.
mitogen-activated protein kinase kinase kinase 7
, TGF-beta-activated kinase TAK1
, TGF-beta activated kinase 1
, TGF-beta-activated kinase 1
, transforming growth factor-beta-activated kinase 1
, mitogen activated protein kinase kinase kinase 7
, transforming growth factor beta-activated kinase 1