Browse our anti-MAP3K7 (MAP3K7) Antibodies

Human Mitogen-Activated Protein Kinase Kinase Kinase 7 (MAP3K7) interaction partners

1. results strongly suggest that TAK1 activation leads to AMPK activation, which activates ULK1 by phosphorylating ULK1(S317) and suppressing mTOR activity and ULK1(S757) phosphorylation.

2. TAK1 up regulates the expression of BMP-2 at all concentration under the inhibition of p38 and JNK.

3. TAK1 as a potential biomarker and therapeutic target for CTCL therapy.

4. USP8 interacted with transforming growth factorbetaactivated kinase1 (TAK1) and deubiquitinated the K63linked ubiquitination of TAK1.

5. 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

6. De novo splicing variant in MAP3K7 was identified in a patient with cardiospondylocarpofacial syndrome with features of hereditary connective tissue disorder.

7. 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.

8. 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]

9. 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.

10. 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.

11. 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.

12. increased TAK1 expression may be involved in the progression of gastric cancer.

13. miR-146a, serving as a tumor suppressor, may significantly promote GC cell apoptosis by inhibition of the NF-kappaB signaling pathway via targeting TAK1.

14. 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.

15. 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.

16. nMet accelerated HCC tumorigenesis and metastasis via the activation of TAK1/NF-kappaB pathway.

17. TAK1 protein expression increased in cartilage tissue from spinal tuberculosis patients.

18. TAK1 regulates Nrf2 through modulation of Keap-p62/SQSTM1 interaction. This regulation is important for homeostatic antioxidant protection in the intestinal epithelium.

19. Overexpression of TAK1 was strongly associated with positive lymph node metastasis in pancreatic ductal adenocarcinoma.

20. 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

Mouse (Murine) Mitogen-Activated Protein Kinase Kinase Kinase 7 (MAP3K7) interaction partners

1. Takinib has utility in the treatment inflammatory disease by locally suppressing TNF production from invading macrophages

2. USP4 deficiency plays a detrimental role in hepatic I/R injury by promoting activation of the TAK1/JNK signalling pathways.

3. Inducible inactivation of TAK1 causes severe muscle wasting in both young and adult mice by inhibiting protein synthesis, inducing proteolysis, and accumulation of dysfunctional mitochondria in skeletal muscles. TAK1 activity is highly upregulated during overload-induced skeletal muscle growth, and inactivation of TAK1 prevents myofiber hypertrophy.

4. cisplatin activates TAK1, which phosphorylates p38 and ERK, leading to excessive autophagy of tubular epithelial cells that exacerbates kidney damage.

5. TAK1 plays an important role in the pathogenesis of ischemia-induced renal fibrosis and may mediate p38-regulated cell apoptosis

6. that TAK1 deletion in tumor endothelial cells resulted in blood vessel and hence tumor regression

7. Inactivation of MAP3K7 in FOXD1-expressing cells results in loss of mesangial PDGFRBeta and juvenile kidney scarring.

8. Study identifies a critical role for TAK1 in maintaining NLRP3 inflammasome quiescence.

9. Results show that phospholipase C beta 2 (PLCbeta2) inhibits the virus-induced expression of pro-inflammatory cytokines by interacting with and inhibiting transforming growth factor-beta-activated kinase 1 (TAK1) activation.

10. this study establishes the importance of TAK1 and IKK activity in the control of GSDMD cleavage and cytotoxicity.

11. 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.

12. TAK1 inhibits HBV primarily at viral transcription level through activation of MAPK-JNK pathway.

13. 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.

14. 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.

15. 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.

16. It is a key regulator of the toll-like receptor signaling pathway.

17. 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.

18. 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.

19. 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

20. 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.