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The results revealed upregulation of MEK3, as well as phosphorylated MEK3 and phosphorylated p38 MAPK (show MAPK14 Proteins), in CMM patients. These results provide a "fingerprint" for mechanistic studies of CMM in the future and highlight the importance of MEK3-p38 MAPK (show MAPK14 Proteins) activation in CMM.
miR (show MLXIP Proteins)-21 targets MKK3 in vivo and in vitro, inhibiting the downstream factors IL-6 (show IL6 Proteins) and TNF-alpha (show TNF Proteins), in ischemia pretreatment protection from ischemia-reperfusion induced kidney injury.
MKK3 overexpression upregulated the cyclin-dependent kinase (show CDK1 Proteins) inhibitors, p16 INK4A and p15 INK4B (show CDKN2B Proteins) in hepatocellular carcinoma cells was Bim1, was downregulated following MKK3 overexpression.
Our results suggest that asthma is associated with MKK3 over-expression in CD8 (show CD8A Proteins)+ cells; we have also demonstrated that MKK3 may be critical for airway neutrophilia
MicroRNA-21 promotes hepatocellular carcinoma HepG2 cell proliferation through repression of mitogen-activated protein kinase-kinase 3.
study detected higher MKK3 activation in isolated peripheral blood mononuclear cells from septic patients compared with nonseptic controls
study concludes MAP2K3 is a reproducible obesity locus that may affect body weight via complex mechanisms involving appetite regulation and hypothalamic inflammation
miR-20a acts in a feedback loop to repress the expression of MKK3 and to negatively regulate the p38 pathway-mediated VEGF-induced endothelial cell migration and angiogenesis
Data suggest aberrant MAP2K protein (MKK3, MKK4 (show MAP2K4 Proteins), MKK6 (show MAP2K6 Proteins), and MKK7 (show MAP2K7 Proteins)) expression indicates that altered cellular signal transduction mediated via JNK (show MAPK8 Proteins) and p38 (show CRK Proteins) may be common in bladder cancer.
the balance between MKK6 (show MAP2K6 Proteins) and MKK3 mediates p38 MAPK (show MAPK14 Proteins) associated resistance to cisplatin in NSCLC
ATF3 (show ATF3 Proteins) upregulation in cardiac fibroblasts in response to hypertensive stimuli protects the heart by suppressing Map2K3 expression and subsequent p38 (show CRK Proteins)-transforming growth factor-beta signaling.
miR (show MLXIP Proteins)-21a-5p inhibited BPA (show DST Proteins) induced adipocyte differentiation by targeting map2k3 through MKK3/p38/MAPK (show MAPK14 Proteins) in 3T3-L1 cells
this study demonstrates that MKK3 influences mitochondrial quality by affecting the expression of mitochondrial proteins, including TCA cycle enzymes, and mitophagy, which consequently regulates the inflammatory response.
Exendin-4 treatment improves cardiac function, attenuates cardiac remodeling, and promotes angiogenesis in the infarcted myocardium through MKK3 and Akt-1 (show AKT1 Proteins) pathway.
MKK3 and MKK6 (show MAP2K6 Proteins) differentially regulate bone loss due to estrogen withdrawal. MKK3 directly mediates osteoclastogenesis while MKK6 (show MAP2K6 Proteins) likely contributes to pro-inflammatory cytokine production that promotes osteoclast formation.
results designate MKK3 as a novel, positive regulator of SCF (show KITLG Proteins)-induced mast cell proliferation and a critical signaling protein for AP-1 (show JUN Proteins)-dependent IL-6 (show IL6 Proteins) production
findings demonstrate a critical role for mitochondria in the pathogenesis of sepsis that involves a previously unrecognized function of MKK3 in mitochondrial quality control
Endothelial MKK3 is neede for inflammatory cell recruitment to the lungs, mitochondrial oxidant-mediated AP-1 (show JUN Proteins), NF-kappaB (show NFKB1 Proteins) activation, & ICAM-1 (show ICAM1 Proteins) expression during LPS (show TLR4 Proteins) challenge.
The protein encoded by this gene is a dual specificity protein kinase that belongs to the MAP kinase kinase family. This kinase is activated by mitogenic and environmental stress, and participates in the MAP kinase-mediated signaling cascade. It phosphorylates and thus activates MAPK14/p38-MAPK. This kinase can be activated by insulin, and is necessary for the expression of glucose transporter. Expression of RAS oncogene is found to result in the accumulation of the active form of this kinase, which thus leads to the constitutive activation of MAPK14, and confers oncogenic transformation of primary cells. The inhibition of this kinase is involved in the pathogenesis of Yersina pseudotuberculosis. Multiple alternatively spliced transcript variants that encode distinct isoforms have been reported for this gene.
MAP kinase kinase 3
, MAPK/ERK kinase 3
, MAPKK 3
, MEK 3
, SAPK kinase 2
, dual specificity mitogen-activated protein kinase kinase 3
, stress-activated protein kinase kinase 2
, mitogen activated protein kinase kinase 3
, protein kinase, mitogen-activated, kinase 3
, MAP kinase kinase 6
, MAPKK 6
, dual specificity mitogen-activated protein kinase kinase 6
, mitogen-activated protein kinase kinase 3