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Advanced glycation end products significantly activated ASK1, MKK3, and MKK6, which led to activation of p38 MAPK, resulting in upregulated fibrotic response in human coronary smooth muscle cells.
The study identifies MKK3 as a negative regulator of mitochondrial function and inflammatory responses to cigarette smoke and suggests that MKK3 could be a therapeutic target.
MEK2 was essential for the phosphorylation of MKK3/MKK6 and p38 MAPK that directly impacted on cyclin D1 expression.
High MKK3 expression is associated with lung cancer.
The results revealed upregulation of MEK3, as well as phosphorylated MEK3 and phosphorylated p38 MAPK, in CMM patients. These results provide a "fingerprint" for mechanistic studies of CMM in the future and highlight the importance of MEK3-p38 MAPK activation in CMM.
miR-21 targets MKK3 in vivo and in vitro, inhibiting the downstream factors IL-6 and TNF-alpha, in ischemia pretreatment protection from ischemia-reperfusion induced kidney injury.
MKK3 overexpression upregulated the cyclin-dependent kinase inhibitors, p16 INK4A and p15 INK4B in hepatocellular carcinoma cells was Bim1, was downregulated following MKK3 overexpression.
Our results suggest that asthma is associated with MKK3 over-expression in CD8+ 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, MKK6, and MKK7) expression indicates that altered cellular signal transduction mediated via JNK and p38 may be common in bladder cancer.
the balance between MKK6 and MKK3 mediates p38 MAPK associated resistance to cisplatin in NSCLC
LFA-1-induced stabilization of ARE-containing mRNAs in T cells is dependent on HuR, and occurs through the Vav-1, Rac1/2, MKK3 and p38MAPK signaling cascade
The p38 MAPK pathway transgene is dispensable for the development of natural killer (NK)T cells; however, NKT cell cytokine production and NKT-mediated liver damage are highly dependent on activation of this pathway.
MAP2K3 is identified as a protein to promote senescence in human breast epithelial cells.
Data provide evidence that p38 Map kinase (MAPK) pathway is activated leading to increased upregulation of mixed lineage kinase 3, MKK3/6, MSK1, and Mapkapk2, upon treatment of BCR/ABL expressing cells with dasatinib.
Results show that oncogenic ras provokes premature senescence by sequentially activating the MEK-ERK and MKK3/6-p38 pathways in normal, primary cells.
role in activating Mirk protein kinase
The study identifies MKK3 as a negative regulator of mitochondrial function and inflammatory responses to cigarette smoke.
MAP2K6 functions in mouse testis determination, via positive effects on Sry, and a minor role for MAP2K3.
ATF3 upregulation in cardiac fibroblasts in response to hypertensive stimuli protects the heart by suppressing Map2K3 expression and subsequent p38-transforming growth factor-beta signaling.
miR-21a-5p inhibited BPA induced adipocyte differentiation by targeting map2k3 through MKK3/p38/MAPK 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 pathway.
MKK3 and MKK6 differentially regulate bone loss due to estrogen withdrawal. MKK3 directly mediates osteoclastogenesis while MKK6 likely contributes to pro-inflammatory cytokine production that promotes osteoclast formation.
results designate MKK3 as a novel, positive regulator of SCF-induced mast cell proliferation and a critical signaling protein for AP-1-dependent IL-6 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, NF-kappaB activation, & ICAM-1 expression during LPS challenge.
mast cell MKK3 signaling contributes to IgE-dependent allergic inflammation and is a specific regulator of FcepsilonRI-induced IL-4 production.
Studies identified FOXM1 as a key downstream target of Ras-MKK3-p38 regulated in vitro cellular invasion.
Activation of distinct p38MAPK isoforms is regulated by the selective and synchronized action of two kinases, MKK3 and MKK6, in response to cell stress.
MKK3 is upregulated in peripheral CD4(+)T cells
MKK3 is a critical component of the TGF-beta1 signaling pathway, and its activation is required for subsequent p38alpha and p38delta MAPK activation and collagen stimulation by TGF-beta1
MKK3 is one of three protein kinases which activate p38 MAPK in vitro.
Cytoprotective effects of carbon monoxide are mediated by selective activation of the MKK3/p38 beta protein MAP kinase pathway.
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