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SMYD3-mediated methylation of MAP3K2 increases mutant K-Ras-induced activation of ERK1/2. (Review)
Restoration of miR17/20a in solid tumor cells enhances the natural killer cell antitumor activity by targeting Mekk2
HBXIP (show HBXIP Proteins) activated ERK1/2 through up-regulating MEKK2.
MEKK2 has a novel function as a regulator of ubiquitylation-dependent paxillin (show PXN Proteins) redistribution in breast tumour cells.
EBV microRNA BART (show BSND Proteins) 18-5p targets MAP3K2 to facilitate persistence in vivo by inhibiting viral replication in B cells.
Inhibitors of apoptosis proteins regulate myogenic differentiation by directly suppressing MEKK2/3-MEK5 (show MAP2K5 Proteins)-ERK5 (show MAPK7 Proteins) signaling.
methylation of MAP3K2 by SMYD3 increases MAP kinase signalling and promotes the formation of Ras-driven carcinomas
results strongly support a role for MEKK2 as a regulator of signaling that modulates breast tumor cell spread area and migration through control of focal adhesion stability
Data suggest that MEKK2 and MLK3 (show MAP3K11 Proteins) represent untargeted kinases in tumor biology for potential therapeutic development.
Hepatitis B virus X protein enhances the growth of hepatoma cells through upregulation of MEKK2.
FGF2 (show FGF2 Proteins)/MEKK2 pathway mediates an alternative nonclassical pathway for beta-catenin (show CTNNB1 Proteins) activation, and this pathway is a key regulator of bone formation by osteoblasts
Stk38 (show STK38 Proteins) protein kinase (show CDK7 Proteins) has a role in inhibiting TLR9 (show TLR9 Proteins)-activated inflammatory responses by promoting MEKK2 ubiquitination in macrophages
MEKK2 is regulated through a phosphorylation-dependent association with 14-3-3 (show YWHAQ Proteins), a group of adapters that modulate dimerization and association between proteins
MEKK2 signaling contributes to right ventricular hypertrophy and altered myocardial inflammatory gene expression in response to hypoxia-induced pulmonary hypertension.
MEKK2 alone can suppress T-cell TGF-beta (show TGFB1 Proteins) responses. MEKK2 or MEKK3 (show MAP3K3 Proteins) can cause ERK1/2 to phosphorylate SMAD2 (show SMAD2 Proteins)/3 and suppress R-SMAD (show SMAD1 Proteins)-dependent transcription. MEKK2 and MEKK3 (show MAP3K3 Proteins) play overlapping roles in regulating Th-cell differentiation via TGF-beta (show TGFB1 Proteins)
Data show that HDAC4 (show HDAC5 Proteins) binds and promotes the deacetylation and activation of a key MAP3 kinase, MEKK2.
Data from experiments with Mekk2(-/-) mice show that MEKK2 may be required for controlling the strength of T cell receptor/CD3 (show CD3E Proteins) signaling.
PB1 (show GPR97 Proteins) domain mediates the association of MEKK2 and MEKK3 (show MAP3K3 Proteins) with MEK5 (show MAP2K5 Proteins) and that the respective PB1 (show GPR97 Proteins) domains of these kinases are critical for regulation of the ERK5 (show MAPK7 Proteins) pathway.
Rap1 (show TERF2IP Proteins) and MEKK2 are critical upstream signaling molecules mediating BDNF (show BDNF Proteins) stimulation of ERK5 (show MAPK7 Proteins) in central nervous system neurons
The protein encoded by this gene is a member of serine/threonine protein kinase family. This kinase preferentially activates other kinases involved in the MAP kinase signaling pathway. This kinase has been shown to directly phosphorylate and activate Ikappa B kinases, and thus plays a role in NF-kappa B signaling pathway. This kinase has also been found to bind and activate protein kinase C-related kinase 2, which suggests its involvement in a regulated signaling process.
mitogen-activated protein kinase kinase kinase 2
, MAP/ERK kinase kinase 2
, MAPK/ERK kinase kinase 2
, MEK kinase 2
, MEKK 2
, mitogen activated protein kinase kinase kinase 2
, protein kinase MEKK2b