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miR (zeige MLXIP Proteine)-34c-3p may regulate triple-negative breast cancer progression by directly targeting the 3'-untranslated region of mitogen-activated protein kinase kinase kinase 2 (MAP3K2).
Study found miR (zeige MLXIP Proteine)-186 expression significantly decreased in lung cancer tissues and cells and MAP3K2 expression increased in the same cancer tissues. Also, results confirmed that MAP3K2 is a target gene of miR (zeige MLXIP Proteine)-186 and both expression correlated with prognosis.
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 (zeige HBXIP Proteine) activated ERK1/2 through up-regulating MEKK2.
MEKK2 has a novel function as a regulator of ubiquitylation-dependent paxillin (zeige PXN Proteine) redistribution in breast tumour cells.
EBV microRNA BART (zeige BSND Proteine) 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 (zeige MAP2K5 Proteine)-ERK5 (zeige MAPK7 Proteine) 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
Erk5 MAP kinase is activated in response to PDGF-BB in the smooth muscle cell line MOVAS in a manner dependent on Mekk2, Mek1/2, Mek5, PI3-kinase and protein kinase C (PKC).
FGF2 (zeige FGF2 Proteine)/MEKK2 pathway mediates an alternative nonclassical pathway for beta-catenin (zeige CTNNB1 Proteine) activation, and this pathway is a key regulator of bone formation by osteoblasts
Stk38 (zeige STK38 Proteine) protein kinase (zeige CDK7 Proteine) has a role in inhibiting TLR9 (zeige TLR9 Proteine)-activated inflammatory responses by promoting MEKK2 ubiquitination in macrophages
MEKK2 is regulated through a phosphorylation-dependent association with 14-3-3 (zeige YWHAQ Proteine), 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 (zeige TGFB1 Proteine) responses. MEKK2 or MEKK3 (zeige MAP3K3 Proteine) can cause ERK1/2 to phosphorylate SMAD2 (zeige SMAD2 Proteine)/3 and suppress R-SMAD (zeige SMAD1 Proteine)-dependent transcription. MEKK2 and MEKK3 (zeige MAP3K3 Proteine) play overlapping roles in regulating Th-cell differentiation via TGF-beta (zeige TGFB1 Proteine)
Data show that HDAC4 (zeige HDAC5 Proteine) 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 (zeige CD3E Proteine) signaling.
PB1 (zeige GPR97 Proteine) domain mediates the association of MEKK2 and MEKK3 (zeige MAP3K3 Proteine) with MEK5 (zeige MAP2K5 Proteine) and that the respective PB1 (zeige GPR97 Proteine) domains of these kinases are critical for regulation of the ERK5 (zeige MAPK7 Proteine) pathway.
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