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anti-Rat (Rattus) MAP3K2 Antibodies:
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Human Monoclonal MAP3K2 Primary Antibody for ICC, ELISA - ABIN969272
Kurada, Li, Mulherkar, Subramanian, Prasad, Prabhakar: MADD, a splice variant of IG20, is indispensable for MAPK activation and protection against apoptosis upon tumor necrosis factor-alpha treatment. in The Journal of biological chemistry 2009
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Human Polyclonal MAP3K2 Primary Antibody for WB - ABIN3043184
Li, Zhang, Zhou, Li, Liu, Wang, Bai, Zhao, Shi, Zhang, Ye: The oncoprotein HBXIP enhances migration of breast cancer cells through increasing filopodia formation involving MEKK2/ERK1/2/Capn4 signaling. in Cancer letters 2014
Compound 1s displayed activity in cell-based assays in which it inhibited ERK5 pathway activation in cells and inhibited cell migration in a scratch assay. Thus, we have identified a scaffold that has promising potential to be developed into a highly selective and potent inhibitor of MEKK2. Information from these SAR studies provides specific guidance for the future design of MEKK2 inhibitor probes.
miR-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-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-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 activated ERK1/2 through up-regulating MEKK2.
MEKK2 has a novel function as a regulator of ubiquitylation-dependent paxillin redistribution in breast tumour cells.
EBV microRNA BART 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-ERK5 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 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.
Calcium regulation of EGF-induced ERK5 activation is mediated through interaction of MEKK2 with the adaptor protein Lad1.
MEKK2 is a potent activator of the c-Jun N-terminal kinase pathway in fibroblast-like synoviocytes in rheumatoid arthritis.
Unlike ERK5 and MEK5, their upstream activator MEKK2 is localized mainly in the cytosol of resting cells, and translocates into the nucleus upon EGF stimulation
MEKK2 is dimerized and activated by the novel protein Mip1.
Through interaction with MEKK2, XIAP functions in an ubiquitin ligase dependent manner to evoke a second wave of NF-kappaB activation, resulting in the modulation of NF-kappaB target gene expression.
Loss of MADD expression resulted in reduced Grb2 and Sos1/2 recruitment to the TNFR1 complex and decreased Ras and MEKK1/2 activation
The ability of MEKK2 to discriminate tumor from normal cells was orthogonally confirmed.
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/MEKK2 pathway mediates an alternative nonclassical pathway for beta-catenin activation, and this pathway is a key regulator of bone formation by osteoblasts
Stk38 protein kinase has a role in inhibiting TLR9-activated inflammatory responses by promoting MEKK2 ubiquitination in macrophages
MEKK2 is regulated through a phosphorylation-dependent association with 14-3-3, 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 responses. MEKK2 or MEKK3 can cause ERK1/2 to phosphorylate SMAD2/3 and suppress R-SMAD-dependent transcription. MEKK2 and MEKK3 play overlapping roles in regulating Th-cell differentiation via TGF-beta
Data show that HDAC4 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 signaling.
PB1 domain mediates the association of MEKK2 and MEKK3 with MEK5 and that the respective PB1 domains of these kinases are critical for regulation of the ERK5 pathway.
Rap1 and MEKK2 are critical upstream signaling molecules mediating BDNF stimulation of ERK5 in central nervous system neurons
A noncanonical function of Map3k2 domain is described for coordinated erk5 kinase and map2k7 signaling.
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