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All these suggest that the MAP3K M1P site is a potential interacting partner of MAP3K SH3 domain, which may mediate the intermolecular recognition between hPTTG1 and MAP3K.
Polymorphisms in MAP3K3, MMP24 (show MMP24 Proteins) and IGF1R (show IGF1R Proteins) are associated with greater height and act additively on height in children of an admixed population.
MAP3K3 overexpression is an independent poor prognostic indicator in ovarian carcinoma.
MAP3K3 may potentially not only serve as diagnostic/prognostic markers for patients with lung cancer but also provide an indicator for future investigations into immunomodulatory therapies for lung cancer.
studies identify gain of MEKK3 signallin (show KLF2 Proteins)g and KL (show KLF4 Proteins)F2/4 function as causal mechanisms for cerebral cavernous malformations pathogenesis that may be targeted to develop new CCM therapeutics
High MEKK3 expression is associated with renal clear cell carcinoma.
MEKK3 expression was significantly higher in patients with renal clear cell carcinoma than in controls.
This (show NBR1 Proteins) study identified an NBR1-MEKK3 complex as a key regulator of JNK s (show NBR1 Proteins)ignaling and adipose tissue inflam (show MAPK8 Proteins)mation in obesity.
Our finding that Verrucous venous malformation contains a MAP3K3 mutation supports our impression that this lesion is a venous anomaly.
MEKK3 expression was positively correlated with survivin (show BIRC5 Proteins).
MiR (show MLXIP Proteins)-188 regulated MAP3K3 expression in bone marrow cells.MAP3K3 is involved in miR (show MLXIP Proteins)-188-induced promotion of bone marrow cells senescence.
this study shows that TAK1 (show NR2C2 Proteins) negatively regulates lipopolysaccharide-induced cytokine secretion in myeloid cells by inhibiting MEKK3 activities
endothelial-specific loss of Mekk3, Klf2 (show KLF2 Proteins) or Klf4 (show KLF4 Proteins) markedly prevents cerebral cavernous malformation lesion formation, reverses the increase in Rho activity, and rescues lethality
CCM2 (show CCM2 Proteins):MEKK3-mediated regulation of Rho-ROCK signalling is required for maintenance of neurovascular integrity, a mechanism by which CCM2 (show CCM2 Proteins) loss leads to disease.
NBR1 (show NBR1 Proteins) is increased in adipose tissue macrophages in obese mice. The NBR1 (show NBR1 Proteins)-MEKK3 complex is important in JNK (show MAPK8 Proteins) activation in macrophages.
MEKK2 (show MAP3K2 Proteins) alone can suppress T-cell TGF-beta (show TGFB1 Proteins) responses. MEKK2 (show MAP3K2 Proteins) or MEKK3 can cause ERK1/2 to phosphorylate SMAD2 (show SMAD2 Proteins)/3 and suppress R-SMAD (show SMAD1 Proteins)-dependent transcription. MEKK2 (show MAP3K2 Proteins) and MEKK3 play overlapping roles in regulating Th-cell differentiation via TGF-beta (show TGFB1 Proteins)
Using Mekk3-deficient murine T cells, the authors concluded MEKK3 expression is required for mounting optimal T cell responses in vivo and is involved in mediating the TCR-dependent Rac1/2 signals for IFN-gamma (show IFNG Proteins) production through the MAPK (show MAPK1 Proteins) pathways.
The signaling defect of elevated interleukin (IL)-12 (show IL12A Proteins) overproducing cells in nonobese diabetic mice could be attributed to, at least partially, the overexpression of a single MAP3K, namely MEKK3.
Strikingly, chimeric mice transplanted with Mekk3(Deltaflox/-) BM exhibited a reduction in tumor growth and vessel density compared with mice transplanted with Mekk3(Deltaflox/+) BM cells.
PB1 (show GPR97 Proteins) domain mediates the association of MEKK2 (show MAP3K2 Proteins) and MEKK3 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.
This gene product is a 626-amino acid polypeptide that is 96.5% identical to mouse Mekk3. Its catalytic domain is closely related to those of several other kinases, including mouse Mekk2, tobacco NPK, and yeast Ste11. Northern blot analysis revealed a 4.6-kb transcript that appears to be ubiquitously expressed. This protein directly regulates the stress-activated protein kinase (SAPK) and extracellular signal-regulated protein kinase (ERK) pathways by activating SEK and MEK1/2 respectively\; it does not regulate the p38 pathway. In cotransfection assays, it enhanced transcription from a nuclear factor kappa-B (NFKB)-dependent reporter gene, consistent with a role in the SAPK pathway. Alternatively spliced transcript variants encoding distinct isoforms have been observed.
mitogen-activated protein kinase kinase kinase 3
, MAP/ERK kinase kinase 3
, MAPK/ERK kinase kinase 3
, MEK kinase 3
, MEKK 3
, mitogen activated protein kinase kinase kinase 3