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All these suggest that the MAP3K M1P site is a potential interacting partner of MAP3K SH3 domain (show ITSN1 ELISA Kits), which may mediate the intermolecular recognition between hPTTG1 and MAP3K.
Polymorphisms in MAP3K3, MMP24 (show MMP24 ELISA Kits) and IGF1R (show IGF1R ELISA Kits) 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 ELISA Kits)g and KL (show KLF4 ELISA Kits)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 ELISA Kits) study identified an NBR1-MEKK3 complex as a key regulator of JNK s (show NBR1 ELISA Kits)ignaling and adipose tissue inflam (show MAPK8 ELISA Kits)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 ELISA Kits).
MiR (show MLXIP ELISA Kits)-188 regulated MAP3K3 expression in bone marrow cells.MAP3K3 is involved in miR (show MLXIP ELISA Kits)-188-induced promotion of bone marrow cells senescence.
this study shows that TAK1 (show NR2C2 ELISA Kits) negatively regulates lipopolysaccharide-induced cytokine secretion in myeloid cells by inhibiting MEKK3 activities
endothelial-specific loss of Mekk3, Klf2 (show KLF2 ELISA Kits) or Klf4 (show KLF4 ELISA Kits) markedly prevents cerebral cavernous malformation lesion formation, reverses the increase in Rho activity, and rescues lethality
CCM2 (show CCM2 ELISA Kits):MEKK3-mediated regulation of Rho-ROCK signalling is required for maintenance of neurovascular integrity, a mechanism by which CCM2 (show CCM2 ELISA Kits) loss leads to disease.
NBR1 (show NBR1 ELISA Kits) is increased in adipose tissue macrophages in obese mice. The NBR1 (show NBR1 ELISA Kits)-MEKK3 complex is important in JNK (show MAPK8 ELISA Kits) activation in macrophages.
MEKK2 (show MAP3K2 ELISA Kits) alone can suppress T-cell TGF-beta (show TGFB1 ELISA Kits) responses. MEKK2 (show MAP3K2 ELISA Kits) or MEKK3 can cause ERK1/2 (show MAPK1/3 ELISA Kits) to phosphorylate SMAD2 (show SMAD2 ELISA Kits)/3 and suppress R-SMAD (show SMAD1 ELISA Kits)-dependent transcription. MEKK2 (show MAP3K2 ELISA Kits) and MEKK3 play overlapping roles in regulating Th-cell differentiation via TGF-beta (show TGFB1 ELISA Kits)
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 ELISA Kits) production through the MAPK (show MAPK1 ELISA Kits) pathways.
The signaling defect of elevated interleukin (IL)-12 (show IL12A ELISA Kits) 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 domain mediates the association of MEKK2 (show MAP3K2 ELISA Kits) and MEKK3 with MEK5 (show MAP2K5 ELISA Kits) and that the respective PB1 domains of these kinases are critical for regulation of the ERK5 (show MAPK7 ELISA Kits) 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