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All these suggest that the MAP3K M1P site is a potential interacting partner of MAP3K SH3 domain (Montrer ITSN1 Kits ELISA), which may mediate the intermolecular recognition between hPTTG1 and MAP3K.
Polymorphisms in MAP3K3, MMP24 (Montrer MMP24 Kits ELISA) and IGF1R (Montrer IGF1R Kits ELISA) 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 (Montrer KLF2 Kits ELISA)g and KL (Montrer KLF4 Kits ELISA)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 (Montrer NBR1 Kits ELISA) study identified an NBR1-MEKK3 complex as a key regulator of JNK s (Montrer NBR1 Kits ELISA)ignaling and adipose tissue inflam (Montrer MAPK8 Kits ELISA)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 (Montrer BIRC5 Kits ELISA).
MiR (Montrer MLXIP Kits ELISA)-188 regulated MAP3K3 expression in bone marrow cells.MAP3K3 is involved in miR (Montrer MLXIP Kits ELISA)-188-induced promotion of bone marrow cells senescence.
this study shows that TAK1 (Montrer NR2C2 Kits ELISA) negatively regulates lipopolysaccharide-induced cytokine secretion in myeloid cells by inhibiting MEKK3 activities
endothelial-specific loss of Mekk3, Klf2 (Montrer KLF2 Kits ELISA) or Klf4 (Montrer KLF4 Kits ELISA) markedly prevents cerebral cavernous malformation lesion formation, reverses the increase in Rho activity, and rescues lethality
CCM2 (Montrer CCM2 Kits ELISA):MEKK3-mediated regulation of Rho-ROCK signalling is required for maintenance of neurovascular integrity, a mechanism by which CCM2 (Montrer CCM2 Kits ELISA) loss leads to disease.
NBR1 (Montrer NBR1 Kits ELISA) is increased in adipose tissue macrophages in obese mice. The NBR1 (Montrer NBR1 Kits ELISA)-MEKK3 complex is important in JNK (Montrer MAPK8 Kits ELISA) activation in macrophages.
MEKK2 (Montrer MAP3K2 Kits ELISA) alone can suppress T-cell TGF-beta (Montrer TGFB1 Kits ELISA) responses. MEKK2 (Montrer MAP3K2 Kits ELISA) or MEKK3 can cause ERK1/2 (Montrer MAPK1/3 Kits ELISA) to phosphorylate SMAD2 (Montrer SMAD2 Kits ELISA)/3 and suppress R-SMAD (Montrer SMAD1 Kits ELISA)-dependent transcription. MEKK2 (Montrer MAP3K2 Kits ELISA) and MEKK3 play overlapping roles in regulating Th-cell differentiation via TGF-beta (Montrer TGFB1 Kits ELISA)
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 (Montrer IFNG Kits ELISA) production through the MAPK (Montrer MAPK1 Kits ELISA) pathways.
The signaling defect of elevated interleukin (IL)-12 (Montrer IL12A Kits ELISA) 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 (Montrer MAP3K2 Kits ELISA) and MEKK3 with MEK5 (Montrer MAP2K5 Kits ELISA) and that the respective PB1 domains of these kinases are critical for regulation of the ERK5 (Montrer MAPK7 Kits ELISA) 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