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