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抗Rat (Rattus) MAP3K3 抗体:
抗Human MAP3K3 抗体:
抗Mouse (Murine) MAP3K3 抗体:
MEKK3 KO reduced both EMT (显示 ITK 抗体) and cell migration, the size of 3D colonies and the percentage of CD44 (显示 CD44 抗体)(+)/CD24 (显示 CD24 抗体)(+)/EpCAM (显示 EPCAM 抗体)(+) CSC, promoter recruitment of YAP (显示 YAP1 抗体)/TAZ (显示 TAZ 抗体) and the expression of their target genes.
All these suggest that the MAP3K M1P site is a potential interacting partner of MAP3K SH3 domain (显示 ITSN1 抗体), which may mediate the intermolecular recognition between hPTTG1 and MAP3K.
Polymorphisms in MAP3K3, MMP24 (显示 MMP24 抗体) and IGF1R (显示 IGF1R 抗体) 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 抗体)g and KL (显示 KLF4 抗体)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 抗体) study identified an NBR1-MEKK3 complex as a key regulator of JNK s (显示 NBR1 抗体)ignaling and adipose tissue inflam (显示 MAPK8 抗体)mation in obesity.
Our finding that Verrucous venous malformation contains a MAP3K3 mutation supports our impression that this lesion is a venous anomaly.
MiR (显示 MLXIP 抗体)-188 regulated MAP3K3 expression in bone marrow cells.MAP3K3 is involved in miR (显示 MLXIP 抗体)-188-induced promotion of bone marrow cells senescence.
this study shows that TAK1 (显示 NR2C2 抗体) negatively regulates lipopolysaccharide-induced cytokine secretion in myeloid cells by inhibiting MEKK3 activities
endothelial-specific loss of Mekk3, Klf2 (显示 KLF2 抗体) or Klf4 (显示 KLF4 抗体) markedly prevents cerebral cavernous malformation lesion formation, reverses the increase in Rho activity, and rescues lethality
CCM2 (显示 CCM2 抗体):MEKK3-mediated regulation of Rho-ROCK signalling is required for maintenance of neurovascular integrity, a mechanism by which CCM2 (显示 CCM2 抗体) loss leads to disease.
NBR1 (显示 NBR1 抗体) is increased in adipose tissue macrophages in obese mice. The NBR1 (显示 NBR1 抗体)-MEKK3 complex is important in JNK (显示 MAPK8 抗体) activation in macrophages.
MEKK2 (显示 MAP3K2 抗体) alone can suppress T-cell TGF-beta (显示 TGFB1 抗体) responses. MEKK2 (显示 MAP3K2 抗体) or MEKK3 can cause ERK1/2 to phosphorylate SMAD2 (显示 SMAD2 抗体)/3 and suppress R-SMAD (显示 SMAD1 抗体)-dependent transcription. MEKK2 (显示 MAP3K2 抗体) and MEKK3 play overlapping roles in regulating Th-cell differentiation via TGF-beta (显示 TGFB1 抗体)
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 (显示 RAC1 抗体)/2 signals for IFN-gamma (显示 IFNG 抗体) production through the MAPK (显示 MAPK1 抗体) pathways.
The signaling defect of elevated interleukin (IL)-12 (显示 IL12A 抗体) 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 (显示 GPR97 抗体) domain mediates the association of MEKK2 (显示 MAP3K2 抗体) and MEKK3 with MEK5 (显示 MAP2K5 抗体) and that the respective PB1 (显示 GPR97 抗体) domains of these kinases are critical for regulation of the ERK5 (显示 MAPK7 抗体) 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