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抗Rat (Rattus) MAP3K4 抗体:
抗Human MAP3K4 抗体:
抗Mouse (Murine) MAP3K4 抗体:
IL-21 expression is promoted by MEKK4 in malignant T cells and is associated with progression risk in cutaneous T-cell lymphoma
Mutations in genes such as AKT2, CCNA1, MAP3K4, and TGFBR1, were associated significantly with Epstein-Barr-positive gastric tumors, compared with EBV-negative tumors.
Map3k4 haploinsufficiency is the cause of T-associated sex reversal.
MTK1 was identified in the HER2/HER3-HRG mediated extracellular acidification and cell migration pathway in breast cancer cells.
MAP3K4 is sufficiently mediate the TGFbeta-induced phosphorylation of p38 MAPK in MEFs and HaCaT cells.
we have identified a reduced IL-1A response, related to a low MAP3K4 expression and high expression of its inhibitor GSK3beta, identifying a novel key player in Crohn's disease.
For the first time we report a significant association between nicotine dependence and DRD5, NPY1R MAP3K4 single nucleotide polymorphism.
The upstream molecule of the TRAIL-induced MAPK activation is MEKK, as opposed to ASK1, via the mediation of its signal through JNK/p38 in a caspase-8-dependent manner.
CIN85 binding to a C-terminal motif within hTTP leads to the increased phosphorylation of hTTP, possibly through enhanced association with MEKK4
Axin utilizes distinct regions for competitive MEKK1 and MEKK4 binding and JNK activation.
MEKK4 is the MAPK kinase kinase for TRAF4 regulation of the JNK pathway
Taken together, these results indicate a novel role for CIN85 in the regulation of cellular stress response via the MAPK pathways.
In this review, the role of MKK4 in cancer development appears complex, as some studies support a pro-oncogenic role for MKK4, while others suggest it may have tumor suppressor functions.
MAP3K4 activity controls epithelial-to-mesenchymal transition through the ubiquitination and degradation of HDAC6.
by forming a complex with MEKK4 in skeletal muscle fibers, Gadd45a increases MEKK4 protein kinase activity, which is both sufficient to induce skeletal muscle fiber atrophy and required for Gadd45a-mediated skeletal muscle fiber atrophy.
suggest a requirement for GADD45gamma in promoting MAP3K4-mediated activation of p38 MAPK signaling in embryonic gonadal somatic cells for testis determination
regulates epithelial-mesenchymal transition in trophoblast stem cells
MTK1 plays an important role in the regulation of cell death and is also involved in the pathogenesis of heart failure.
During Th1 differentiation, the GADD45beta/GADD45gamma/MEKK4 pathway integrates upstream signals transduced by both T cell receptor and IL12/STAT4, leading to augmented interferon-gamma production in a process independent of STAT4.
MEKK4 plays a critical role in regulating MKK4 activity and apoptotic cell death during neural tube development.
Hindbrains of exencephalic MEKK4(K1361R) embryos show a striking increase in neuroepithelial cell apoptosis and a dramatic loss of phosphorylation of MKK3 and -6, mitogen-activated protein kinase kinases (MKKs) regulated by MEKK4 in the p38 pathway.
MEKK4 regulates epithelial-to-mesenchymal transition in the endocardial cushions of the developing heart.
our results demonstrate a link between MEKK4 and filamin-a that impacts neuronal migration initiation
GSK3beta binding to MEKK4 blocks MEKK4 dimerization that is required for MEKK4 activation, effectively inhibiting MEKK4 stimulation of the JNK and p38 MAPK pathways
G alpha o mediates WNT-JNK signaling through dishevelled 1 and 3, RhoA family members, and MEKK 1 and 4 in mammalian cells
Results define MEKK4 as a signaling hub for FGF4 activation of JNK that is required for maintenance of trophoblast stem cells in an undifferentiated state.
a role for the signalling pathway in mouse sex determination
The central core of each mitogen-activated protein kinase (MAPK) pathway is a conserved cascade of 3 protein kinases: an activated MAPK kinase kinase (MAPKKK) phosphorylates and activates a specific MAPK kinase (MAPKK), which then activates a specific MAPK. While the ERK MAPKs are activated by mitogenic stimulation, the CSBP2 and JNK MAPKs are activated by environmental stresses such as osmotic shock, UV irradiation, wound stress, and inflammatory factors. This gene encodes a MAPKKK, the MEKK4 protein, also called MTK1. This protein contains a protein kinase catalytic domain at the C terminus. The N-terminal nonkinase domain may contain a regulatory domain. Expression of MEKK4 in mammalian cells activated the CSBP2 and JNK MAPK pathways, but not the ERK pathway. In vitro kinase studies indicated that recombinant MEKK4 can specifically phosphorylate and activate PRKMK6 and SERK1, MAPKKs that activate CSBP2 and JNK, respectively but cannot phosphorylate PRKMK1, an MAPKK that activates ERKs. MEKK4 is a major mediator of environmental stresses that activate the CSBP2 MAPK pathway, and a minor mediator of the JNK pathway. Two alternatively spliced transcripts encoding distinct isoforms have been described.
mitogen-activated protein kinase kinase kinase 4
, MAP three kinase 1
, MAP/ERK kinase kinase 4
, MAPK/ERK kinase kinase 4
, MEK kinase 4
, MEKK 4
, SSK2/SSK22 MAP kinase kinase kinase, yeast, homolog of
, dJ473J16.1 (mitogen-activated protein kinase kinase kinase 4)
, predicted protein of HQ0412
, T-associated sex reversal
, mitogen activated protein kinase kinase kinase 4