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抗Rat (Rattus) MAP3K4 抗体:
抗Human MAP3K4 抗体:
抗Mouse (Murine) MAP3K4 抗体:
IL-21 (显示 IL17C 抗体) 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 (显示 AKT2 抗体), CCNA1 (显示 CCNA1 抗体), MAP3K4, and TGFBR1 (显示 TGFBR1 抗体), 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 (显示 ERBB2 抗体)/HER3 (显示 ERBB3 抗体)-HRG (显示 NRG1 抗体) mediated extracellular acidification and cell migration pathway in breast cancer cells.
MAP3K4 is sufficiently mediate the TGFbeta (显示 TGFB1 抗体)-induced phosphorylation of p38 MAPK (显示 MAPK14 抗体) in MEFs and HaCaT cells.
we have identified a reduced IL-1A (显示 IL1A 抗体) response, related to a low MAP3K4 expression and high expression of its inhibitor GSK3beta (显示 GSK3b 抗体), identifying a novel key player in Crohn's disease.
For the first time we report a significant association between nicotine dependence and DRD5 (显示 DRD5 抗体), NPY1R (显示 NPY1R 抗体) MAP3K4 single nucleotide polymorphism.
The upstream molecule of the TRAIL-induced MAPK (显示 MAPK1 抗体) activation is MEKK (显示 MAP3K1 抗体), as opposed to ASK1 (显示 MAP3K5 抗体), via the mediation of its signal through JNK (显示 MAPK8 抗体)/p38 (显示 CRK 抗体) in a caspase-8 (显示 CASP8 抗体)-dependent manner.
CIN85 (显示 SH3KBP1 抗体) binding to a C-terminal motif within hTTP leads to the increased phosphorylation of hTTP, possibly through enhanced association with MEKK4
Axin (显示 AXIN1 抗体) utilizes distinct regions for competitive MEKK1 (显示 MAP3K1 抗体) and MEKK4 binding and JNK (显示 MAPK8 抗体) activation.
MAP3K4 activity controls epithelial-to-mesenchymal transition through the ubiquitination and degradation of HDAC6 (显示 HDAC6 抗体).
by forming a complex with MEKK4 in skeletal muscle fibers, Gadd45a (显示 GADD45A 抗体) increases MEKK4 protein kinase (显示 CDK7 抗体) activity, which is both sufficient to induce skeletal muscle fiber atrophy and required for Gadd45a (显示 GADD45A 抗体)-mediated skeletal muscle fiber atrophy.
suggest a requirement for GADD45gamma (显示 GADD45G 抗体) in promoting MAP3K4-mediated activation of p38 MAPK (显示 MAPK14 抗体) signaling in embryonic gonadal somatic cells for testis determination
MTK1 plays an important role in the regulation of cell death and is also involved in the pathogenesis of heart failure.
During Th1 (显示 HAND1 抗体) differentiation, the GADD45beta (显示 GADD45B 抗体)/GADD45gamma (显示 GADD45G 抗体)/MEKK4 pathway integrates upstream signals transduced by both T cell receptor and IL12 (显示 IL12A 抗体)/STAT4 (显示 STAT4 抗体), leading to augmented interferon-gamma (显示 IFNG 抗体) production in a process independent of STAT4 (显示 STAT4 抗体).
MEKK4 plays a critical role in regulating MKK4 (显示 MAP2K4 抗体) activity and apoptotic cell death during neural tube development.
MEKK4 is the MAPK (显示 MAPK1 抗体) kinase kinase for TRAF4 (显示 TRAF4 抗体) regulation of the JNK (显示 MAPK8 抗体) pathway
Hindbrains of exencephalic MEKK4(K1361R) embryos show a striking increase in neuroepithelial cell apoptosis and a dramatic loss of phosphorylation of MKK3 (显示 MAP2K3 抗体) and -6, mitogen-activated protein kinase (显示 MAPK1 抗体) kinases (MKKs (显示 MKKS 抗体)) regulated by MEKK4 in the p38 (显示 CRK 抗体) pathway.
MEKK4 regulates epithelial-to-mesenchymal transition in the endocardial cushions of the developing heart.
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