Aperçu des produits pour anti-MAP3K4 (MAP3K4) Anticorps

Human Mitogen-Activated Protein Kinase Kinase Kinase 4 (MAP3K4) interaction partners

1. IL-21 expression is promoted by MEKK4 in malignant T cells and is associated with progression risk in cutaneous T-cell lymphoma

2. Mutations in genes such as AKT2, CCNA1, MAP3K4, and TGFBR1, were associated significantly with Epstein-Barr-positive gastric tumors, compared with EBV-negative tumors.

3. Map3k4 haploinsufficiency is the cause of T-associated sex reversal.

4. MTK1 was identified in the HER2/HER3-HRG mediated extracellular acidification and cell migration pathway in breast cancer cells.

5. MAP3K4 is sufficiently mediate the TGFbeta-induced phosphorylation of p38 MAPK in MEFs and HaCaT cells.

6. 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.

7. For the first time we report a significant association between nicotine dependence and DRD5, NPY1R MAP3K4 single nucleotide polymorphism.

8. 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.

9. CIN85 binding to a C-terminal motif within hTTP leads to the increased phosphorylation of hTTP, possibly through enhanced association with MEKK4

10. Axin utilizes distinct regions for competitive MEKK1 and MEKK4 binding and JNK activation.

11. MEKK4 is the MAPK kinase kinase for TRAF4 regulation of the JNK pathway

12. Taken together, these results indicate a novel role for CIN85 in the regulation of cellular stress response via the MAPK pathways.

13. 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.

Mouse (Murine) Mitogen-Activated Protein Kinase Kinase Kinase 4 (MAP3K4) interaction partners

1. MAP3K4 activity controls epithelial-to-mesenchymal transition through the ubiquitination and degradation of HDAC6.

2. 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.

3. Map3k4 haploinsufficiency is the cause of T-associated sex reversal.

4. suggest a requirement for GADD45gamma in promoting MAP3K4-mediated activation of p38 MAPK signaling in embryonic gonadal somatic cells for testis determination

5. regulates epithelial-mesenchymal transition in trophoblast stem cells

6. MTK1 plays an important role in the regulation of cell death and is also involved in the pathogenesis of heart failure.

7. 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.

8. MEKK4 plays a critical role in regulating MKK4 activity and apoptotic cell death during neural tube development.

9. MEKK4 is the MAPK kinase kinase for TRAF4 regulation of the JNK pathway

10. 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.

11. MEKK4 regulates epithelial-to-mesenchymal transition in the endocardial cushions of the developing heart.

12. our results demonstrate a link between MEKK4 and filamin-a that impacts neuronal migration initiation

13. GSK3beta binding to MEKK4 blocks MEKK4 dimerization that is required for MEKK4 activation, effectively inhibiting MEKK4 stimulation of the JNK and p38 MAPK pathways

14. G alpha o mediates WNT-JNK signaling through dishevelled 1 and 3, RhoA family members, and MEKK 1 and 4 in mammalian cells

15. 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.

16. a role for the signalling pathway in mouse sex determination