Aperçu des produits pour anti-MAP2K2 (MAP2K2) Anticorps

Human Mitogen-Activated Protein Kinase Kinase 2 (MAP2K2) interaction partners

1. Here the authors identified a direct interaction of both MEK1 and MEK2 with AKT. The interaction between MEK and AKT affects cell migration and adhesion, but not proliferation. The specific mechanism of action of the MEK-AKT complex involves phosphorylation of the migration-related transcription factor FoxO1.

2. Data show that SAM and SH3 domain containing 1 protein (SASH1) binds with mitogen-activated protein kinase kinase 2 (MAP2K2), and SASH1 mutations promote binding between SASH1 and MAP2K2.

3. findings demonstrate the interaction of tRNA with MEK2 in pancreatic cancer cells and suggest that tRNA may impact MEK2 activity in cancer cells

4. Report a synthetic lethal interaction of cetuximab in combination with MEK1/2 inhibition for the NRAS mutant subgroup of metastatic colorectal cancer.

5. There are no other biomarkers correlated with treatment responses following MEK1/2 inhibition.

6. MEK2 was essential for the phosphorylation of MKK3/MKK6 and p38 MAPK that directly impacted on cyclin D1 expression.

7. High MEK2 expression is associated with inflammation.

8. there were significant decreases in intercellular adhesion molecules 1 (ICAM1), ezrin (EZR), mitogen-activated protein kinase kinase 2 (MAP2K2), and nitric oxide synthase 3 (NOS3) gene expressions in metabolic syndrome patients.

9. The patient showed a paternally inherited 16p13.11 microduplication and a de novo 19p13.3 microdeletion involving the mitogen-activated protein kinase kinase 2 gene (MAP2K2), in which mutations cause the cardio-facio-cutaneous (CFC) syndrome

10. Data show that mitogen-activated protein kinase kinases MEK1/2 inhibitor pimasertib (MEKI) sensitized the cells to apoptosis through its ability to promote a G1 cell cycle arrest.

11. the purpose of this paper was to investigate MAPK downstream signalling molecules in Natural killer cell phenotypes from Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients.

12. at clinically relevant concentrations, cDDP binds to and inhibits MEK1/2 and both the binding and inhibitory activity are related to its interaction with Cu bound to MEK1/2

13. Endocytosis separates EGF receptors from endogenous fluorescently labeled HRas and diminishes receptor signaling to MAP kinases in endosomes.

14. MEK1 levels are upregulated at transcriptional level whereas MEK2 levels are downregulated at posttranslational level.

15. MEK1/2 inhibitor trametinib showed similar PFS and a response rate as docetaxel in patients with previously treated KRAS-mutant-positive non-small cell lung carcinoma.

16. We report on a fourth familial case with transmission of CFC syndrome from father to son due to a novel heterozygous sequence change c.376A>G (p.N126D) in exon 3 of MEK2 gene.

17. MK2 attenuates dendritic cell-mediated Th1 differentiation and autoimmune encephalomyelitis.

18. We documented three novel mutations in the BRAF gene in cardio-facio-cutaneous syndrome patients and correlated clinical findings with causative mutations in the BRAF or MEK1/MEK2 genes

19. CCR7 can also promote survival of mDCs through a novel MEK1/2-ERK1/2-AMPK signaling axis.

20. Our cohort of seven individuals with MEK2 deletions has overlapping features associated with RASopathies.

Mouse (Murine) Mitogen-Activated Protein Kinase Kinase 2 (MAP2K2) interaction partners

1. data suggest that, although short-term suppression of Mek1/2 in ES cells helps to maintain an inner cell mass-like epigenetic state, prolonged suppression results in irreversible changes that compromise their developmental potential

2. Erk5 MAP kinase is activated in response to PDGF-BB in the smooth muscle cell line MOVAS in a manner dependent on Mekk2, Mek1/2, Mek5, PI3-kinase and protein kinase C (PKC).

3. fluid shear stress induces autocrine TGF-beta/ALK5-induced target gene expression in renal epithelial cells, which is partially restrained by MEK1/2-mediated signaling.

4. FGF2 is an extracellular inducer of COUP-TFII expression and may suppress the osteogenic potential of mesenchymal cells by inducing COUP-TFII expression prior to the onset of osteogenic differentiation

5. REDD1 is required for normal insulin-stimulated signaling, and a subtle balance exists between MEK1/2, REDD1, and mTOR

6. MEK1 and MEK2 can substitute for each other but a minimum amount of MEK is critical for placenta development and embryo survival

7. MK2/3 cascade plays a strategic role in controlling synaptic plasticity and cognition.

8. MK2 attenuates dendritic cell-mediated Th1 differentiation and autoimmune encephalomyelitis.

9. analysis of p38-MK2-activated Rsk signaling in toll-like receptor-stimulated dendritic cells

10. both MEK1 and MEK2 have crucial roles in the integration of mesenchymal and epithelial signals essential for the development of the entire respiratory tract

11. MK2 is responsible for resistance of p53-deficient tumors to cisplatin

12. MK2 plays a critical role in the development of apoptosis.

13. rapamycin treatment led to an increased MKP1 expression in BMDM from WT but failed to do so in BMDMs lacking the AKT1 isoform or MEK1 and MEK2.

14. review focuses on the role of the MEK1 and MEK2 kinases in the development of extraembryonic tissues and in the formation of the placenta

15. AT(2)R-mediated eNOS NO production and vasorelaxation through a MEK pathway are enhanced in aortas from db/db mice.

16. Crucial role of the ERK/MAPK cascade in the formation of extraembryonic structures.

17. Dox-induced up-regulation of IL-6 and GM-CSF was largely abolished after pretreatment of MTEC1 with MEK1/2 inhibitor U0126.

18. MEK1 AND MEK2 are critical for maintaining a functional population of adult Leydig cells and for fertility

19. Novel changes in NF-{kappa}B activity during progression and regression phases of hyperplasia: role of MEK1,2, ERK1,2, and p38

20. A critical role is indicated for p38 effector kinase MK2 in the regulation of tumor necrosis factor (TNF)-alpha messenger RNA (mRNA) translation through the TRIF signaling pathway.

Arabidopsis thaliana Mitogen-Activated Protein Kinase Kinase 2 (MAP2K2) interaction partners

1. the AtMKK2-AtMPK10 MAPK module regulates leaf venation complexity by altering polar auxin transport efficiency

2. Treatment of Arabidopsis with a membrane rigidifier, DMSO, causes MPK4 activation concomitantly with MEKK1 and MKK2 phosphorylation.

3. Ca(2+) signaling occurred upstream of the MEKK1-MKK2 pathway. MEKK1 was phosphorylated by calcium/calmodulin-regulated receptor-like kinase (CRLK1), which suggested that CRLK1 is one of candidates located upstream of MEKK1.

4. Data indicate that MEKK2 is required for the mekk1, mkk1 mkk2, and mpk4 autoimmune phenotypes.

5. Data suggest that the MEKK1-MKK1/MKK2-MPK4 kinase cascade negatively regulates MEKK2 and activation of MEKK2 triggers SUMM2-mediated immune responses.

6. Data indicate that MKK2 plays a role in abiotic stress tolerance and plant disease resistance.

7. double loss-of-function mutant (mkk1/2) of MKK1 and MKK2 is shown to have marked phenotypes in development and disease

8. Activation of MPK4 by flg22 is impaired in the mkk1 mkk2 double mutants, suggesting that MKK1 and MKK2 function together with MPK4 and MEKK1 in a MAP kinase cascade to negatively regulate innate immune responses in plants.