Browse our anti-MAP2K2 (MAP2K2) Antibodies

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

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

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

3. Report a synthetic lethal interaction of cetuximab in combination with MEK1 (show MAP2K1 Antibodies)/2 inhibition for the NRAS (show NRAS Antibodies) mutant subgroup of metastatic colorectal cancer.

4. There are no other biomarkers correlated with treatment responses following MEK1 (show MAP2K1 Antibodies)/2 inhibition.

5. MEK2 was essential for the phosphorylation of MKK3 (show MAP2K3 Antibodies)/MKK6 (show MAP2K6 Antibodies) and p38 MAPK (show MAPK14 Antibodies) that directly impacted on cyclin D1 (show CCND1 Antibodies) expression.

6. High MEK2 expression is associated with inflammation.

7. there were significant decreases in intercellular adhesion molecules 1 (ICAM1 (show ICAM1 Antibodies)), ezrin (EZR (show EZR Antibodies)), mitogen-activated protein kinase kinase 2 (MAP2K2), and nitric oxide synthase (show NOS Antibodies) 3 (NOS3 (show NANOS3 Antibodies)) gene expressions in metabolic syndrome patients.

8. 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 (show PTPN11 Antibodies)) syndrome

9. Data show that mitogen-activated protein kinase (show MAPK1 Antibodies) kinases MEK1 (show MAP2K1 Antibodies)/2 inhibitor pimasertib (MEKI) sensitized the cells to apoptosis through its ability to promote a G1 cell cycle arrest.

10. the purpose of this paper was to investigate MAPK (show MAPK1 Antibodies) downstream signalling molecules in Natural killer cell phenotypes from Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients.

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

1. data suggest that, although short-term suppression of Mek1 (show MAP2K1 Antibodies)/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 (show TGFB1 Antibodies)/ALK5 (show TGFBR1 Antibodies)-induced target gene expression in renal epithelial cells, which is partially restrained by MEK1 (show MAP2K1 Antibodies)/2-mediated signaling.

4. FGF2 (show FGF2 Antibodies) is an extracellular inducer of COUP-TFII (show NR2F2 Antibodies) expression and may suppress the osteogenic potential of mesenchymal cells by inducing COUP-TFII (show NR2F2 Antibodies) expression prior to the onset of osteogenic differentiation

5. REDD1 (show DDIT4 Antibodies) is required for normal insulin (show INS Antibodies)-stimulated signaling, and a subtle balance exists between MEK1 (show MAP2K1 Antibodies)/2, REDD1 (show DDIT4 Antibodies), and mTOR (show FRAP1 Antibodies)

6. MEK1 (show MAP2K1 Antibodies) and MEK2 can substitute for each other but a minimum amount of MEK (show MDK Antibodies) is critical for placenta development and embryo survival

7. MK2 (show KCNA2 Antibodies)/3 cascade plays a strategic role in controlling synaptic plasticity and cognition.

8. MK2 (show KCNA2 Antibodies) attenuates dendritic cell-mediated Th1 (show HAND1 Antibodies) differentiation and autoimmune encephalomyelitis.

9. analysis of p38 (show CRK Antibodies)-MK2 (show KCNA2 Antibodies)-activated Rsk (show RPS6KA1 Antibodies) signaling in toll (show TLR4 Antibodies)-like receptor-stimulated dendritic cells

10. both MEK1 (show MAP2K1 Antibodies) and MEK2 have crucial roles in the integration of mesenchymal and epithelial signals essential for the development of the entire respiratory tract

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

1. the AtMKK2-AtMPK10 (show MAPK10 Antibodies) MAPK (show MAPK1 Antibodies) module regulates leaf venation complexity by altering polar auxin transport efficiency

2. Treatment of Arabidopsis with a membrane rigidifier, DMSO, causes MPK4 (show MAPK4 Antibodies) activation concomitantly with MEKK1 (show MAP3K1 Antibodies) and MKK2 phosphorylation.

3. Ca(2 (show CA2 Antibodies)+) signaling occurred upstream of the MEKK1 (show MAP3K1 Antibodies)-MKK2 pathway. MEKK1 (show MAP3K1 Antibodies) was phosphorylated by calcium/calmodulin-regulated receptor-like kinase (CRLK1), which suggested that CRLK1 is one of candidates located upstream of MEKK1 (show MAP3K1 Antibodies).

4. Data indicate that MEKK2 (show MAP3K2 Antibodies) is required for the mekk1 (show MAP3K1 Antibodies), mkk1 (show MAP2K1 Antibodies) mkk2, and mpk4 (show MAPK4 Antibodies) autoimmune phenotypes.

5. Data suggest that the MEKK1 (show MAP3K1 Antibodies)-MKK1 (show MAP2K1 Antibodies)/MKK2-MPK4 (show MAPK4 Antibodies) kinase cascade negatively regulates MEKK2 (show MAP3K2 Antibodies) and activation of MEKK2 (show MAP3K2 Antibodies) 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 (show MAP2K1 Antibodies)/2) of MKK1 (show MAP2K1 Antibodies) and MKK2 is shown to have marked phenotypes in development and disease

8. Activation of MPK4 (show MAPK4 Antibodies) by flg22 is impaired in the mkk1 (show MAP2K1 Antibodies) mkk2 double mutants, suggesting that MKK1 (show MAP2K1 Antibodies) and MKK2 function together with MPK4 (show MAPK4 Antibodies) and MEKK1 (show MAP3K1 Antibodies) in a MAP kinase (show MAPK1 Antibodies) cascade to negatively regulate innate immune responses in plants.