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In melorheostosis, all the identified MAP2K1 mutations affected a region of the MEK1 protein that normally suppresses its activity, thus, they caused MEK1 to become overactive.
FGF2 mediates mouse spermatogonial stem cell selfrenewal via upregulation of Etv5 and Bcl6b through MAP2K1 activation.
Fold Gene Description change elF2 signaling E1F1AX Eukaryotic translation initiation factor 1A, -1.343 X-Linked EIF2B3 Eukaryotic translation initiation factor 2B, -1.361 subunit 3 gamma, 58kDa EIF3B Eukaryotic translation initiation factor 3, -1.385 subunit B EIF4G1 Eukaryotic translation initiation factor 4 -1.306 gamma, 1 MAP2K1 Mitogen-activated protein kinase inase 1 1.306 PPP1R15A Protein phosphatase 1, regulatory subunit 15A 1.784 RPL7L1 Ribosomal protein L7-like 1 -1.283 RPL14 Ribosomal protein L14 -1.297 RPL36 Ribosomal protein L36 -1.424 RPL36A Ribosomal protein L36a -1.400 RPS2 Ribosomal protein S2 -1.376 RPS7 Ribosomal protein S7 -1.619 RPS15 Ribosomal protein S15 -1.641 Table 4 Molecular docking of CPT to P13K (PDB ID: 1E8Y) and eIF4A (PDB ID:2G9N).
The following sequences were used: shRNA Mek1 sequence Map2k1: 5'-GGCAGCTAATTGACTCTATGGCGAACCATAGAGTCAATTAGCTGCC-37, and scramble sequence: 5'-GGACTCGGGCCACCGGGTACGAATACCCGGTGGCCCGAGTCC-3'.
Meanwhile, MAPK signaling pathway molecules including MEKK1, ASK1 (MAP3K5), MLK2 (MAP3K10), MLK3, NIK, MEK1 (MAP2K1), MEK2 (MAP2K2), MEK4 (MAP2K4), MEK7 (MAP2K7), ERK1 (MAPK3), JNK1 (MAPK8) and JNK2 (MAPK9) were significantly up-regulated and revealed 2.00-4.09 fold increases in expression level (Table 1).
Among neural-derived cells, integrated mRNA-miRNA functional analyses of mature neurons (MNs), neural progenitor cells (NPCs), and neuroblastoma cells (NBCs) revealed that several very highly expressed genes (e.g., Robo1, Nrp1, Epha3, Unc5c, Dcc, Pak3, and Limk4) and a few underexpressed miRNAs (e.g., miR-152, miR-146b, and miR-339-5p) in MNs are associated with one important cellular process-axon guidance; some very highly expressed mitogenic pathway genes (e.g., Map2k1, Igf1r, Rara, and Runx1) and underexpressed miRNAs (e.g., miR-370, miR-9, and miR-672) in NBCs are associated with cancer pathways .
AKT1 CTNNB1 FGFR1 GNAS KRAS NRAS PIK3R5 STAT1 AKT2 EGFR FGFR2 HRAS MAP2K1 NTRK1 PKHD1 TEC AKT3 ERBB2 FGFR3 IDH1 MAP2K2 NTRK2 PRKCB1 TP53 (HER2) ALK ERCC6 FGFR4 IDH2 MAP2K7 NTRK3 RAF1 BRAF FBX4 FOXL2 IGF1R MET PDGFRA RET CDK4 FBXW7 GNA11 KDR MYC PIK3R1 SMO CSF1R FES GNAQ KIT NEK9 PIK3R4 SOS1
Seven genes only (FOS, CDKN2D, MAP2K1, MAPK7, MAPK13, PDK1, and SFN) were characterised by an increase in their expression, whereas the expression of other genes was reduced.
Targeted therapy with an inhibitor of mutated BRAF (vemurafenib) has been proved effective in Langerhans cell histiocytosis (LCH) harboring BRAF valine at position 600 (V600E) mutation.[sup] MAP2K1 mutations are mutually exclusive with BRAF mutations and might have implications for the use of BRAF targeted therapy.[sup] Here, we reported a case of PLCH proven by lung biopsy.
As well as the above genes and pathways, other molecular changes can bring about lung adenocarcinoma, such as mutations in ROS (10,11), ERCC1 (12), RB (13), AKT(14), PTEN (15), and MAP2K1 (16).
An in vivo study with cocoa-extracted polyphenols reported the suppression of TNF-[alpha]-induced VEGF expression (involved in RA) via the inhibition of phosphoinositide 3-kinase (PI3K) and MAPK kinase-1 (MAP2K1) activities.
MAP2K1 (MEK1) mutations define a distinct subset of lung adenocarcinoma associated with smoking.
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