MAP2K1

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MAP2K1

A gene on chromosome 15q22.1-q22.33 that encodes a dual-specificity protein kinase which is an essential component of the MAP-kinase signal transduction pathway. MAP2K1 binds to extracellular ligands (e.g., as growth factors, cytokines and hormones) to their cell surface
receptors, activating RAS and RAF1, which in turn activates dual-specificity protein kinases MAP2K1/MEK1 and MAP2K2/MEK2; these act in the MAPK/ERK cascade and catalyse the phosphorylation of threonine and tyrosine residues, leading to the activation of the extracellular signal-regulated kinases MAPK3/ERK1 and MAPK1/ERK2,  and amplification of the transduction signal within the MAPK/ERK cascade.
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Moreover, the signal-transducing mechanisms of LPS-induced regulation of SP-A expression arise through TLR4-dependent cascade phosphorylations of MEK1, ERK1/2, and p38MAPK, leading to the nuclear translocation and activation of NF-?
Hydrogen peroxide activates extracellular signal regulated kinase via protein kinase C, Raf-1, and MEK1.
low] HBECs were treated with a P13K inhibitor (wortman-nin), an Akt inhibitor, or an MEK1 inhibitor (U0126) chat blocks Erkl/2 activation.
As the effects of Nc-5-s on LPS-induced cytokine secretion by THP-1 monocytes may in part be mediated through activation of the ERK1 /2 kinase, we investigated whether a known MEK1 /2 inhibitor, U0126, affected LPS-induced cytokine secretion by THP-1 cells in the same way as Nc-5-s.
Experiments with transfected cells that expressed constitutively activated MAPK kinase MEK1 and a specific inhibitor of p38 have shown that inactivation of ERKs and activation of p38 might be associated with the induction of apoptosis by arsenic trioxide (Iwama et al.
Arsenic trioxide (ATO) and MEK1 inhibition synergize to induce apoptosis in acute promyelocytic leukemia cells.
Adenocarcinoma-associated mutations (EGFR, KRAS, BRAF, MAP2K1/ MEK1, neuroblastoma RAS viral [v-ras] oncogene homolog [NRAS], and ERBB2/HER2, as well as ALK) or SCCassociated mutations (phosphoinositide 3 kinase [PI3K and AKT1) may be found in LCC, and tend to segregate with an IHC profile associated with the corresponding tumor subtype.
6A), the same effect as the p38 MAPK inhibitor SB203580, the MEK1 /2 inhibitor PD098059 and the JNK inhibitor SP600125 (Fig.
These genes include protein kinases (AKT, MEK1, PIM3), growth factors (VEGF, PLGF), GTPases (RHOC, RAB11A, DEXRAS1), cytokine signaling proteins (MCP1, SOCS1, SOCS3, WSB1, IL17R), and a Wnt signaling factor (WNT4).
The protein expression levels of elements of different cascades related to cell cycle progression, like Akt/PKB, MEK1 /2, and ERK1 /2 were found to be changed as depicted in Fig.