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FOXF1 (Montrer FOXF1 Kits ELISA) promotes prostate tumor growth and progression by activating ERK5 signaling
Erk5 MAP kinase (Montrer MAPK1 Kits ELISA) is activated in response to PDGF (Montrer PDGFA Kits ELISA)-BB in the smooth muscle cell line MOVAS in a manner dependent on Mekk2 (Montrer MAP3K2 Kits ELISA), Mek1 (Montrer MAP2K1 Kits ELISA)/2, Mek5 (Montrer MAP2K5 Kits ELISA), PI3-kinase (Montrer PIK3CA Kits ELISA) and protein kinase C (PKC (Montrer PKC Kits ELISA)).
Using compound selectivity engineering and CRISPR/Cas9 genome editing, distinct functions for Erk5 and Brd4 (Montrer BRD4 Kits ELISA) in pluripotency regulation of mouse embryonic stem cells have been revealed.
These results suggest that YAP (Montrer YAP1 Kits ELISA) promotes muscle differentiation by activating the Abl (Montrer ABL1 Kits ELISA)/Src (Montrer SRC Kits ELISA)/MEKK3 (Montrer MAP3K3 Kits ELISA)/MEK5 (Montrer MAP2K5 Kits ELISA)/ERK5 kinase cascade.
our results offer a preclinical proof of concept for ERK5 as a target to enhance T-cell infiltrates in prostate cancer
This study indicated that MAN can protect osteoblast against oxidative damage by modulation of ERK5/Nrf2 (Montrer NFE2L2 Kits ELISA) signaling, which can be new agent for osteoporosis.
These findings suggest that atherogenic conditions critically regulate platelet CD36 (Montrer CD36 Kits ELISA) signaling by increasing superoxide radical anion and hydrogen peroxide through a mechanism that promotes activation of MAPK (Montrer MAPK1 Kits ELISA) ERK5.
Fluid shear stress acts on the Galphaq (Montrer GNAQ Kits ELISA)-ERK5 signaling pathway to upregulate Cyclin B1 (Montrer CCNB1 Kits ELISA) and CDK1 (Montrer CDK1 Kits ELISA) expression, thereby resulting in MC3T3-E1 cell proliferation.
Finally, we demonstrated that miR (Montrer MLXIP Kits ELISA)-24 plays the modulational role by directly repressing MAPK7, a key number in the MAPK (Montrer MAPK1 Kits ELISA) signaling pathway. These data indicate that miR (Montrer MLXIP Kits ELISA)-24 is a novel positive regulator of adipocyte differentiation by targeting MAPK7, which provides new insights into the molecular mechanism of miRNA-mediated cellular differentiation.
the activation of ERK5-AKT (Montrer AKT1 Kits ELISA)-FoxO3a (Montrer FOXO3 Kits ELISA) signaling pathways by fluid shear stress resulted in a decreased expression of FasL (Montrer FASL Kits ELISA) and Bim (Montrer BCL2L11 Kits ELISA) and an inhibition of caspase-3 (Montrer CASP3 Kits ELISA) activation, which exerts a protective effect that prevents osteoblasts from apoptosis.
CCh induced TGF-beta1 (Montrer TGFB1 Kits ELISA) self-sustaining signaling loops by potentiating ERK5 signaling and promoted myofibroblast activity. This autocrine signaling mechanism may be an attractive therapeutic target to block the fibrotic response, which was modulated by the combination of glycopyrronium and indacaterol.
In the current study, five structures of the ERK5 kinase domain co-crystallized with ERK5 inhibitors are reported. Interestingly, three of the compounds bind at a novel allosteric binding site in ERK5, while the other two bind at the typical ATP-binding site.
Our results indicate that overexpression of MAPK7 in human OS cells could promote cell proliferation, migration and invasion, whereas knockdown of MAPK7 expression had the opposite effect. All the results suggest that MAPK7 may serve as a potent target for drug development.
Statin mediated ERK5 activation and the resulting decrease in cardiac endothelial cell permeability may contribute to the cardioprotective effects of statins in reducing doxorubicin-induced cardiotoxicity.
expression of miR (Montrer MLXIP Kits ELISA)-143 in osteosarcoma cells inhibited cell proliferation and migration/invasion. Bioinformatics and luciferase reporter assays confirmed that MAPK7 was targets gene of miR (Montrer MLXIP Kits ELISA)-143.
miR (Montrer MLXIP Kits ELISA)-143 down-regulated its target ERK5, leading to the suppression of epithelial-mesenchymal transition induced by GSK-3beta (Montrer GSK3b Kits ELISA)/Snail (Montrer SNAI1 Kits ELISA) signaling of breast cancer.
this study revealed the functional and mechanistic links between CDK5 (Montrer CDK5 Kits ELISA) and the oncogenic ERK5-AP-1 (Montrer FOSB Kits ELISA) signaling pathway in the pathogenesis of colorectal cancer.
Present study revealed the positive role of ERK5/AP-1 (Montrer FOSB Kits ELISA) in benzidine-provoked urocystic epithelial-mesenchymal transition and the curcumin promising use in bladder cancer prevention and intervention via ERK5/AP-1 (Montrer FOSB Kits ELISA) pathway.
Data showed that expression of the MKK7 (Montrer MAP2K7 Kits ELISA) gene in wild-type plants is induced by pathogen infection. Reducing mRNA levels of MKK7 (Montrer MAP2K7 Kits ELISA) by antisense RNA expression not only compromises basal resistance, but also blocks the induction of SAR (Montrer SRL Kits ELISA).
The protein encoded by this gene is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals, and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation and development. This kinase is specifically activated by mitogen-activated protein kinase kinase 5 (MAP2K5/MEK5). It is involved in the downstream signaling processes of various receptor molecules including receptor type kinases, and G protein-coupled receptors. In response to extracelluar signals, this kinase translocates to cell nucleus, where it regulates gene expression by phosphorylating, and activating different transcription factors. Four alternatively spliced transcript variants of this gene encoding two distinct isoforms have been reported.
, MAP kinase 4
, MAPK 4
, extracellular signal-regulated kinase 4
, mitogen activated protein kinase 4
, MAP kinase isoform p63
, BMK1 kinase
, MAP kinase 7
, MAPK 7
, big MAP kinase 1
, extracellular signal-regulated kinase 5
, extracellular-signal-regulated kinase 5
, extracellular signal regulated kinase 5
, mitogen activated protein kinase 7
, mitogen-activated kinase 7
, Big MAP kinase 1
, Extracellular signal-regulated kinase 5