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These data highlight that MAPK7 represents a promising target for combination treatment with MEK inhibition in KRAS mutant Non Small Cell Lung Carcinoma.
The study provide evidence that nitrogen-containing bisphosphonates activate the MEK5/ERK5 cascade and reveal an essential role of ERK5 in osteogenic differentiation and mineralization of skeletal precursors.
MAPK7 is a target gene of miR-143a-3p in 3T3-L1 cells.
Data show that ERK5 is consistently expressed and active in human melanoma tissues. Inhibition of ERK5 pathway drastically reduce the growth of melanoma cells and xenografts harboring wild-type (wt) or mutated BRAF. These data support a key role of the ERK5 pathway for melanoma growth in vitro and in vivo.
Regulation of atypical MAP kinases ERK3 and ERK4 by the phosphatase DUSP2 has been reported.
that Capn4 promotes cell proliferation by increasing MAPK7 expression
ERK5 is highly expressed in human tumor-associated macrophages.ERK5 plays a role in the tumor-associated macrophage polarization via STAT3.
The reduction of MAPK7 pathway activity and the loss of MAPK7 gene expression induce damaged osteogenesis via RPS6KA3 and/or its substrates.
Findings revealed that ERK5-mediated EMT was critically involved in benzidine-correlated BC progression.
MiR-143-3p inhibits the proliferation, cell migration and invasion of human breast cancer cells by modulating the expression of MAPK7
High ERK5 expression is associated with malignant pleural mesothelioma.
Small interfering RNA knockdown of MAPK7 demonstrated that MAPK7 regulates a subset of WNK1-regulated genes and controls the migration and cell proliferation
The data suggest that miR-143 might represent a novel genetic element to enhance production of difficult-to-express proteins in CHO cells which may be partly mediated by down-regulation of MAPK7.
our findings suggest that rare coding variants in MAPK7 predispose to AIS, providing clues to understanding the mechanisms of AIS.
ERK5 associates with CKII to play essential roles in GPIb-IX-mediated platelet activation via the PTEN/PI3K/Akt pathway.
For gain and loss of function studies, constitutively active MEK5 (CA-MEK5) and ERK5 shRNA lentiviruses were used to activate or knock down extracellular signal-regulated kinase 5 (ERK5). Our results confirmed that low concentrations of H2O2 promoted HUVECs angiogenesis in vitro, and ERK5 is an essential mediator of this process. Therefore, ERK5 may be a potential therapeutic target for promoting angiogenesis
ERK5 expression was increased in 58% of cases and associated with the presence of metastasis and more advanced stages in clear cell renal cell carcinoma patients. ERK5 may be a new prognostic marker in this type of tumor.
FOXF1 promotes prostate tumor growth and progression by activating ERK5 signaling
CCh induced TGF-beta1 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.
These findings highlight the importance of the Mek5-Erk5-Smurf-Smad-Sox9 axis in mammalian skeletogenesis.
ERK5 provides a common bypass route in intestinal epithelial cells, which rescues cell proliferation upon abrogation of ERK1/2 signalling, with therapeutic implications in colorectal cancer.
the data revealed that puerarin inhibited the monocyte adhesion in vitro and in vivo and thus reduced atherosclerotic lesions in apoE-/- mice; the protective effects were mediated by activation of ERK5/KLF2 signaling pathway.
Extracellular-signal-regulated kinase 5 plays an essential role in the gestational augmentation of beta-cell proliferation.
This study was undertaken to explore the mechanism whereby ERK5 inhibition instigates pancreatic beta-cell apoptosis via an endoplasmic reticulum stress-dependent signaling pathway.
the present study demonstrated that ERK5 positively regulates TS-induced urocystic EMT in vivo. These findings indicate the important role of ERK5 in TS-associated carcinogenesis and provide a potential strategy for the search of a novel interventional target in TS-associated bladder tumorigenesis.
These findings define an antagonistic function of ATM and MAPK7 in the thymocyte response to DNA damage, and suggest that the lack of MAPK7 inhibits thymic lymphoma growth in Atm-/- mice by partially restoring the DNA damage response in thymocytes.
Erk5 role in the cardiac mitochondria and the Pgc-1alpha regulation
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).
Using compound selectivity engineering and CRISPR/Cas9 genome editing, distinct functions for Erk5 and Brd4 in pluripotency regulation of mouse embryonic stem cells have been revealed.
These results suggest that YAP promotes muscle differentiation by activating the Abl/Src/MEKK3/MEK5/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 signaling, which can be new agent for osteoporosis.
These findings suggest that atherogenic conditions critically regulate platelet CD36 signaling by increasing superoxide radical anion and hydrogen peroxide through a mechanism that promotes activation of MAPK ERK5.
Fluid shear stress acts on the Galphaq-ERK5 signaling pathway to upregulate Cyclin B1 and CDK1 expression, thereby resulting in MC3T3-E1 cell proliferation.
Finally, we demonstrated that miR-24 plays the modulational role by directly repressing MAPK7, a key number in the MAPK signaling pathway. These data indicate that miR-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-FoxO3a signaling pathways by fluid shear stress resulted in a decreased expression of FasL and Bim and an inhibition of caspase-3 activation, which exerts a protective effect that prevents osteoblasts from apoptosis.
Data, including data from studies in knockout mice, suggest that Erk5/Mapk7 is required for tobacco smoke-triggered gastric epithelial-mesenchymal transition; can be suppressed by dietary factors (here, supplementation with epigallocatechin-3-gallate); suppression of Erk5/Mapk7 activation reverses tobacco smoke-triggered epithelial-mesenchymal transition in gastric mucosa.
ERK5 activation is essential for osteoclast differentiation.
Data showed that expression of the MKK7 gene in wild-type plants is induced by pathogen infection. Reducing mRNA levels of MKK7 by antisense RNA expression not only compromises basal resistance, but also blocks the induction of SAR.
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.
, 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
, LOW QUALITY PROTEIN: mitogen-activated protein kinase 7
, bmk I
, mitogen-activated protein kinase 7 L homeolog