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For gain and loss of function studies, constitutively active MEK5 (Montrer MAP2K5 Protéines) (CA-MEK5 (Montrer MAP2K5 Protéines)) 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 (Montrer MOK Protéines) patients. ERK5 may be a new prognostic marker in this type of tumor.
FOXF1 (Montrer FOXF1 Protéines) promotes prostate tumor growth and progression by activating ERK5 signaling
CCh induced TGF-beta1 (Montrer TGFB1 Protéines) 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.
These findings suggest that atherogenic conditions critically regulate platelet CD36 (Montrer CD36 Protéines) signaling by increasing superoxide radical anion and hydrogen peroxide through a mechanism that promotes activation of MAPK (Montrer MAPK1 Protéines) ERK5.
expression of miR (Montrer MLXIP Protéines)-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 Protéines)-143.
miR (Montrer MLXIP Protéines)-143 down-regulated its target ERK5, leading to the suppression of epithelial-mesenchymal transition induced by GSK-3beta/Snail (Montrer SNAI1 Protéines) signaling of breast cancer.
the present study demonstrated that ERK5 positively regulates TS-induced urocystic EMT (Montrer ITK Protéines) 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 (Montrer ATM Protéines) and MAPK7 in the thymocyte response to DNA damage, and suggest that the lack of MAPK7 inhibits thymic lymphoma growth in Atm (Montrer ATM Protéines)-/- 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 (Montrer BRD4 Protéines) in pluripotency regulation of mouse embryonic stem cells have been revealed.
These results suggest that YAP (Montrer YAP1 Protéines) promotes muscle differentiation by activating the Abl (Montrer ABL1 Protéines)/Src (Montrer SRC Protéines)/MEKK3 (Montrer MAP3K3 Protéines)/MEK5 (Montrer MAP2K5 Protéines)/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 Protéines) signaling, which can be new agent for osteoporosis.
Data showed that expression of the MKK7 (Montrer MAP2K7 Protéines) gene in wild-type plants is induced by pathogen infection. Reducing mRNA levels of MKK7 (Montrer MAP2K7 Protéines) by antisense RNA expression not only compromises basal resistance, but also blocks the induction of SAR (Montrer SRL Protéines).
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