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Using compound selectivity engineering and CRISPR/Cas9 genome editing, distinct functions for Erk5 and Brd4 (显示 BRD4 ELISA试剂盒) in pluripotency regulation of mouse embryonic stem cells have been revealed.
These results suggest that YAP (显示 YAP1 ELISA试剂盒) promotes muscle differentiation by activating the Abl (显示 ABL1 ELISA试剂盒)/Src (显示 SRC ELISA试剂盒)/MEKK3 (显示 MAP3K3 ELISA试剂盒)/MEK5 (显示 MAP2K5 ELISA试剂盒)/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 (显示 NFE2L2 ELISA试剂盒) signaling, which can be new agent for osteoporosis.
These findings suggest that atherogenic conditions critically regulate platelet CD36 (显示 CD36 ELISA试剂盒) signaling by increasing superoxide radical anion and hydrogen peroxide through a mechanism that promotes activation of MAPK (显示 MAPK1 ELISA试剂盒) ERK5.
Fluid shear stress acts on the Galphaq (显示 GNAQ ELISA试剂盒)-ERK5 signaling pathway to upregulate Cyclin B1 (显示 CCNB1 ELISA试剂盒) and CDK1 (显示 CDK1 ELISA试剂盒) expression, thereby resulting in MC3T3-E1 cell proliferation.
Finally, we demonstrated that miR (显示 MLXIP ELISA试剂盒)-24 plays the modulational role by directly repressing MAPK7, a key number in the MAPK (显示 MAPK1 ELISA试剂盒) signaling pathway. These data indicate that miR (显示 MLXIP ELISA试剂盒)-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 (显示 AKT1 ELISA试剂盒)-FoxO3a (显示 FOXO3 ELISA试剂盒) signaling pathways by fluid shear stress resulted in a decreased expression of FasL (显示 FASL ELISA试剂盒) and Bim (显示 BCL2L11 ELISA试剂盒) and an inhibition of caspase-3 (显示 CASP3 ELISA试剂盒) 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.
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 (显示 MLXIP ELISA试剂盒)-143 in osteosarcoma cells inhibited cell proliferation and migration/invasion. Bioinformatics and luciferase reporter assays confirmed that MAPK7 was targets gene of miR (显示 MLXIP ELISA试剂盒)-143.
miR (显示 MLXIP ELISA试剂盒)-143 down-regulated its target ERK5, leading to the suppression of epithelial-mesenchymal transition induced by GSK-3beta (显示 GSK3b ELISA试剂盒)/Snail (显示 SNAI1 ELISA试剂盒) signaling of breast cancer.
this study revealed the functional and mechanistic links between CDK5 (显示 CDK5 ELISA试剂盒) and the oncogenic ERK5-AP-1 (显示 FOSB ELISA试剂盒) signaling pathway in the pathogenesis of colorectal cancer.
Present study revealed the positive role of ERK5/AP-1 (显示 FOSB ELISA试剂盒) in benzidine-provoked urocystic epithelial-mesenchymal transition and the curcumin promising use in bladder cancer prevention and intervention via ERK5/AP-1 (显示 FOSB ELISA试剂盒) pathway.
miR (显示 MLXIP ELISA试剂盒)-200b-3p suppresses glioma tumor growth, invasion, and reverses EMT (显示 ITK ELISA试剂盒) through downregulated its target ERK5.
Results indicate that MAPK7 may be modulating the growth, proliferation, migration and invasion of osteosarcoma cells.
Data showed that expression of the MKK7 (显示 MAP2K7 ELISA试剂盒) gene in wild-type plants is induced by pathogen infection. Reducing mRNA levels of MKK7 (显示 MAP2K7 ELISA试剂盒) by antisense RNA expression not only compromises basal resistance, but also blocks the induction of SAR (显示 SRL ELISA试剂盒).
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