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Human ERK2 Protein expressed in Wheat germ - ABIN1310256
Abeydeera, Egli, Cox, Mercier, Conde, Pallan, Mizurini, Sierant, Hibti, Hassell, Wang, Liu, Liu, Martinez, Sood, Lybrand, Frydman, Monteiro, Gomer, Nawrot, Yang: Evoking picomolar binding in RNA by a single phosphorodithioate linkage. dans Nucleic acids research 2016
Human ERK2 Protein expressed in Baculovirus infected Insect Cells - ABIN2001936
Slack, Seternes, Gabrielsen, Keyse: Distinct binding determinants for ERK2/p38alpha and JNK map kinases mediate catalytic activation and substrate selectivity of map kinase phosphatase-1. dans The Journal of biological chemistry 2001
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P38 activation repressed the cooperation of TTP with Ago2, thus ensuring that ARE-mRNA does not associate with processing bodies and remains stable.
these results suggest that sustained presence of lipid inflammatory mediator LTD4 could induce human airway epithelial cell proliferation through ERK1/2 phosphorylation, either directly via CysLT1 receptor or by transactivating EGFR.
lncRNA OECC is overexpressed in colorectal cancer and may play an oncogenic role through NF-kappaB and p38 MAPK pathway activation via miR-143-3p.
These results indicate that BSNQ and OSNQ induce apoptosis in human hepatoma Hep3B cells via ROS-mediated p38/MAPK, Akt and STAT3 signaling pathways, suggesting that these 1,4-naphthoquinone derivatives may provide promising new anticancer agents to treat HCC.
TRIM65 silencing inhibited cell proliferation, promoted cell apoptosis and arrested cell cycle, highly like through blocking ERK1/2 pathway.
Nuclear accumulation of symplekin promotes cellular proliferation and dedifferentiation in an ERK1/2-dependent manner.
Hydrogen bond analyses also prove that Mg(2+) binding increases occupancies of hydrogen bonds formed between ATP and residues K52, Q103, D104, and M106. We expect that this study can provide a significant theoretical hint for designs of anticancer drugs targeting ERK2
AKR1C3 is a novel epithelial-mesenchymal transition driver in prostate cancer metastasis through activating ERK signaling
Its activation may play a role in therapeutic resistance and disease relapse in head and neck squamous cell carcinoma by maintenance of the cancer stem cell phenotype.
that eukaryotic elongation factor 2 kinase might inhibit TGF-beta1-induced normal lung fibroblast (NHLF) proliferation and differentiation and activate NHLF cell apoptosis and autophagy through p38 MAPK signaling
The activation of p38 in response to low doses of ultraviolet radiation was postulated to be protective for p53-inactive cells. Therefore, MCPIP1 may favor the survival of p53-defective HaCaT cells by sustaining the activation of p38.
the present study demonstrated that scopoletin inhibited MMP1 and proinflammatory cytokine expression by inhibiting p38 MAPK phosphorylation.
High MAPK1 expression is associated with Prostate Cancer.
Role for ERK1/2-dependent activation of FCHSD2 in cancer cell-selective regulation of clathrin-mediated endocytosis.
MiR-451, which is down-regulated in human gastric cancer samples, potently modulated multiple metastatic phenotypes including cell migration, invasion, proliferation, and epithelial-mesenchymal transition. These effects were achieved via down-regulation of the miR-451 target gene, ERK2.
These results demonstrate that betaine acts through ERK1/2-PPARgamma signalling pathway to regulate lipid metabolism in adipogenic-differentiated skeletal muscle cells, which could provide some useful information for controlling muscle lipid accumulation by manipulating ERK1/2 and PPARgamma signalling pathway.
Autophagy protects bone marrow mesenchymal stem cells from palmitate-induced apoptosis through the reactive oxygen speciesJNK/p38 MAPK signaling pathways.
The present study demonstrated that the downregulation of filaggrin in the epidermis by toluene is mediated by ERK1/2 and STAT3-dependent pathways.
The results of the present study suggested that the therapeutic effect of TGP on psoriasis may be mediated by modulation of the p38 MAPK/NFkappaB p65 signaling pathway. The results of the present study contribute to the understanding of the role of TGP in the treatment of psoriasis. The present study provides insights suggesting that p38 MAPK may be a novel regulatory signaling pathway for the treatment of psoriasis.
L5-LDL, a naturally occurring mild oxidized LDL, induced G-CSF and GM-CSF production in human macrophages through LOX-1, ERK2, and NF-kappaB dependent pathways
SIRT6 attenuates cisplatin-induced acute kidney injury by binding to the promoters of ERK1 and ERK2 and deacetylated histone 3 at Lys9 (H3K9) thereby inhibiting ERK1/2 expression.
results demonstrate the mechanism for the maintenance of the undifferentiated state of embryonic stem cells via the inhibition of the FGF4-PKCzeta-MEK-ERK1/2 pathway by O-GlcNAcylation on PKCzeta.
Selective inhibition or knockdown of Rac1 decreased IL-6 and IL-8 release in 16HBE cells induced by cigarette smoke extract (CSE), which correlated with CSE-induced Rac1-regulated Erk1/2 mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription-3 (STAT3) signaling.
M-CSF-evoked ERK1/2 activation was decreased, whereas AKT activation was enhanced in SHP2-deficient BMMs. ERK1/2, via its downstream target RSK2, mediates this negative feedback by negatively regulating phosphorylation of M-CSF receptor at Tyr721 and, consequently, its binding to p85 subunit of PI3K and PI3K activation.
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.
MAPKs play a critical role in the control of cellular responses to cytokines and stressors and involved in the LPS-induced signaling pathway by which iNOS is expressed.
The Macrophage Activation Induced by Bacillus thuringiensis Cry1Ac Protoxin Involves ERK1/2 and p38 Pathways and the Interaction with Cell-Surface-HSP70
persistent distention/stretch on colonic smooth muscle cells could suppress SCF production probably through Ca(2+) -ERK-AP-1-miR-34c deregulation.
This indicates that TcpC may promote MIP2 production in kidney cells through the p38 MAPK signaling pathway. Taken together, the data of the present study demonstrated that TcpC can induce MIP2 production, which may contribute to the characteristic histological change associated with pyelonephritis.
the hippocampal MAPK oscillation and theta rhythmic oscillations in Nf1 (+/-) mice were disturbed and hinted about a possible mechanism for the brain dysfunction in Nf1 (+/-) mice.
Stress-specific p38 MAPK activation is sufficient to drive EGFR endocytosis but not its nuclear translocation
This indicated that RANK might be the binding target of baicalin. In sum, our findings revealed baicalin increased osteoclast maturation and function via p-ERK/Mitf signalling. In addition, the results suggest that baicalin can potentially be used as a natural product for the treatment of bone fracture
ERK2 role in the osteoclast differentiation.Insulin induces RANK expression via ERK1/2, which contributes to the enhancement of osteoclast differentiation.
Suppressing P38 promoted adipogenic trans-differentiation and intensified adipolytic metabolism in differentiated cells. However, inhibition of ERK1/2 had the opposite effects on adipogenesis and no effect on adipolysis. Blocking JNK weakly blocked trans-differentiation but stimulated adipolysis and induced apoptosis.
Betacellulin promotes the proliferation of corneal epithelial stem cells through the phosphorylation of Erk1/Erk2.
A stimulation induced PARP1 binding to phosphorylated Erk2 in the chromatin of cerebral neurons caused Erk-induced PARP1 activation, rendering transcription factors and promoters of immediate early genes (IEG) accessible to PARP1-bound phosphorylated Erk2.
Collectively, this study firstly demonstrated that PRMT1 exert podocyte-injury effects in mouse glomerulus through Ang /ERK pathway, which reveals a potential therapeutic target for DN.
North American ginseng inhibits myocardial NOX2-ERK1/2-TNF-alpha signaling pathway and improves cardiac function in endotoxemia, suggesting that NA ginseng may have the potential in the prevention of clinical sepsis.
NF-alpha1 is critical for regulating antiproliferation and cell fate determination, through differentiating embryonic stem cells to GFAP-positive astrocytes for normal neurodevelopment.
These findings suggested that USP14 induces NF-kappaB activity and ERK1/2 phosphorylation triggered by microbial infection.
The present results suggest that demecolcine might contribute to the activation of the Mos/MAPK pathway and affect spindle structure
MAPK1 upregulated milk protein synthesis through the Stat5 and mTOR pathways.
Chronic hypoxia induces Egr-1 via activation of ERK1/2 and contributes to pulmonary vascular remodeling.
ER Ca(2+) release enhances eNOS Ser-635 phosphorylation and function via ERK1/2 activation.
Cyclin-dependent kinase inhibition did not affect the expression (mRNA and protein levels) and localization of maturation promoting factor(MPF) and MAPK, and had nearly no effect on kinase activities during maturation.
Thrombospondin 1, fibronectin, and vitronectin are differentially dependent upon RAS, ERK1/2, and p38 for induction of vascular smooth muscle cell chemotaxis.
results suggest that Nav1.7-Ca2+ influx-protein kinase C-alpha pathway activated ERK1/ERK2 and p38, which increased phosphorylation of glycogen synthase kinase-3beta, decreasing tau phosphorylation
These data suggest that Gab1-ERK1/2 binding and their nuclear translocation play a crucial role in Egr-1 nuclear accumulation.
Role of CaMKII in hydrogen peroxide activation of p38 MAPK/heat shock protein 27 pathway and ERK1/2
data demonstrate that hypoxia-induced adventitial fibroblast proliferation requires activation and interaction of PI3K, Akt, mTOR, p70S6K, and ERK1/2.
This study demonstrates for the first time that cyclic mechanical stretch induces the proliferation of bovine satellite cells and suppresses their myogenic differentiation through the activation of ERK.
findings indicate that exposure to DHEA, at concentrations found in human blood, causes vascular endothelial proliferation by a plasma membrane-initiated activity that is Gi/o and ERK1/2 dependent.
These results suggest that bGPR40 mediates LCFA signaling in mammary epithelial cells and thereby plays an important role in cell proliferation and survival.
Results suggest that estrogen receptors and the ERK1/2 signaling pathway are involved in the anti-apoptotic action of LY117018 in vascular endothelial cells.
The intracellular mechanism of action of CART in regulation of FSH-induced MAPK signaling.
IFN-alpha mediated activation of ERK1/2 appeared to be responsible for the increased phosphorylation of tyrosine hydroxylase.
MAPK1 role in the oocyte maturation
Excess PLAC8 promotes an unconventional ERK2-dependent EMT in colon cancer.
ERK1/2-Akt1 crosstalk regulates arteriogenesis in mice and zebrafish.
eena plays an important role in the development of the myeloid cell through activation of the ERK1/ERK2 pathway
ERK1 and ERK2 target common and distinct gene sets, confirming diverse roles for these kinases during embryogenesis; for ERK2 genes involved in cell-migration, mesendoderm differentiation and patterning were identified.
These results demonstrate that induction of Hsp70 in response to heat stress is dependent on ERK activation in Pac2 cells.
Data define distinct roles for ERK1 and ERK2 in developmental cell migration processes during zebrafish embryogenesis.
Here the authors show that CPEB4 activity is regulated by ERK2- and Cdk1-mediated hyperphosphorylation. These phosphorylation events additively activate CPEB4 in M-phase by maintaining it in its monomeric state.
The reciprocal feedback observed between MPF and ERK2 in meiosis is not observed during mitotic M-phase in cell-free Xenopus embryo extracts.
The data suggest a MKK3 * MPK1 * RBK1 phosphorylation cascade that may provide a dynamic module for altering cell expansion.
MKP1 is a negative regulator of signaling pathways required for some, but not all, early and late pathogen-associated molecular pattern responses.
MKP1 and PTP1 act redundantly to suppress salicylic acid and camalexin biosynthesis, and regulate growth homeostasis and PR gene expression in an MPK3- and MPK6-dependent manner.
Regulation of AtMPK1/2 kinase activity in Arabidopsis might be under the control of signals involved in different kinds of stress.
Early activation of MAPK p44/42 is involved in deoxynivalenol -induced disruption of intestinal barrier function and tight junction network signaling.
Agonist stimulation of vascular smooth muscle increases PKC activity, which, in turn, increases MKP-1 activity and maintains MAPK1 activity at submaximal values.
sub-vasomotor concentration of ET-1 leads to vascular dysfunction by impairing endothelium-dependent NO-mediated dilation via p38 kinase-mediated production of superoxide from NADPH oxidase following ETA receptor activation
Treatment with ERK inhibitors or ERK1/2 knockdown significantly suppressed porcine epidemic diarrhea virus progeny production.
This study reveals a new function of the gE glycoprotein of pseudorabies virus and suggests that pseudorabies virus, through activation of ERK1/2 signaling, has a substantial impact on T cell behavior.
CSF2 stimulates proliferation of trophectoderm cells by activation of the PI3K-and ERK1/2 MAPK-dependent MTOR signal transduction cascades.
PGRN inhibits adipogenesis in porcine preadipocytes partially through ERK activation mediated PPARgamma phosphorylation.
Data show that proinflammatory cytokines induction was ERK1/2 and JNK1/2 dependent.
The authors show that porcine circovirus type 2 (PCV2) activates ERK1/2 in PCV2-infected PK15 cells dependent on viral replication.
20-HETE activates the Raf/MEK/ERK pathway in renal epithelial cells through an EGFR- and c-Src-dependent mechanism.
Data show that treatment with GH or IGF-I reduced leptin receptor expression, and increased Phosphorylation of ERK1/2 in response to acute leptin.
Cyclosporine A/sirolimus alter claudin-1 expression in renal proximal tubular cells via ERK1/2 signaling pathway to alter barrier function.
role of ERK1 and 2 in mediating IGF-I-stimulated vascular smooth muscle cell proliferation and chemotaxis [ERK1, ERK2]
endogenous ceramides are important second messengers in IL-1beta-induced apoptosis in pig thyroid cells through inhibition of adenylyl cyclase and ERK1/2 activities
Phorbol 12-myristate 13-acetate activation of ERK and JNK signaling is relevant in the regulation of gene expression during follicular development, ovulation, and luteinization.
There was no correlation of infarct size with expression or phosphorylation of ERK2 in ischemic postconditioning.
Retinal ischemia-reperfusion alters expression of mitogen-activated protein kinases, particularly ERK1/2, in the neuroretina and retinal arteries.
Saccharomyces cerevisiae inhibits the Enterotoxigenic Escherichia coli-induced expression of pro-inflammatory transcripts and this inhibition was associated to a decrease of ERK1/2 and p38 MAPK phosphorylation
ERK2 phosphorylation in response to Insulin-like Growth Factor-1 does not require activation of the Insulin-like Growth Factor-1 receptor tyrosine kinase
The protein encoded by this gene is a member of the MAP kinase family. MAP kinases, also known as extracellular signal-regulated kinases (ERKs), 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. The activation of this kinase requires its phosphorylation by upstream kinases. Upon activation, this kinase translocates to the nucleus of the stimulated cells, where it phosphorylates nuclear targets. Two alternatively spliced transcript variants encoding the same protein, but differing in the UTRs, have been reported for this gene.
, MAP kinase 1
, MAP kinase 2
, MAP kinase isoform p42
, MAPK 2
, extracellular signal-regulated kinase 2
, mitogen-activated protein kinase 2
, protein tyrosine kinase ERK2
, MAPK 1
, mitogen activated protein kinase 1
, extracellular-signal-regulated kinase 2
, mitogen-activated protein kinase 1
, MAP kinase
, mitogen-activated protein kinase 1b
, myelin basic protein kinase-like protein
, mitogen-activated protein kinase 1a
, extracellular signal-regulated kinase-2
, extracellular regulated protein 2