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Human Polyclonal MAPK3 Primary Antibody for ICC, IHC (p) - ABIN3044377
Li, Zhu, Liu, Liu, Wang, Xiong, Shen, Hu, Zheng: ZFX knockdown inhibits growth and migration of non-small cell lung carcinoma cell line H1299. in International journal of clinical and experimental pathology 2013
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Human Polyclonal MAPK3 Primary Antibody for WB - ABIN1881527
Munshi, Wu, Mukhopadhyay, Ottaviano, Sassano, Koblinski, Platanias, Stack et al.: Differential regulation of membrane type 1-matrix metalloproteinase activity by ERK 1/2- and p38 MAPK-modulated tissue inhibitor of metalloproteinases 2 expression controls transforming growth ... in The Journal of biological chemistry 2004
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Chicken Monoclonal MAPK3 Primary Antibody for IF, IP - ABIN967952
Boulton, Cobb: Identification of multiple extracellular signal-regulated kinases (ERKs) with antipeptide antibodies. in Cell regulation 1991
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Chicken Polyclonal MAPK3 Primary Antibody for ICC, FACS - ABIN361833
Boulton, Gregory, Cobb: Purification and properties of extracellular signal-regulated kinase 1, an insulin-stimulated microtubule-associated protein 2 kinase. in Biochemistry 1991
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Human Polyclonal MAPK3 Primary Antibody for IF (p), IHC (p) - ABIN744143
Zhao, Zhang, Liu, Zhang, Hao, Li, Chen, Shen, Tang, Min, Meng, Wang, Yi, Zhang: Hydrogen Sulfide and/or Ammonia Reduces Spermatozoa Motility through AMPK/AKT Related Pathways. in Scientific reports 2016
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Mouse (Murine) Polyclonal MAPK3 Primary Antibody for - ABIN550154
Johnson, Lapadat: Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases. in Science (New York, N.Y.) 2002
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Human Polyclonal MAPK3 Primary Antibody for WB - ABIN540798
Kolch: Meaningful relationships: the regulation of the Ras/Raf/MEK/ERK pathway by protein interactions. in The Biochemical journal 2001
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Human Polyclonal MAPK3 Primary Antibody for WB - ABIN540648
Smalley: A pivotal role for ERK in the oncogenic behaviour of malignant melanoma? in International journal of cancer. Journal international du cancer 2003
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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.
High ERK1 expression is associated with resistance to mTOR inhibition in glioblastoma.
High ERK1 expression is associated with pancreatic cancer cell invasion.
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.
High ERK1 expression is associated with gastric cancer.
Data suggest that Thr264 in TRPV3 is key ERK1 phosphorylation site mediating EGFR-induced sensitization of TRPV3 to stimulate signaling pathways involved in regulating skin homeostasis. (TRPV3 = transient receptor potential cation channel subfamily V member-3; ERK1 = extracellular signal-regulated kinase-1; EGFR = epidermal growth factor receptor)
Role for ERK1/2-dependent activation of FCHSD2 in cancer cell-selective regulation of clathrin-mediated endocytosis.
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.
The present study demonstrated that the downregulation of filaggrin in the epidermis by toluene is mediated by ERK1/2 and STAT3-dependent pathways.
RASSF7 promotes cell proliferation through activating MEK1/MEK2-ERK1/ERK2 signaling pathway in hepatocellular carcinoma.
SHP-2 may augment the ERK1/2 activity and cell proliferation activity in IL-21 signaling.
intact keratin filaments are regulators for PKB/Akt and p44/42 activity, basal and in response to stretch.
Immune profiling of human prostate epithelial cells in health and pathology determined by expression of p38/TRAF-6/ERK MAP kinases pathways has been reported.
Integrated ERK1/ERK2 response to B-cell receptor stimulation and SF3B1 gene mutations refine prognosis in chronic lymphocytic leukemia.
These findings identified the relationship between ERK1/2 Snitrosylation and phosphorylation.
A cellular threshold for active ERK1/2 levels determines Raf/MEK/ERK-mediated growth arrest versus death responses.
ERK1/2/p53/PUMA signaling axis is related to cisplatin-induced cell death in ovarian cancer cells.
results demonstrated that OEA exerts anti-inflammatory effects by enhancing PPARalpha signaling, inhibiting the TLR4-mediated NF-kappaB signaling pathway, and interfering with the ERK1/2-dependent signaling cascade (TLR4/ERK1/2/AP-1/STAT3), which suggests that OEA may be a therapeutic agent for inflammatory diseases.
the physiological role of the negative crosstalk between the cAMP/PKA/AKAP4 and the PKC/ERK1/2 pathways is to regulate capacitation and acrosome reaction.
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.
Low ERK1 Phosphorylation is associated with low liver regeneration.
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.
In a retinitis pigmentosa mouse model, TrkC activity generates phosphorylated Erk, which upregulates glial TNF-alpha, causing selective neuronal death.
A. fumigatus increased PAR-2 expression and elevated disease, PMN infiltration, and proinflammatory cytokine expreERK1 Kinasession through PAR-2, which may be modified by p-ERK1/2.
ERK1 and ERK2 play specific roles in beta cells. ERK2 cannot always compensate for the lack of ERK1 but the absence of a clear-cut phenotype in Erk1 (-/-) mice shows that ERK1 is dispensable in normal conditions.
The Macrophage Activation Induced by Bacillus thuringiensis Cry1Ac Protoxin Involves ERK1/2 and p38 Pathways and the Interaction with Cell-Surface-HSP70.
hBD-1 potentiates the induction of in vitro osteoclastogenesis by RANKL via enhanced phosphorylation of the p44/42 MAPKs.
ERK1 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.
Taken together, the results of our present study indicated that DHCE could inhibit cellular proliferation and induce cell apoptosis in myeloma cells mediated through different mechanisms, possibly through inhibiting the IL-6/STAT3 and ERK1/2 pathways. And it may provide a new therapeutic option for MM patients.
Betacellulin promotes the proliferation of corneal epithelial stem cells through the phosphorylation of Erk1/Erk2.
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.
Cortical neuron-specific deletion of extracellular signal-regulated kinases Erk1 or Erk2 significantly increased the duration of wakefulness.
pERK1/2 is a regulator of CD44 expression, and increased CD44 expression leads to a pro-sclerotic and migratory parietal epithelial cell phenotype in focal segmental glomerulosclerosis.
MAPK3 role in the oocyte maturation
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 ERK1 different specific genes involved in dorsal-ventral patterning and subsequent embryonic cell migration 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.
MAPK3/1 is involved in luteinizing hormone-mediated decrease of C-type natriuretic peptide and this process is related to the EGFR and MAPK3/1 signal 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.
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.
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.
Early activation of MAPK p44/42 is involved in deoxynivalenol -induced disruption of intestinal barrier function and tight junction network signaling.
Pseudorabies virus glycoprotein gE-mediated ERK 1/2 phosphorylation also occurs in epithelial cells and in these cells, gE-mediated ERK 1/2 signaling is associated with degradation of the pro-apoptotic protein Bim.
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.
The food contaminant deoxynivalenol activates the mitogen activated protein kinases in the intestine.
Porcine circovirus type 2 (PCV2) might induce autophagy via the AMPK/ERK/TSC2/mTOR signaling pathway in the host cells, representing a pivotal mechanism for PCV2 pathogenesis
Data show that proinflammatory cytokines induction was ERK1/2 and JNK1/2 dependent.
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
ERK1 phosphorylation in response to Insulin-like Growth Factor-1 does not require activation of the Insulin-like Growth Factor-1 receptor tyrosine kinase
Retinal ischemia-reperfusion alters expression of mitogen-activated protein kinases, particularly ERK1/2, in the neuroretina and retinal arteries.
Cyclosporine A/sirolimus alter claudin-1 expression in renal proximal tubular cells via ERK1/2 signaling pathway to alter barrier function.
Data show that treatment with GH or IGF-I reduced leptin receptor expression, and increased Phosphorylation of ERK1/2 in response to acute leptin.
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 ERK1 in ischemic postconditioning.
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.
The results suggest that the MPK-1/ERK regulatory network, including FBF-1, FBF-2, and LIP-1, controls the number of sperm by regulating the timing of the sperm-oocyte switch in C. elegans.
data support a role for the Cek1mediated pathway in fungal cell wall maintenance, virulence and antifungal discovery
Cek2 has a cryptic role in cell-wall biogenesis and its role is not entirely redundant to Cek1.
knockdown of SUV420H1 reduced phosphorylated ERK1 and total ERK1 proteins, and interestingly suppressed ERK1 at the transcriptional level
Secreted aspartic protease-mediated proteolytic cleavage of Msb2 is required for activation of the Cek1 mitogen activated protein kinase pathway in response to environmental cues.
The authors propose that a Msb2, Cek1 and Ace2 signalling pathway addresses PMT genes as downstream targets and that different modes of regulation have evolved for PMT1 and PMT2/PMT4 genes.
Dfi1 function promotes matrix-dependent activation of Cek1 kinase during growth.
Msb2 is involved in the transmission of the signal toward Cek1 mediated by the Cdc42 GTPase.
abscisic acid and jasmonate mediate inactivation of the immune-associated MAP kinases (MAPKs), MPK3 and MPK6, in Arabidopsis thaliana ABA induced expression of genes encoding the protein phosphatases 2C (PP2Cs), HAI1, HAI2, and HAI3 through ABF/AREB transcription factors
Constitutive active-MPK3 plants are more resistant to the hemibiotrophic pathogen Pseudomonas syringae DC3000.
constitutively active (CA)-MPK3 crosses with summ1 and summ2, two known suppressors of mpk4, resulted in a partial reversion of the CA-MPK3 phenotypes.
that MPK3/MPK6 phosphorylate and destabilize ICE1, which negatively regulates CBF expression and freezing tolerance in plants
Changes in PUB22 Ubiquitination Modes Triggered by MITOGEN-ACTIVATED PROTEIN KINASE3 Dampen the Immune Response
MPK3 role in ultraviolet induced stomatal closure
Study propose that the pathogen-responsive MPK3/MPK6 cascade and ABA are two essential signaling pathways that control, respectively, the organic acid metabolism and ion channels, two main branches of osmotic regulation in guard cells that function interdependently to control stomatal opening/closure.
Data report that MPK3/MPK6 and their substrate ERF6 promote the biosynthesis of IGSs and the conversion of I3G to 4MI3G, a target of PEN2/PEN3-dependent chemical defenses in plant immunity.
Data show that the protein kinases MPK3 and MPK6 can both interact with SPOROCYTELESS/NOZZLE (SPL) in vitro and in vivo and can phosphorylate the SPL protein in vitro.
MKK4, MKK5, MKK7, and MKK9, are responsible for the activation of MPK3 and MPK6 by melatonin, indicating that melatonin-mediated innate immunity is triggered by MAPK signaling through MKK4/5/7/9-MPK3/6 cascades.
Phosphatase AP2C1, as well as AP2C1-targeted MPK3 and MPK6, are important regulators of plant-nematode interaction, where the co-ordinated action of these signalling components ensures the timely activation of plant defence.
Results demonstrated the contribution of MPK3 and MPK6 to riboflavin-induced resistance.
These results indicate that the MVB pathway is positively regulated by pathogen-responsive MPK3/6 through LIP5 phosphorylation and plays a critical role in plant immune system
MKK3-MPK6 is activated by blue light in a MYC2-dependent manner.
MPK3 and MPK6 target a subclass of 'VQ-motif'-containing proteins to regulate immune responses.
MicroRNA biogenesis factor DRB1 is a phosphorylation target of mitogen activated protein kinase MPK3 in both rice and Arabidopsis
MPK3 represses the constitutive and flg22-induced expression of defence genes in Arabidopsis thaliana.
These results suggest that the MKK9-MPK3/MPK6 cascade is part of the phosphate signaling pathway in plants.
AZI1 overexpression in the mpk3 genetic background partially alleviates the salt-hypersensitive phenotype of this mutant, but functional MPK3 appears to be required for the full extent of AZI1-conferred robustness.
HSFA4A is a substrate of the MPK3/MPK6 signaling and that it regulates stress responses in Arabidopsis.
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 in a signaling cascade that regulates various cellular processes such as proliferation, differentiation, and cell cycle progression in response to a variety of extracellular signals. This kinase is activated by upstream kinases, resulting in its translocation to the nucleus where it phosphorylates nuclear targets. Alternatively spliced transcript variants encoding different protein isoforms have been described.
MAP kinase isoform p44
, MAPK 1
, extracellular signal-regulated kinase 1
, extracellular signal-related kinase 1
, insulin-stimulated MAP2 kinase
, microtubule-associated protein 2 kinase
, MAP kinase 3
, p44 MAP kinase
, pp42/MAP kinase
, mitogen-activated protein kinase 3
, MAP kinase 1
, MAPK 3
, mitogen-activated 3
, mitogen-activated protein kinase 1
, extracellular signal-regulated kinase-1
, likely protein kinase