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Validated All-in-One™ qPCR Primer for MAPK1(NM_002745.4) Search again
Product ID:
HQP014848
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ERK, ERK-2, ERK2, ERT1, MAPK2, NS13, P42MAPK, PRKM1, PRKM2, p38, p40, p41, p41mapk, p42-MAPK
Gene Description:
mitogen-activated protein kinase 1
Target Gene Accession:
NM_002745.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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. [provided by RefSeq].
Gene References into function
- Vav associates with ERK2.
- MEK1 interacts with and phosphorylates ERK2. This interaction is mediated via a conserved N-terminal docking site in MEK1. Note that this interaction was demonstrated using rat ERK2.
- MEK2 interacts with ERK2. This interaction is mediated via a conserved N-terminal docking site in MEK2. Note that this interaction was demonstrated using rat ERK2.
- Angiogenin induces transient phosphorylation of extracellular signal-related kinase 1/2 (Erk1/2) in cultured human umbilical vein endothelial cells.
- Unregulated activation of STAT-5, ERK1/2 and c-Fos may contribute to the phenotypic transformation from myelodysplastic syndrome to acute leukaemia. Impaired ERK1/2 signalling pathways were activated only by GM-CSF but not by Epo.
- C-terminal halves of ERK2 and ERK3DeltaC are primarily responsible for subcellular localization in resting cells; and the N-terminal folding domain of ERK2 is required for its activation in cells, interaction with MEK1, and accumulation in the nucleus
- suggests that upon activation Ras becomes associated with IRAK, Traf-6, and TAK-1, possibly aiding the assembly of this multiprotein signaling complex required for p38 MAPK activation by IL-1
- Based on a MEK1-derived peptide, we developed inhibitors of ERK activation in vitro and in vivo.
- Extracellular signal-regulated kinase (ERK1 and ERK2) activation is required for GP Ibalpha-dependent endothelial cell migration.
- residues located at different positions are important for discriminating between ERK and p38 MAPKs
- Cooperativity between the Ras-ERK and Rho-Rho kinase pathways in urokinase-type plasminogen activator-stimulated cell migration
- ERK and p38 MAP kinase pathways cooperate in mediating cytokine-induced proliferation of OCI-AML5 cell line
- mediates regulation of p73 by c-Abl
- ERK1/2 activation is a regulator of progesterone synthesis in hGL cells
- p42/44MAPK regulates baseline permeability and cGMP-induced hyperpermeability in endothelial cells
- Glucocorticoids synergistically enhance nontypeable Haemophilus influenzae-induced Toll-like receptor 2 expression via a negative cross-talk with p38 MAP kinase.
- Hepatitis C virus core protein expression activates extracellular signal-regulated kinase (ERK)
- role of activation in TFF-peptide-stimulated bronchial epithelial cell migration and tumor necrosis factor-alpha-induced interleukin-6 and IL-8 secretion
- ML-1-induced IL-6 and IL-8 production is mediated through the activation of ERK1/2
- ERK negatively regulates the epidermal growth factor-mediated interaction of Gab1 and the phosphatidylinositol 3-kinase
- The functional role of mitogen-activated protein kinase (MAPK) signaling and c-Jun induction in phorbol 12-myristate 13-acetate (PMA)-induced human 12(S)-lipoxygenase gene expression
- role of activation in IGFBP-5 stimulation of growth and IGF-I secretion in intestinal smooth muscle
- Activation of p38 MAP-kinase and caldesmon phosphorylation are essential for urokinase-induced human smooth muscle cell migration.
- Activation of the p42 MAPK pathway contributes to the underlying mechanism of IL-12 suppression by soluble CD40 ligand.
- mediates activation of neutrophils by lipopolysaccharide
- Down-regulation of ERK1 and ERK2 activity during differentiation of the intestinal cell line HT-29.
- Mechanism of 17-beta-estradiol-induced Erk1/2 activation in breast cancer cells. A role for HER2 AND PKC-delta
- eNOS expression might be regulated by PI-3K and the ERK1/2 signaling pathway
- Results show that oncogenic ras provokes premature senescence by sequentially activating the MEK-ERK and MKK3/6-p38 pathways in normal, primary cells.
- Eicosapentaenoic acid and docosahexaenoic acid modulate MAP kinase enzyme activity in human T-cells
- ERK2 activity and dual-phosphorylation were undetectable in expanding and self-renewing hematopoietic progenitors (HP). Adding IL-3, inducing maturation and cell death in HP, led to sustained high levels of ERK2 activity and dual-phosphorylation.
- The signaling pathway triggered by both 8-iso-PGFalpha and low concentrations of U46619 to induce platelet adhesion and shape change implicates Syk, the p38 MAP kinase, and actin polymerization.
- role in stabilizing p21(Cip1) by phosphorylation
- p38MAPK is activated by phosphorylated ATF6 and induces HSPA5 binding
- NBMPR-sensitive equilibrative nucleoside transporters are targets for p38 MAPK inhibitors
- the NOx-induced cell proliferation via activation of p38 might contribute to lung tissue damage caused by NOx
- Provant Wound Closure System induces activation of p44/42 MAP kinase in normal cultured human fibroblasts
- p38 MAP kinase regulation of AP-2 binding in TGF-beta1-stimulated chondrogenesis of human trabecular bone-derived cells
- ERK activation by cAMP does not require RAP1
- Role of ERK2 in BRCA1-induced apoptosis
- Formation of an hER alpha-COUP-TFI complex enhances hER alpha AF-1 through Ser118 phosphorylation by ERK2.
- p38 MAP kinase activation appears to be an important upstream signaling event associated with increased endothelial permeability and vascular endothelial cadherin redistribution
- The alpha-MSH-induced differentiation of COLO 853 human melanoma cells proceeds via a p38 MAP kinase-mediated pathway and is associated with decreased pRB phosphorylation and accumulation of cells in the G(1) phase.
- p38 MAPK is a pivotal regulator of basophil function downstream of PI 3-K activation and calcium mobilization.
- Physiological levels of interleukin-18 stimulate multiple neutrophil functions through p38 MAP kinase activation.
- These results show that p38 MAPK provides a costimulatory signal for IL-4-induced gene responses by directly stimulating the transcriptional activation of STAT6.
- Control of mycobacterial replication in human macrophages: roles of extracellular signal-regulated kinases 1 and 2 and p38 mitogen-activated protein kinase pathways.
- ITGB1 activated by ERK1/2, p38 MAPK after hypoxia
- description of the signaling of JNK and p38 MAPK in apoptosis after stimulation by antioxidants
- connective tissue growth factor induced fibronectin production, cell migration, and cytoskeletal rearrangement are associated with recruitment of Src and phosphorylation of p42/44 MAPK and protein kinase B
- A new ERK2 binding protein, Naf1, attenuates the EGF/ERK2 nuclear signaling.
- Data show that arsenic trioxide induces activation of the small G-protein Rac1 and the alpha and beta isoforms of the p38 mitogen-activated protein (MAP) kinase in several leukemia cell lines.
- glucocorticoids synergistically enhance NTHi-induced TLR2 expression via specific up-regulation of the MAPK phosphatase-1 (MKP-1) that, in turn, leads to dephosphorylation and inactivation of p38 MAPK
- EPO induces long-lasting phosphorylation of MAPK p42/44 in vascular endothelial cells, activating signal pathways increasing the thrombogenicity of their extracellular matrices.
- role in stimulus-induced platelet activating factor synthesis by regulating individual enzymes of the remodeling pathway in neutrophils
- Data suggest that mitogen-activated protein kinase phosphatase 1 (MKP-1) participates in a negative-feedback loop which regulates p38 function and that dexamethasone may inhibit proinflammatory gene expression in part by inducing MKP-1 expression.
- Inhibition of p38 MAPK inhibits IL-6 and VEGF secretion in bone marrow stromal cells triggered by adherence of multiple myeloma cells.
- expression of extracellular signal-regulated kinase, ERK2, and its relationship with clinicopathological characteristics of breast cancer
- p38 is activated by various kinds of stresses and regulates TEL transcription factor
- LMP1 inhibits transforming growth factor-beta 1-mediated induction of MAPK/p21 in Epstein-barr virus infected gastric epithelial cell line GT38
- Release of proteinase 3 and human neutrophil elastase can result in their entry into endothelial cells coincident with the activation of proapoptotic-signaling events through ERK, JNK, and p38 MAPK.
- report the activation of the extracellular signal-regulated kinases (ERKs) 1 and 2 (p44 and p42 MAP kinase) through the human serotonin receptors 5-HT(4(b)) and 5-HT(7(a))
- results suggest that activation of p38 MAPK, either directly or via lipoxygenase activation, participates in aldosterone's stimulatory effects of ANG II in adrenal cells.
- Ubiquitylation of MEKK1 inhibits its phosphorylation of MKK1 and MKK4 and activation of the ERK1/2 and JNK pathways
- activation by Pro33 polymorphism of integrin beta3
- hypertonic stress increases T cell interleukin-2 expression through a mechanism that involves ATP release, P2 receptor, and p38 MAPK activation
- MEK2 and p38 in IFN-gamma-mediated signal transduction and induction of C/EBP beta expression and activity associated with interleukin-6 (IL-6) secretion in colon epithelial cells.
- Activation of p38 and inactivation of ERK are involved in CsA-induced erythroid differentiation of K562 cells.
- Decreased phosphorylation of protein kinase B and erk1/erk2 in neutrophils from patients with myelodysplastic syndrome
- Data show that p-MEK1/2 and p-ERK1/2 are present in neurons in the initial stages of neurofibrillary degeneration in Alzheimer's disease, before deposition of beta-amyloid.
- IL-2 decreased the expression of ERK2, whereas polysaccharide K did not.
- Persistent activation of ERK1/2 by lead acetate increases nucleotide excision repair synthesis and confers anti-cytotoxicity and anti-mutagenicity.
- Activation of p38 MAPK by double-stranded RNA in biliary epithelial cells.
- Helicobacter pylori-induced ERK2 activation, especially by the cagA(+) strain, may play a protective role against gastric epithelial cell apoptosis partially through maintenance of bcl-2 gene expression
- inhibition amplifies ajoene-induced cell death in human promyeloleukemic cells
- pp90RSK- and protein kinase C-dependent pathway regulates p42/44MAPK-induced LDL receptor transcription in HepG2 cells.
- a randomized double-blind study to determine the role of p38 MAPK in the procoagulant response to lipopolysaccharide
- The protein tyrosine phosphatase HePTP regulates nuclear translocation of of this protein.
- Western blot demonstrated that phosphorylation of ERK is dramatically induced (11.6-fold ) by TPA during 15 min to 1 h and significantly induced (2.5-fold) by Saikosaponin alpha at 30 min.
- EDD, elk1, rsk1 protein, tpr protein, are identified as novel ERK2 substrates.
- p38 Mitogen-activated protein kinase and extracellular signal-regulated kinases play distinct roles in the activation of dendritic cells by two representative haptens, NiCl2 and 2,4-dinitrochlorobenzene.
- acute hyperglycemia-mediated mononuclear cell activation is dependent on activation of ras, p42/p44 mitogen-activated protein kinase phosphorylation, and subsequent NF-kappaB activation
- Physiological concentration of insulin causes modest but sustained activation of p38 MAPK pathway in human skeletal muscle. Effect of exercise on p38 phosphorylation lasts 3 h. Role in increased insulin sensitivity of skeletal muscle after exercise.
- data provides first evidence of a new role of extracellular signal-regulated kinase and p38 mitogen activated protein kinase on the translational machinery
- HDL induced a potent signal through a Ras/MAPK pathway mediated by a pertussis toxin-sensitive G-protein coupled receptor to the angiogenic phenotype in HCECs.
- stretch of airway smooth muscle causes production of interleukin-8 by activating CCAAT/enhancer-binding protein and activator protein-1 transcription factor through activation of extracellular regulated kinase-1 and 2 and p38 kinase signaling pathways
- EGF & ionizing radiation up-regulate the DNA repair genes XRCC1 & ERCC1 in DU145 & LNCaP prostate carcinoma, showing a complex control of DNA repair activation that may be more generally dependent on MAPK (ERK1/2) signaling than previously noted.
- p38 and ERK1/2 have roles in coordinating cellular migration and proliferation in epithelial wound healing
- TAO (thousand-and-one amino acid) protein kinases mediate signaling from carbachol to this enzyme and ternary complex factors.
- MKP-1 degradation is mediated via the ubiquitin-proteasome pathway, thus facilitating long-term activation of ERK1/2 against cytotoxicity
- The 1,25(OH)(2)D3-responsive element in cystatin A gene is identical to TRE, T2 (-272 to -278). Suppression of Raf-1/MEK1/ERK1,2 signaling pathway increases cystatin A expression of normal human keratinocytes.
- antiproliferative effect of the heme oxygenase-1 pathway in airway smooth muscle in vitro and in vivo through a bilirubin-mediated redox modulation of phosphorylation of ERK1/2
- IL1beta and TNFalpha activation of MSK1 and CREB and cAMP-response element signaling cascades occurs via ERK/p38 MAP kinases and are crucial aspects of the intracellular mechanisms that mediate MUC5AC gene expression
- altered property of decidualized cells is thought to be caused by attenuation of interleukin-1 beta-induced p38 mitogen-activated protein kinase phosphorylation
- ERK and p38 MAPK were constitutively active in all cases of the B-cell tumor studied
- Eosinophils induced neurite retraction via two distinct pathways: by generation of tyrosine kinase-dependent reactive oxygen species and by p38 MAP kinase.
- Lipopolysaccharide-induced matrix metalloproteinase (MMP)-1 production by monocytes is regulated by p38 MAP kinase mainly through a PGE2-dependent pathway.
- p38 delta is the major p38 isoform driving suprabasal hINV gene expression and that p38 delta directly regulates ERK1/2 activity via formation of a p38 delta-ERK1/2 complex
- ERK1/2 signaling is regulated by B-raf in melanocytes
- trophoblast cells cause activation of p38 mitogen-activated protein kinase in endometrial epithelial cells and induce apoptosis and displacement of endometrial epithelial cells
- Neutrophil elastase-induced PGE2 release involved activation of p44/42, but not p38, MAP kinases.
- Amyloid beta-protein expression and secretion are regulated via activation of ERK1/2 by HGF in cells transfected with APP751.
- Constitutive induction of p-Erk1/2 accompanied by reduced activities of protein phosphatases 1 and 2A and MKP3 due to reactive oxygen species during cellular senescence.
- p38 MAPK and NF-kappaB signaling regulate steady-state levels of COX-2 expression, p38 MAPK additionally affects stability of COX-2 mRNA in cytokine-stimulated human airway myocytes
- P38 MAPK is important for uPA expression in gastric tumor cells by enhancing the promoter activity of uPA
- p38 MAP kinase modulates Smad-dependent changes in human prostate cell adhesion. Smad3 is phosphorylated by p38 MAP kinase in vitro.
- constitutively activated in choroidal melanoma cell lines, independent of Ras, and regulated by B-RafV599E
- ERK-1/ERK-2 active in salivary gland mucoepidermoid carcinoma. Activation is associated with more aggressive tumor behavior and higher proliferative activity. Deregulation contributes to mucoepidermoid carcinoma phenotype. Target for anticancer drugs.
- Basal p38 MAPK phosphorylation is increased in skeletal muscle from Type 2 diabetic patients. Aberrant p38 MAPK signalling might contribute to the pathogenesis of insulin resistance.
- results indicate that activation of PKC is responsible for GnRH-induced phosphorylation of both ERK1/2 and Pyk2, and that Pyk2 activation does not contribute to GnRH signaling
- The beta1-integrin-ligand disengagement resulted in capillary disruption and stimulated p38 MAPK and extracellular signal-regulated kinase activity.
- Alterations in MAPK pathways in part regulate peripheral microvascular dysfunction after CPB in humans.
- p38 MAPK activation could play a relevant role in the exacerbated platelet activation associated with oxidative stress as found in diabetes
- IGF-I signals osteoblast mitogenesis and survival through parallel, partly overlapping intracellular pathways involving PI-3 kinase, p42/44 MAPKs, and G beta gamma subunits.
- activation of p38 MAPK caused a decrease in EEA1 colocalization with phagosomes, arresting maturation into the phagolysosome
- p38 activity is regulated in neoplasms by Akt.
- the P2X1-ERK2-Myosin Light Chain Kinase axis contributes to collagen-induced platelet activation by enhancing platelet degranulation
- JNK and p38 MAPK have roles in UVA-induced signaling pathways leading to AP-1 activation and c-Fos expression
- activation of Sphingosine kinase 1 results directly from phosphorylation of Ser225, and evidence shows that the activating kinase is ERK1/2 or a close relative
- Jak2 is required for Ang II-induced ERK2 inactivation via induction of MKP-1 gene expression.
- results suggest that ERK may play important roles in the control of microvilli structure and possibly, in brush border-associated responses in differentiated intestinal epithelial cells.
- phosphorylation of PPARgamma was mediated through the ciglitazone-induced activation of Erk1/2
- nNOS can differentially regulate the ERK signal transduction pathway in a manner dependent on the presence of l-arginine and the production of NO*.
- Both pyrophosphate-resembling (p-) and nitrogen-containing (n-) bisphosphonates induce activation of p38 mitogen activated protein (MAP) kinase pathway in MDA-MB-231 breast cancer cells in vitro.
- Treatment of insulin receptor-overexpressing cells with insulin or vanadyl sulfate resulted in a time-dependent transient increase in phosphorylation and activation of extracellular signal-regulated kinases 1 and 2.
- Elevated levels of phosphorylated ERK 1/2 were detected in monocytes after 2 h of NANase treatment, persisting for 2 additional hours. Desialylation of cell surface glycoconjugates also led to increased production of IL-6, MIP-1alpha, and MIP-1beta.
- CPPD crystal associated inflammatory response is regulated through the activation of p38 kinase to sub-apoptotic levels.
- Phospho-ERK immunoreactivity was often associated with mitochondrial proteins (MnSOD, 60 kDa and 110 kDa mitochondrial antigens), and some vesicular-appearing phospho-ERK granules appeared to envelop enlarged mitochondria.
- JCV-induced signal activates the mitogen-activated protein kinases ERK1 and ERK2 when JC virus is binding to human glial cells
- Stress-related signaling pathways in epithelial cells are modulated by hypoxia and confer protection from reoxygenation, since hypoxia and chemical inhibition of p38mapk and MEK1/2 similarly increase cytolysis resulting from O2-.
- p42MAPK has a role in glucose-enhanced interleukin-6-induced VEGF165 expression
- A novel regulatory network RAFTK/Pyk2, Src and p38 appears to be critical for VEGF-induced endothelial cell migration.
- p38 MAP kinase has a role in platelet activation by von Willebrand factor
- Activation of p38 is necessary but not sufficient for toll-like receptor synergizing with IFN-gamma in regulating Tap-1 expression in macrophages
- ERK1/2 activation with calcium requires Galphai2 coupling and dynamin-independent receptor internalization
- results suggest that physiological levels of beta-arrestin1 may act as "dominant-negative" inhibitors of beta-arrestin2-mediated extracellular signal-regulated kinases 1 and 2 activation
- epidermal p44/42 and p38 mitogen-activated protein kinases are activated by acute cutaneous barrier disruption
- Virtually all TNF-alpha-inducible genes were dependent on I kappa B kinase 2 (IKK2)/NF-kappa B activation, whereas a minor number was additionally modulated by p38; genes suppressed by IKK2/NF-kappa B were newly identified
- Data show that respiratory syncytial virus stimulates sphingosine kinase activity in lung epithelial cells, leading to activation of antiapoptotic sphingosine 1-phosphate and subsequently activation of Akt and extracellular signal-related kinase.
- extracellular signal-regulated kinases 1 and 2 are activated by cyclic AMP
- p38(MAPK) regulates BSEP trafficking from Golgi to canalicular membrane, and Golgi may serve as BSEP pool in certain forms of cholestasis or when p38(MAPK) activity is inhibited. Activation of p38(MAPK) can recruit Golgi-associated BSEP.
- p38 MAPK is critical for discoidin domain receptor 1b-mediated, increased NF-kappa B trans-activity during differentiation of human monocytes into macrophages.
- p38 MAP kinase has an important role in regulating MMM-9 release from eosinophils and regulating fMLP-induced MMP-9 release
- RSV attachment to A549 cells activates both ERK-1 and ERK-2 pathways within 5 min. Inhibition of ERK pathways significantly decreases RSV infection, demonstrating that the activation of the ERK-1/2 is required in RSV-induced early gene expression.
- p38 is activated by ultraviolet rays mediated by Gbetagamma in a Cdc42-dependent way
- ERK2 is regulated by IQGAP1
- ERK1 and ERK2 have roles in functional activation of estrogen receptor alpha in human tumor cells by leptin
- ERK1/2 is activated in non-small-cell lung cancer and associated with advanced tumours
- examination of expression of p53, p21, and phosphorylated p42/44 mitogen-activated protein kinase in human pulmonary arterial smooth muscle cells
- ERK may contribute to non-caspase-dependent pathways of injury after ER stress in SH-SY5Y human neuroblastoma cells.
- p38MAPK has a role in controlling p21WAF1 regulation on vascular smooth muscle cells along with transcription factor Sp1
- mechanical pressure-induces phosphorylation of p38 mitogen-activated protein kinase in epithelial cells via Src and protein kinase C
- p38 pathway activation selectively induces cell death in K-ras-mutated human colon cancer cells by mechanisms involving the suppression of vitamin D receptor activity
- The signal transduction pathway of VEGF transcription in HepG(2) cells may be through PI3K pathway, but not through p42/p44 MAPK pathway.
- some protease inhibitors might act as stress and induced TF expression with direct phosphorylation of JNK and p38, followed by phosphorylation and activation of AP-1 in monocytic cells
- Acute vasoconstrictor effects of insulin in skeletal muscle arterioles are mediated by activation of ERK1/2 in endothelium. This effect antagonizes insulin-induced, PI3-kinase-dependent vasodilatation in skeletal muscle arterioles.
- Lipoteichoic acid-stimulated p42/p44 MAPK phosphorylation is mediated through a TLR2 receptor and involves tyrosine kinase, PLC, PKC, Ca(2+), MEK, and PI 3-kinase.
- sustained activation of p44/42 MAPK perhaps forms the stimulatory signal induced by low TGF-beta1, whereas activation of p38 forms the inhibitory pathway
- insulin stimulates Na(+),K(+)-ATPase activity and translocation to plasma membrane in HSMCs via phosphorylation of the alpha-subunits by ERK1/2 mitogen-activated protein kinase.
- ERK1/2 and p38 MAPK have roles in suppressing apoptosis of colon cancer cells via cyclic AMP
- The character of extracellular signal-regulated kinase 2 activation, transient or sustained, acts as a signal integrator to quantify the strength of T cell receptor engagement and direct the cellular response.
- The p38 mitogen-activated protein kinase pathway is necessary for CD40L to condition dendritic cells to become competent antigen presenters to T cells, to induce strong allogeneic responses, and to expand virus-specific memory CD8+ T cell responses.
- Agonist-mediated metalloproteinase activation in C9 cells led to shedding of heparin-binding EGF (HB-EGF) and stimulation of ERK1/2 phosphorylation
- phosphorylation of p6(gag) protein by virus-associated ERK-2 is involved in the budding stage of HIV-1 life cycle
- ERK1/2 is important for ER cytoplasmic localization in breast cancer cells
- I kappa B-NF kappa B participates on ERK2-mediated survival mechanisms
- ERK2 binds to vinexin and is activated by epidermal growth factor and cell adhesion
- augmented p38 activation of CD14 monocytes associated with suppressed p38 activation of CD8 lymphocytes was found in SARS patients.
- Activation of FAK and ERK1/2 by MCSP appear to involve independent mechanisms.
- ERK1 and ERK2 play a major role in ovarian cancer pathogenesis and down-regulation of this master signaling pathway is highly effective for the inhibition of ovarian tumor growth.
- ERK 1/2- and p38 MAPK-modulated TIMP-2 expression regulates MT1-MMP activity and control TGF-beta1-induced pericellular collagenolysis
- role of ERK in the cytotoxicity mediated upon activation of the D1 dopamine receptor.
- These results suggest that bFGF can negatively modulate p38 and positively modulate ERK1/2 to antagonize activin A-mediated growth inhibition and Hb synthesis in K562 cells.
- p38 MAPK and Bcl-XL expression play critical roles in the survival of UVA-irradiated HaCaT cells
- p38 MAPK mediates gamma-irradiation-induced endothelial cell apoptosis
- Activated by Trypanosoma cruzi infections in cultured human umbilical vein endothelial and vascular smooth muscle cells
- Cystathionine gamma-lyase has a role in regulating cell proliferation via a H2S-dependent modulation of ERK1/2 phosphorylation and p21Cip/WAK-1
- Data show how the ability of receptors such as angiotensin type 1A to interact with beta-arrestin 2 determines both the mechanism of extracellular signal-regulated kinase 1 and 2 activation as well as the physiological consequences of this activation.
- Data suggest that the p38-mitogen-activated protein kinase-activated protein kinase 2 signaling pathway may be substantially involved in interferon-alpha-mediated anti-hepatitis C virus activity.
- Erk2 links extracellular signaling to centrosome dynamics by Nek2A
- SNT-2 negatively regulates ERK2 signaling activated via EGF stimulation through direct binding to ERK2
- mechanotransduction induced by hydrostatic loading especially activated ERK2; accumulation of Hsp70 was independent of ERK2 phosphorylation
- nuclear accumulation of active ERK1/2 is a discrete regulated step that can direct the function of the kinase in response to specific stimuli
- Resistin induces HASMC proliferation through both ERK 1/2 and Akt signaling pathways.
- Interleukins 2 and 15 regulate Ets1 expression via ERK1/2 and MNK1 in human natural killer cells
- The blockage of TLR-4 activation by EGCG resulted in inactivation of extracellular signal response kinase 1/2 and of nuclear factor-kappaB, the downstream molecules of TLR-4 signaling induced by H. pylori
- IL-6 release from monocytes under hyperglycemia appears to be mediated via upregulation of PKC, through p38MAPK and NF-kappaB
- Data suggest that Rit is involved in a novel pathway of neuronal development and regeneration by coupling specific trophic factor signals to sustained activation of the B-Raf/ERK and p38 MAP kinase cascades.
- a novel Ras-independent ERK1/2 activation system in which p110gamma/Raf-1/MEK1/2 and PKA/B-Raf/MEK1/2 cooperate to activate ERK1/2.
- Protein phosphatase 2A activity associated with Golgi membranes during the G2/M phase may regulate phosphorylation of ERK2.
- ERK1/2 and JNK1/2 signaling is stimulated by radiation and can promote cell cycle progression in human colon cancer cells
- Results indicate that polymyxin B induces a partial maturation of human dendritic cells through increased adhesion and activation of the IkappaB-alpha/NF-kappaB pathway, and that increased ERK1/2 activation inhibits maturation.
- the protective effect of phorbol-12-myristate-13-acetate on anchorage-independent survival of melanoma cells is partly mediated by MEK-independent activation of ERK1/2 and inactivation of downstream pro-apoptotic effector proteins
- MMP-1 expression is maintained at a low level by Cdc42 via a repression of the Rac1 and ERK1/2 pathways when cell/extracellular-matrix interactions via integrins induce cytoskeleton organization
- ERK1/2 signaling has a critical role in the regulation of BRCA1 function on controlling the G2/M checkpoint responses
- Contributes to insulin signalling upstream of nitric-oxide-dependent cyclic GMP production.
- OSBP was found to function as a cholesterol-binding scaffolding protein coordinating the activity of two phosphatases to control the extracellular signal-regulated kinase (ERK) signaling pathway
- RAS-MEK-ERK1/2 signaling pathway can sensitize cells to TRAIL-induced apoptosis by up-regulating DR4 and DR5
- DDSP (dehydroepiandrosterone-enhanced dual specificity protein phosphatase) negatively regulates the p38 mitogen-activated protein kinase pathway. [DDSP]
- Although E. histolytica strongly induced activation of ERK1/2 and p38 MAPK in neutrophils, the activation of ERK1/2, not p38 MAPK, was closely associated with ROS-mediated apoptosis
- ERK1/2 mediated GRK2 protection could be a general phenomenon as proteasome inhibition increased G protein-coupled receptor kinase 2 expression in two other cell lines, HEK293 and NIH3T3
- EGFR-dependent ERK1/2 activity in keratinocytes takes part to a homeostatic mechanism regulating inflammatory responses
- ERK2 and p38 have complementary effects in the control of platelet adhesion to collagen in a shear stress-dependent manner
- In cholesteatoma, co-expression of p21 and pERK1/2 was prominent, whereas in retro-auricular skin there was hardly any co-expression.
- activation by leptin is associated with gastric cancer cell proliferation
- These data support ROS production and p42/44 MAP kinase phosphorylation being involved in a common strain-induced signaling pathway.
- Induction of c-jun depends on activation of p38-mitogen-activated protein kinase (MAPK) by an Aryl hydrocarbon receptor-dependent mechanism.
- GIT1 has a role as a scaffold for ERK1/2 activation in focal adhesions
- a linear pathway for Nef-induced FasL expression that encompasses p38 and AP-1 has been elucidated. Furthermore, chemical inhibition of the p38 pathway attenuates HIV-1-mediated bystander killing of CD8 cells in vitro
- intracellular M. leprae activates Erk1/2 directly by p56Lck by means of a PKCepsilon-dependent and MEK-independent signaling pathway
- Flow activates ERK1/2 and endothelial nitric oxide synthase via a pathway involving PECAM1, SHP2, and Tie2.
- late sustained ERK1/2 activation plays a role in coxsackievirus B3 replication; virus infection affected several host genes through ERK1/2 activation
- Spatially separate docking sites on ERK2 regulate distinct signaling events in vivo.
- in primary fibroblasts stabilization of Ras protein by ROS and ERK1/2 amplifies the response of the cells to growth factors and in systemic sclerosis represents a critical factor in the onset and progression of the disease
- ERK activation and p21 and N-cadherin upregulation are required for genistein-induced neuronal differentiation
- Results highlight the centrosome as a site to organize phosphorylation of Cep55 by Erk2/Cdk1 and Plk1, enabling it to relocate to the midbody to function in mitotic exit and cytokinesis.
- findings suggest the ERK/MAPK and PI3K pathways may regulate VEGF expression in part through regulating the action of these repressor proteins
- activation of focal adhesion kinase is involved with the aggressive capability in pancreatic cancer through Ras/ERK signaling pathway
- PP2A ABalphaC and ABdeltaC holoenzymes function as positive regulators of Raf1-MEK1/2-ERK1/2 signaling by targeting Raf1
- A3 receptor stimulation activates p44/p42 and p38 mitogen-activated protein kinases, which are required for A3-induced increase of HIF-1alpha and Ang-2
- x-ray crystallographic structure of the human ERK2 complexed with a pyrazolo[3,4-c]pyridazine derivative
- ERK/PLD2 pathway contributes to fMLP-mediated oxidant production
- Study is the first to report ERK2 substitution mutation in a human cancer cell line which resulted in constitutive phosphorylation.
- overexpression of SphK1 up-regulated MMP1 protein, MMP1 mRNA, and MMP1 promoter activity, and this action of SphK1 required activation of the ERK1/2-Ets1 and NF-kappaB pathways
- GSK-3, acting through PKCdelta, is a negative regulator of ERK1/2
- the beta2 adrenergic receptor has a role in beta-arrestin-dependent, G protein-independent ERK1/2 activation
- Results describe the opposite effect of ERK1/2 and JNK on p53-independent p21WAF1/CIP1 activation involved in the arsenic trioxide-induced human epidermoid carcinoma A431 cellular cytotoxicity.
- Transient expression of centaurin-alpha1 in COS-7 cells results in specific activation of ERKs.
- in gastric epithelial cells, H. pylori up-regulates MMP-1 in a type IV secretion system-dependent manner via JNK and ERK1/2
- a novel signaling pathway involving MKK-2 and ERK1/2 may down-regulate the activity of PABP and eIF4E by controlling their phosphorylation and compensates for the effect of excess cellular PABP
- HSD-3.8 (SPAG1), interacts with G-protein beta 1 subunit and activates extracellular signal-regulated kinases 1 and 2
- Prostacyclin receptor up-regulates the expression of angiogenic genes in human endometrium via cross talk with epidermal growth factor Receptor and the extracellular signaling receptor kinase 1/2 pathway.
- Data show that p38 MAPK is necessary for HGF sensitization of ovarian cancer cells to low-doses of CDDP and PTX and might be sufficient to overcome activation of survival pathways.
- These results indicate that PI3K plays different roles in the activation of Ras/ERK1/2 signaling by insulin and EGF, and that insulin-stimulated, but not EGF-stimulated, ERK1/2 and Akt signalings diverge at PI3K.
- IR-induced ERK1/2 activation involves EGFR through a Src-dependent pathway that is distinct from EGFR ligand activation
- beta-arrestin and G proteins activate parathyroid hormone receptor-stimulated ERK1/2 pathways
- These findings reveal that prolonged ERK1-2/MAPK stimulation results in FADD-independent caspase 8 activation and cell death.
- dynamin has roles in the IL-5 signaling pathway and in receptor endocytosis and termination of the ERK1/2 signaling pathway
- intracellular generation of NO* by nNOS leads to S-nitrosylation of H-Ras, which interferes with Raf-1 activation and propagation of signalling through ERK1/2
- seminal plasma and PGE(2) can promote the expression of tumorigenic and angiogenic factors, in cervical adenocarcinoma cells via the EP4 receptor, EGFR, and ERK1/2 signaling pathways
- Report shows that adenosine downregulation of DPPIV of colon cancer cells is mediated by an increase in protein tyrosine phosphatase activity that leads to a decrease in the tyrosine phosphorylation of ERK1/2 MAP kinase that links to the decline in DPPIV
- As such, caveolae and caveolin-1 coordinate PDGF receptor signaling, leading to myocyte proliferation, and inhibit constitutive activity of p42/p44 MAPK to sustain cell quiescence.
- HSP25 and HSP70i activate HSF1 and have roles in inhibition of ERK1/2 phosphorylation
- data show that the HTLV-1 MA protein may be phosphorylated by cellular ERK-2 kinase and indicate that phosphorylation of L-domain-containing proteins may be a common post-translational modification required for appropriate retroviruses budding
- TNFalpha-signaling pathway mediating ERK inhibition suggesta a role for Lnk in the interplay between PI3K and ERK triggered by TNFalpha in vascular endothelial cells.
- ERK1/2 is activated by a chimeric neurokinin 1 receptor-beta-arrestin1 fusion protein
- Rho kinase, myosin-II, and p42/44 MAPK are potentially important players in different aspects of bile canalicular lumen morphogenesis.
- results strongly suggest the existence of a bidirectional molecular connection alpha(v)beta(3)-ERK1/ERK2 MAPK that would regulate breast cancer cells survival and proliferation
- LRRC4 plays a major role in suppressing U251 cell proliferation by regulating the extracellular signal-regulated kinase (ERK)/Akt/NF-kappaBp65, STAT3, and JNK2/c-Jun pathways.
- ERK5 and ERK1/2 differ in their mechanisms of gene regulation, and ERK5 may control hypoxia-responsive genes by a mechanism independent of HIF-1alpha expression control
- The authors examined downstream signaling targets to study the BMP-Smad and BMP-p38 mitogen-activated protein kinase (MAPK) pathways in FOP.
- Data show that inorganic phosphate controls cell growth by activating ERK1/2 cascades and by facilitating the translocation of Mnk1 from cytosol into nucleus through an Akt-mediated MEK pathway.
- the presence of dsRNA during viral infections and subsequent activation of p38 MAPK is a potential molecular pathway for viral induction of hemorrhagic fevers
- These results imply that ERK2 may be important for the differentiation of tubular-type cholangiocarcinoma(CCA).
- Expression and activation of ERK2 in the human endometrium was increased particularly during the secretory phase. May be induced by ovarian steroid hormones.
- CCN2 was critically involved in osteolytic metastasis and was induced by PKA- and PKC-dependent activation of ERK1/2 signaling by PTHrP.
- Results show that activation of c-Jun N-terminal protein kinase, ERKs 1 and 2, and p38 MAP kinase is critical for Hs683 glioma cell migration induced by GDNF.
- Results suggest that Dok-4, through activation of the Rap1-ERK1/2 pathway, regulates GDNF-mediated neurite outgrowth during neuronal development.
- TGF-beta1 regulates COX-2 expression in human mesangial cells through the activation of ERK1/2, p38 MAPK, and PI3K.
- Results describe the roles of MEK1/ERK and AKT/PKB pathways on the effects of granulocyte macrophage colony-stimulating factor (GM-CSF) and M-CSF on tumor progression of lung cancer.
- DAZ cannot bind simultaneously to DAZAP1 and poly(A)-binding protein (PABP), and suggest that the phosphorylation-induced dissociation of DAZ and DAZAP1 may allow the former to stimulate translation by interacting with PABP.
- Reduction of extracellular signal-regulated protein kinase phosphorylation is associated with squamous cell carcinoma of the larynx.
- Wip1 overexpression abrogates the homeostatic balance maintained through the p38-p53-Wip1 pathway, and contributes to malignant progression by inactivating wild-type p53 and p38 MAPK as well as decreasing p16 protein levels in human breast tissues.
- In 293T cells, Vaccinia Virus apparently utilizes its M2L protein to interfere with a step (s) that would otherwise enable ERK2 phosphorylation and the consequential activation of an NF-kappaBeta response.
- heterotrimeric G protein-dependent ERK1/2 activation is mediated by IGF-1 and IGF-2 by transactivating sphingosine 1-phosphate receptors
- activations of ERK1/2 promotes basal dopamine cell survival and protects dopamine cells from oxidative stress
- phosphorylation of Ser-641/643 by MAPK promotes the nuclear accumulation and transcriptional activity of hypoxia-inducible factor-1alpha by blocking its CRM1-dependent nuclear export
- The results point to an absolute requirement of enhancer-promoter communication for maintaining the active state of the HNF-4 gene and provide evidence for a molecular bookmarking mechanism.
- C-reactive protein (CRP) activates the MAP-K pathway of renal distal tubular cells (DTC). CRP upregulated RANTES expression of DTC in a significant and dose-dependent manner.
- ERK1/2 critically regulates 5-LO activity in the absence of additional downstream targets in the survival signalling preventing peroxynitrite toxicity.
- These data indicate that the muscle-type nAChR, rather than the alpha7 type, is highly expressed in NSCLC and leads to downstream activation of the p44/42 MAPK pathway
- RAS/MEK/ERK signal transduction cascade may provide a potential therapeutic approach in lymphomas and related malignancies that exhibit high levels of MCT-1 protein.
- In conclusion, we report that the transcription factor Sp1 involved in the p38MAPK-mediated control of p21WAF1 regulation on VSMC in response to BITC has now been identified.
- ERK1/2 activity is required in early G2 for a timely entry into mitosis but that it does not directly regulate cell cycle progression from late G2 through mitosis in normal or transformed mammalian cells.
- Inhibition of overactive ras-MEK-ERK pathway in HepG2 cells can correct the defect in VLDL assembly leading to the secretion of VLDL-sized particles, similar to primary hepatocytes, implicating the MEK-ERK cascade in VLDL assembly in the HepG2 model.
- phosphorylation is a mechanism for regulation of insulin receptor substrate-1/2, Akt, and ERK1/2
- apoptosis induced by cannabinoid receptor CB1 and CB2 agonists leads to activation of ERK1/2 leading to G1 cell cycle arrest in prostate cancer cells
- ERK2 uses two weak docking interactions to specifically assemble the complex, perhaps in doing so denying Ser-26 access to the active site
- inhibition of ITD/Flt3 activity did not prevent the phosphorylation of ERK, STAT5 or Akt in some primary AML cells. In parallel, in these cells, Flt3 and ERK or Akt cooperate to regulate cell survival
- These results suggest the existence of an ERK1/2-driven negative feed-back regulation of ERK5 signaling in epidermal growth factor-stimulated HK-2 cells, which is mediated by MKP-3, DUSP5 and/or MKP-1.
- Leptin and TGF-beta1 synergistically augmented activation of signalling components of mitogen-activated protein kinase (MAPK), STAT3 and Smad but did not modulate the expression of LEPR-B.
- activation of ERK1/2 in colorectal cancer may indicate aggressive tumor behavior and may constitute an independent prognostic factor; data suggest that mutations of the k-ras oncogene may induce activation of ERK1/2
- L-phenylalanine and other amino acids enhance the Ca2+o-sensitivity of calcium-channel stimulated ERK1/2 phosphorylation.
- results firmly establish that angiotensin II activates p44/42 MAPK through protein kinase C epsilon in H295R cells
- Directed trafficking of plasma membrane epidermal growth factor receptor is an essential element of signal transduction leading to p42/p44 MAP kinase activation.
- These experiments demonstrate that D(2) receptor (short splice variant, D(2S)R) stimulation increases DAT cell surface expression. Furthermore, they show that the increase in DAT function is ERK1/2-dependent but PI3K-independent.
- These results suggest that the formation of SUMO-1 foci is regulated by the MEK-ERK pathway and may induce apoptosis.
- Our results suggest that the Hedgehog and ERK1/2 pathways are important for CCA cell proliferation.
- These data imply that PARP activation following exposure to ionizing radiation is enhanced through EGFR-ERK signaling.
- These results implicate IR-induced ERK1/2 activation as an important regulator of G2/M checkpoint response to IR in MCF-7 cells.
- These results strongly suggest that hypoxia-induced apoptosis is regulated through signal transduction in which inactivation of ERK1/2 leads to activation of p38, which then triggers caspase cascade as an execution mechanism of apoptosis.
- These results suggest that in human tracheal smooth muscle cells, activation of p42/p44 MAPK, p38, and JNK pathways, at least in part, mediated through NF-kappaB, is essential for lipopolysaccharide-induced VCAM-1 gene expression.
- CDA1 induces p53- and MEK/ERK1/2 MAPK-dependent expression of p21 by acting through the p53 responsive element in the p21 promoter and this contributes to its antiproliferative activity
- Increased expression of stress-activated kinases and IKK and their phosphorylated forms in omental fat occurs in obesity.
- These data demonstrate that IGF-I induces COX-2 expression in human ovarian cancer cells, which is mediated by three parallel signaling cascades--PI3K, MAPK, and PKC pathways that differentially regulate COX-2 expression.
- phosphorylated-ERK1/2 expression was an independent predictor of complete remission achievement in adult acute lymphoblastic leukemia
- In A2780 cell line, ERK1/2 interacts with Cdc25C in interphase and phosphorylates Cdc25C in mitosis. Inhibition of ERK activation partially inhibits T48 phosphorylation, Cdc25C activation, and mitotic induction.
- Results indicated that p-ERK1/2 expression was an independent prognostic indicator for overall survival.
- The results suggest that multiple cellular signaling pathways can reactivate the virus in a genetically homogeneous cell population. Further analysis revealed that the Raf/MEK/ERK/Ets-1 pathway mediates Ras-induced reactivation.
- receptor and nonreceptor PTKs have roles in modulating H2O2-induced ERK1/2 and PKB signaling [review]
- PI3K/Akt activity strongly correlated with proliferation and invasion and p44/42 MAPK was correlated with only invasion.
- High D-glucose increases L-arginine transport and eNOS expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC.
- Fak/Src signaling to the PI3-K/Akt-1 and MEK/Erk pathways undergoes a differentiation state-specific uncoupling in enterocytes.
- KGF triggers negative feedback between ERK1/2 and AKT pathways to regulate cell proliferation/differention.
- These results demonstrate that 9-cis-Retinoic acid transduces the signal through p38 MAPK and ERK1/2 for CCR1 and CCR2 up-regulation.
- Lipid raft cholesterol regulates apoptotic cell death in prostate cancer cells through EGFR-mediated Akt and ERK pathways.
- cyclin D2 expression in normal and malignant hematopoietic cells is regulated by ubiquitin/proteasome-dependent degradation triggered by Thr280 phosphorylation by GSK3beta or p38, which is induced by inhibition of the PI3K pathway
- This review discusses the mechanisms by which activated ERK1/ERK2 regulate growth and cell cycle progression of somatic cells.
- These results suggest the existence of an activation threshold of the ERK1/2 pathway setting by Ca(2+)/CaM-dependent mechanisms, which appears to be the critical factor controlling cell survival or death decision under trophic factor withdrawal.
- Activation and phosphorylation of the extracellular signal-regulated kinase 1/2 and AKT pathways are involved in cervical adenocarcinoma metastases to pelvic lymph nodes.
- Spry2 plays a role as tumor suppressor in NSCLC by antagonizing receptor tyrosine kinase-induced signaling at different levels.
- Extracellular signal-regulated kinase-2 phosphorylates RORalpha4 in vitro
- GSTP1 contributes to doxorubicin and cisplatin resistance in osteosarcoma, which may be mediated in part by the activation of extracellular signal-regulated kinase 1/2
- administration of IL-6 could activate receptor gp80/gp130 signaling pathways including downstream extracellular signal-regulated kinase 1/2 and STAT3 phosphorylation in EPCs.
- activation of the Erk1/2 by increasing calcium concentration in the incubation medium may compensate for the loss of Akt activation
- ERK1/2-dependent dissociation of Bim(EL) from Mcl-1 and Bcl-x(L) may play a role in regulating Bim(EL) degradation
- inhibition of the p44/42-MAPK phosphorylation by high-dose acetaminophen could abolish the doxorubicin-induced cell death pathway
- The results of the present study suggest that lysophosphatidic acid (LPA), the receptor LPA(1), ERK2 and p38alpha are important regulators for prostate cancer cell invasion and thus could play a significant role in the development of metastasis.
- These results point to a pivotal role for p38 MAPK pathway during GTP-mediated erythroid differentiation of K562 cells.
- Results suggest that CTGF plays a crucial role in migratory/invasive processes in human breast cancer by a mechanism involving activation of the integrin-alphavbeta3-ERK1/2-S100A4 pathway.
- phosphorylation is inhibited by RBP4 in diabetic adipocytes
- These results suggest that inactivation of p44/42 MAPK enhances T(3)-induced GLUT5 gene expression in Caco-2 cells through increasing TRalpha-1 transactivity and binding activity to the GLUT5-TRE, probably due to de-phosphorylation of TRalpha-1.
- Short waves increase proliferation in human chondrocytes through activation of the ERK pathway.
- STI571 influence through inducing urokinase-type plasminogen activator and interleukin-8, in which the induction of early growth response-1 expression and extracellular signal-regulated kinase 1/2 phosphorylation might be involved.
- ERK1/2 is involved in monitoring actin dysfunction to control the onset of mitosis, suggesting the presence of an actin checkpoint at the G(2)/M transition in primary mammalian cells.
- The results show that Hcy activated both ERK(1/2)/p38MAPK pathway and NF-kappaB-DNA-binding activity.
- These observations raise the possibility that the GITRL-mediated inflammatory activation of macrophages is involved in the pathogenesis of inflammatory diseases.
- Leptin induces CRP expression in HCAECs via activation of the leptin receptor, increased ROS production, and phosphorylation of ERK1/2
- that endogenous IGF-1 and IGF-2 receptors can independently initiate ERK1/2 signaling and point to a potential physiologic role for IGF-2 receptors in the cellular response to IGF-2
- ERK2-mediated C-terminal serine phosphorylation of p300 was a key event in the regulation of EGF-induced keratin 16 expression.
- Connexin43 expression can be influenced by Ang II and IGF-1 through ERK and p38 pathways and may contribute to the pathogenesis of vein graft disease following coronary artery bypass grafting.
- The positive feedback loop between TOPK and ERK2 increases tumorigenesis properties of HCT116 colorectal cancer cells, and TOPK-regulated signaling may serve as a potential therapeutic target in colorectal cancer
- PKA and VEGFR2 converge at the MEK/ERK1/2 pathway to protect serum starved neuronal cells from a caspase-dependent cell death.
- IL-17 is a potent inducer of CRP expression via p38 MAPK and ERK1/2-dependent NF-kappaB and C/EBPbeta activation.
- analysis of an ERK2-catalyzed reaction that predicts initial reaction velocities under varying concentrations of ATP and substrate
- These results suggest that SKAP55 modulates signal transduction from the T cell antigen receptor to Ras by binding to RasGRP1.
- ERK expression in patients with IE was significantly increased compared with the controls. This suggested a probable role of ERK in the pathogenesis of IE.
- WNK2 is involved in the modulation of growth factor-induced cancer cell proliferation through the MEK1/ERK1/2 pathway.
- expression levels of pSTAT3, pAkt, and ERK1/2 were significantly higher in squamous cell carcinoma, Bowen's disease or basal cell carinoma than in actinic keratosis or vowenoid papulosis
- These results are evidence that the Sprouty2 mechanism of ERK inhibition is independent of Grb2 binding.
- ERK2 can regulate TPPP activity via the phosphorylation of Thr(14) and/or Ser(18) in its unfolded N-terminal tail
- neuropeptide Y has a role in prostate neoplasm growth through MAP kinase/ERK 1/2 activation [review]
- ERK1/2 signaling may be involved in the regulation of FA oxidation independently of its effects on FA uptake.
- These results establish that unlike HBx, MHBs(t) enhances TRAIL-induced hepatocyte apoptosis through a novel mechanism that involves ERK2.
- Identify novel links between the physiological state of the cell, the activation of MEK/ERK1/2 signaling, and the nucleocytoplasmic distribution of AMPK.
- Hence, our data provide the first evidence that LIV-1 mRNA is overexpressed in cervical cancer in situ and is involved in invasion of cervical cancer cells through targeting MAPK-mediated Snail and Slug expression.
- ERK1/2 functions as an alternative pathway in BMP-4 signaling in human umbilical vein endothelial cells. Capillary sprouting induced by BMP-4 is dependent on ERK phosphorylation.
- These findings provide evidence that mutations in fibronectin, induce anoikis in human squamous cell carcinoma cells by modulating integrin alpha v-mediated phosphorylation of FAK and ERK.
- In human proximal tubular cells ERK1/2 signaling represents an important component of oncostatin M inhibitory effect on N-cadherin expression.
- Streptococcus intermedius histon-like DNA binding protein (Si-HLP) stimulation induced the activation of cell signal transduction pathways, extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK).
- Cbl is not required for ERK1/2-dependent Bim(EL) turnover in fibroblasts and epithelial cells.
- A pathway comprising PKCs>Raf-1>MEK-1>ERK-1/-2 mediates the effect of gastrin on the CgA promoter, and strongly suggests that enhanced phosphorylation of Sp1 and CREB is crucial for CgA transactivation through the G protein-coupled CCK-B/gastrin receptor
- RU486 attenuates the activation of ERK1/2, decreases the expression of COX-2, and affects PGE2 production by inhibiting hCG-induced COX-2 expression.
- IL-17 induces MMP-1 in human cardiac fibroblasts directly via p38 MAPK- and ERK-dependent AP-1, NF-kappaB, and C/EBP-beta activation.
- Activated protein C may provide cytoprotective activity by activating the ERK pathway, which upregulates EGR-1 thereby suppressing the expression of TRAIL by PAR-1/S1p1 dependent but EPCR independent mechanism.
- These observations suggest that within in vivo-like conditions Src may have a leading role in the induction of sustained ERK1/2 activation through the Src/Ras/Raf pathway.
- study demonstrates that the ERK1/2 MAP kinase is markedly activated in ystic fibrosis (CF) airway epithelial cells after prolonged oxidative stress and causes an increase in both the production of IL-8 and the expression of CXCR1/2 receptors
- IL-15 but not IL-21 caused an increased phosphorylation of Shc and ERK1/2.
- Shp2E76K induces cytokine-independent survival of TF-1 cells by a novel mechanism involving up-regulation of Bcl-XL through the Erk1/2 pathway.
- IFNalpha-induced apoptosis requires activation of ERK1/2, PKCdelta, and JNK downstream of PI3K and mTOR, and it can occur in a nucleus-independent manner, thus demonstrating that IFNalpha induces apoptosis in the absence of de novo transcription.
- Our study found a direct relationship between the increasing grade of the dysplastic cervical lesions and the intensity of ERK2 staining, thus implying a role of ERK2 as an early event in cervical carcinogenesis.
- By selectively modulating the downstream effects of Spry2, Tesk1 may thus serve as a molecular determinant of the signaling outcome.
- These results indicate that MMP-9 inhibition induces apoptosis due to altered beta1-integrin expression in medulloblastoma and ERK activation plays an active role and functions upstream of NF-kappaB activation to initiate the apoptotic signal.
- Data show that activation and nuclear translocation of ERK1/2 require Cyclophilin A.
- These results suggest that coupling of Grb2 to Gab1 mediates the hepatocyte growth factor-induced strong activation of the ERK pathway, which is required for the inhibition of HepG2 cell proliferation.
- beta-arrestin2 supported protein kinase C-independent ERK1/2 activation by the AT1a rceptor
- molecular mechanisms leading to glutamate-induced proliferation by determining ERK1/2 and CREB phoshporylation in chick RPE cells in primary culture and the human-derived RPE cell line ARPE-19
- AngII activated the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), but not p38 or c-Jun NH2-terminal MAP kinases. Inhibition of ERK1/2 activation reduced the AngII-induced VEGF synthesis.
- it was shown that recognition of C. albicans filaments by neutrophils is mediated via the MEK/ERK cascade and independent of JNK or p38 activation.
- Taurine was shown to increase cell proliferation and generate an increase in [Mg2+]i accompanied by ERK 1/2 activation in human osteoblast cells.
- Calcitonin decreases ERK1/2 phosphorylation in cancer cells showing constitutive phosphorylated ERK1/2.
- Chorionic gonadotropin promotes trophoblast invasion and migration through activation of ERK and AKT signaling involving their downstream effector MMP-2.
- The production of GRO-alpha, IL-6 and IL-8 was shown to account for the ability of the HeLa cell culture medium to stimulate the migration of monocytes/macrophages, suggesting a key role for p38 MAPK and ERK1/ERK2.
- Altered osteoblast proliferation in human osteoporosis may result from dysregulation of IGF-I receptor signaling, including constitutive activation of the IRS-2/Erk signaling pathway.
- Rho kinase and ERK1/2 play more important roles than RhoA in PGE(2)-mediated migration stimulation of first-trimester trophoblasts.
- Mutational analysis of ERK2 reveals a (157)TTCD(160) motif required for recognition of caspase-9 that acts independently of the putative common docking domain
- attenuation of the Erk1/2 signaling pathway is essential for andrographolide-mediated inhibition of v-Src transformation
- These results clearly indicate that CCDC134 is a novel member of the secretory family and down-regulates the Raf-1/MEK/ERK and JNK/ SAPK pathways.
- RSVL activates the kinase-G system to counteract HP-induced ERK1/2 activation and coronary arterial proliferation
- AEA is able to decrease differentiating gene expression by increasing DNA methylation in human keratinocytes, through a p38, and to a lesser extent p42/44, mitogen-activated protein kinase-dependent pathway triggered by CB1R.
- OSBP is able to sense both membrane cholesterol and oxidized sterols and link this information to the ERK1/2 signaling pathway.
- extracellular signal-regulated kinase-2(ERK2) regulates mitochondrial membrane potential in humans lens epithelial cells
- a novel, stimulus-specific, and phosphatase-specific mechanism of ERK2 regulation in the nucleus by DUSP1, -2, and -4.
- indicate the involvement of focal adhesion kinase-dependent activation of ERK in Toll like receptor-mediated eosinophil stimulation
- processing of pre-TNF alpha in LPS-stimulated macrophages is regulated by TPL2-mediated activation of ERK1 and ERK2
- [Review] ERK2 activity generated by cytokines, free radicals or other inflammatory factors after stroke may worsen ischemic damage, whereas the ERK1/2 activity produced by exogenous growth factors, estrogen, and preconditioning favors neuroprotection.
- Concordant overexpression of p-FAK and p-ERK1/2 in extramammary Paget's disease (EMPD) is associated with the grade of malignancy of EMPD.
- Prorenin and renin-induced ERK 1/2 activation are independent of angiotensin II. The signal transduction is different from that evoked by angiotensin II.
- G2/M cell cycle arrest is induced by genistein via stable activation of ERK1/2 pathway in MDA-MB-231 breast cancer cells
- ERK1/2-mediated phosphorylation of CIITA down-regulates CIITA activity by priming it for nuclear export, thus providing a means for cells to tightly regulate the extent of antigen presentation.
- Overexpression of MSLN resulted in sustained activation of extracellular signal-regulated kinase 1/2 and suppression of Bim.
- Data show that diallyl sulfide induces apoptosis in human colon cancer cells, and that caspase-3, NF-kappaB, and ERK-2 are involved.
- The formation of an ERK.GSK3beta complex retained pERK1/2 in the cytoplasm.
- These data suggest that TNF-induces autophagy through ERK1/2 and that inhibition of autophagy increases cellular sensitivity to TNF.
- Data suggest that TPA stimulates reactive oxygen species generation as a second messenger to activate Erk1/2 via a redox-mediated inhibition of Erk1/2-directed phosphatase in ML-1 cells.
- Prostaglandin E1 inhibits IL-6-induced MCP-1 expression by interfering specifically in IL-6-dependent ERK1/2.
- Epidermal growth factor receptor signaling to Erk1/2 and STATs control the intensity of the epithelial inflammatory responses to rhinovirus infection.
- even upon over-expression DUSP6 fails to inactivate ERK5, confirming that it is indeed an ERK1/2-specific DUSP
- results show that IL-15 can improve the function of NK cells via up-regulating NKG2D expression, and also augmenting the expression of cytotoxic effector molecules and the phosphorylation of STAT1 and ERK1/2, which may also contribute the NK lysis
- Phosphorylated ERK1/2 was present in almost all tumours and p-ERK1/2 may be a prognostic marker at the invasive front of oral squamous cell carcinomas.
- Probiotic-secretory proteins protect the intestinal epithelium from hydrogen peroxide-induced insult by a PKC beta1/epsilon- and ERK1/2-dependent mechanism.
- Results highlight the importance of a high intracellular Zn(2+) content and the VHR/ZAP-70/ERK1,2-associated pathways in the modulation of LNCaP prostate cancer cell growth.
- Tissue factor pathway inhibitor prevented ERK2 phosphorylation in endothelial cells to influence angiogenesis.
- ERK1/2 as an important signaling mediator for the inhibitory effect of THP-1-MacCM on TG accumulation during 3T3-L1 adipogenesis.
- the capacity of IMP to inhibit signal propagation through Raf to MEK is a consequence of disrupting KSR1 homooligomerization and B-Raf/c-Raf hetero-oligomerization
- Data show that in airway smooth muscle cells from asthmatics, the presence of a strong proliferative stimulus (10% FBS) reduces ERK activation resulting in a shift to the PI 3-kinase pathway.
- Preeclampsia is associated with decreased activation of ERK1/2 in invasive trophoblasts in vivo.
- Pyk2/ERK 1/2 mediate Sp1- and c-Myc-dependent induction of telomerase activity by epidermal growth factor
- increased expression of ERK1 and activated p38 can predict poor human sperm quality
- Ablation of ERK2 gene expression (but not ERK1) by RNA interference significantly reduced proliferation of human mesenchymal stem cells.
- These results suggest that induction of OspF is enhanced during Shigella invasion of dendritic cells and decreases the phosphorylation level of Erk1/2.
- when HARE binds HA, that leads to activation of ERK1/2, important mediators of intracellular signal transduction.
- Results suggest that repetitive deformation stimulates intestinal epithelial motility across fibronectin in a manner that requires both Src activation and a novel Src-independent FAK-Tyr 925-dependent pathway that activates ERK.
- These data demonstrate the role of Cx43 in the proliferation and migration of human saphenous vein smooth muscle cells and angiotensin II-induced Cx43 expression via mitogen-activated protein kinases (MAPK)-AP-1 signaling pathway.
- activation of ERK1/2 is implicated in the pathobiology of glioblastoma.
- c-FLIPL promotes the motility of HeLa cells by activating FAK and ERK, and increasing MMP-9 expression.
- Data suggest that PLD2 is an early player upstream of the Ras-ERK1/2-IL-2 pathway in T-cells via phosphatidic acid and diacylglycerol production.
- the induction of inflammatory genes by farnesol is mediated by the activation of the NF-kappaB pathway and involves MEK1/2-ERK1/2-MSK1-dependent phosphorylation of p65/RelA(Ser(276))
- inflammatory levels of NO inhibit epithelial cell migration, because of suppression of ERK1/2 signaling, and activation of HIF-1alpha and p53, with potential consequences for epithelial repair and remodeling during airway inflammation
- human 14-3-3gamma binds to the ERK1/2 molecular scaffold KSR1, which is mediated by the C-terminal stretch of 14-3-3gamma
- Sphingosine kinases and sphingosine-1-phosphate are critical for transforming growth factor beta-induced ERK1 and ERK2 activation and promotion of migration and invasion of esophageal cancer cells
- ATP activated MAPKs through the P2Y2 purinoceptor/PLC/PKC/ERK signaling pathway and induced translocation of ERK1/2 into the nucleus.
- distinct phosphorylation of PKCdelta on tyrosines 64 and 187 specifically activates the Erk1/2 pathway by the down-regulation of MKP-1, resulting in the persistent phosphorylation of Erk1/2 and cell apoptosis
- The ERK-RSK1 activation by growth factors delays G2/M transition and this might be required to maintain genomic integrity during growth factor stimulation.
- the MET proto-oncogene and the downstream extracellular signal-regulated kinase 2 (ERK2) are regulated by MicroRNA miR-199a*
- Lumican induces cell migration by activating ERK 1/2 signaling and ERK 1/2 stimulates expression of integrin beta1.
- We demonstrate a role for PI3-K, p42/44 MAPK and p38 MAPK in the stimulation of cytotrophoblast cell motility by EGF.
- these data demonstrate a novel mitochondrial role for ERK in maintaining mitochondrial membrane potential and ATP production in human alveolar macrophages.
- B-Raf-initiated inactivation of Bad and Bim only partly contributes to the anti-apoptotic activities of this oncogene and that other points within the cell death machinery are also targeted by deregulated ERK signaling
- These data support a role for ERK1/2 in a postattachment step, although the precise mechanism remains under investigation.
- The absence of cytoplasmic ERK activation in poor prognosis T1-2 melanomas may be associated with activation of some other uncharacterized pathway leading to tumor progression and adverse outcome.
- ErbB2 inhibition leads to a persistent phosphorylation of ERK1/2, which negatively regulates the downstream signaling and cell growth
- Inhibition of chemotaxis by PPAR-gamma ligands correlated with decreases in extracellular signal-regulated kinase-1 and -2 activation, actin polymerization, and adherence to a fibrinogen substrate.
- These findings suggest that siRNA-mediated downregulation of MAPK1 could be an attractive strategy for cancer therapy.
- Abnormally high levels of ERK1/2 activity may be involved in endometriosis, possibly by stimulating endometrial cell survival.
- Inhibition of ERK1/2 and activation of p38 are involved in diallyl disulfide induced apoptosis of leukemia HL-60 cells.
- The human angiotensin AT(1) receptor supports G protein-independent extracellular signal-regulated kinase 1/2 activation and cellular proliferation.
- ERK1/2 phosphorylation and c-Jun expression were significantly lowered in gastric cancer compared with the non-cancer adjacent tissues.
- The increase in COX2 expression and the activation of Erk1/2 regulated by Cot are essential for the induction of cell migration.
- the Gab1-SHP2-ERK1/2 signaling pathway comprises an inhibitory axis for IGF-I-dependent myogenic differentiation.
- Erk protein is implicated in human medulloblastoma.
- an important interaction between BRCA1 and ERK1/2 in the regulation of cellular response after IR-induced DNA damage in MCF-7 cells.
- data indicate that mitochondrial localization of ERK2 activity is sufficient to recapitulate the effects of 6-OHDA on mitophagy and autophagic cell death
- Only the GERD patients without Barrett's esophagus demonstrated an acid-induced increase in ERK1/2 phosphorylation.
- ERK1/2-mediated Ser-177 phosphorylation has a role in modulating HDV antigenomic RNA replication, possibly through RNAPII regulation
- These results identify a novel signaling pathway involving Jak2-dependent Gab2 phosphorylation leading to Erk1/2 activation and cell proliferation in response to granulocyte colony-stimulating factor.
- In vascular smooth muscle cells shedding of membrane-bound epidermal growth factor (EGF) receptor ligands and activation of the nonreceptor tyrosine kinases Pyk2 and Src contributed to the thrombin-induced ERK1/2 phosphorylation.
- Histamine-induced Egr-1 expression is dependent on the activation of the H1 receptor, and rapidly and transiently activates PKCdelta, ERK1/2, p38 kinase, and JNK prior to Egr-1 induction.
- E2, a sex hormone, stimulates MUC5B gene overexpression by interaction with estrogen receptor alpha (ERalpha) and by acting through extracellular signal-regulated kinase 1/2 (ERK1/2)-mitogen-activated protein kinase (MAPK).
- Serum induction initially stimulates MKL1 nuclear localization due to a decrease in G-actin levels, but MKL1 is then downregulated by nuclear export due to ERK1/2 phosphorylation.
- germinating but not resting conidia of A. fumigatus results in interleukin (IL)-8 synthesis that is controlled by phosphatidylinositol 3-kinase, p38 MAPK, and ERK1/2. MyD88 pathway is activated by A. fumigatus and leads to NF-kappaB activation
- Myosin light-chain kinase contributes to the proliferation and migration of breast cancer cells through cross-talk with activated ERK1/2.
- DIDS-sensitive Cl- channels play a key role in the Low-density lipoprotein-induced cell proliferation of human aortic smooth muscle cells via the activation of Erk1/2 and PI3K/Akt and the upregulation of Egr-1.
- The state of activation of components of mTOR, Ras/Raf kinase/ERK, and nuclear factor (NF)-kappaB signal transduction pathways, as well as cell cycle protein analyte correlates in gastric adenocarcinoma cases, was examined.
- MAPK-containing signaling complexes are positioned on sensitive promoters with their protein substrates to modulate transcription in situ in response to incoming signals
- A 3 amino acid domain (SPS) that is phosphorylated upon stimulation to induce nuclear translocation of ERK2, is identified.
- Crystal structures for inhibitor-kinase complexes in which the inhibitor has different binding orientations and hydrogen-bonding patterns with extracellular-signal regulated kinase 2 and insulin receptor tyrosine kinase, are reported.
- regulation of ERK1/2 by MKP-3 is countered by the complex regulation of MKP-3 by ERK1/2.
- pneumolysin selectively induced expression of MKP1 via a TLR4-dependent MyD88-TRAF6-ERK pathway, which inhibited the PAK4-JNK signaling pathway,leading to up-regulation of MUC5AC mucin production
- CysLTs induce MIP-1alpha and MIP-1beta production mediated by ERK via binding to the CysLT(1) receptor in human monocytes/macrophages.
- ERK2 CD domain mutation from a human cancer cell line enhanced anchorage-independent cell growth and abnormality in Drosophila.
- IL-17F may be involved in psoriasis via, in part, the activation of ERK1/2 and the induction of IL-8 in keratinocytes
- These results indicate that intron 1 of DUSP6 plays a crucial role in transcriptional regulation of DUSP6 in a feedback loop manner responding to MAPK1 via ETS2 in human cells.
- HMGB1 induced the activation of p38MAPK, ERK1/2 and Akt.
- the craniofacial and cardiac outflow tract defects observed in patients with a distal 22q11.2 micro-deletion are explained by deficiencies in neural crest autonomous ERK2 signaling.
- TC1 was involved in the mitogen-activated ERK1/2 signaling pathway and positively regulated G(1)- to S-phase transition of the cell cycle.
- The goal of the study was to delineate the specificity of RGS proteins modulating induced ERK phosphorylation.
- these results indicate the importance of C. burnetii modulation of host signaling and demonstrate a critical role for Akt and Erk1/2 in successful intracellular parasitism and maintenance of host cell viability.
- the molecular interactions of arrestin2 and arrestin3 and their individual domains with the components of the two MAPK cascades, ASK1-MKK4-JNK3 and c-Raf-1-MEK1-ERK2
- Fast regulation of AP-1 activity through interaction of lamin A/C, ERK1/2, and c-Fos at the nuclear envelope.
- EGF induces uPAR expression via ERK-1/2, AP-1, and NF-kappaB signaling pathways and, in turn, stimulates cell invasiveness in human gastric cancer AGS cells
- Specific phosphorylation events on ERK1/2 integrate differing upstream signals to induce cardiac hypertrophy.
- PGE2 greatly induced HCC cell adhesion, migration, and invasion by activating FAK/paxillin/Erk pathway
- elevated expression of activated ERK1/2 may play a role in lung metastasis of salivary adenoid cystic carcinoma
- Data show that there are both promoter-specific and cell stage-specific roles for the ERK1/2 signaling pathway on 1,25(OH)(2)D(3)-mediated CYP24 gene induction in enterocyte-like Caco-2 cells.
- Aldosterone induces collagen synthesis via activation of extracellular signal-regulated kinase 1 and 2 in renal proximal tubules.
- CIRP enhanced extracellular signal-regulated kinase 1 and 2 (ERK1/2) phosphorylation, and treatment with an MEK inhibitor decreased the proliferation caused by CIRP.