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Validated All-in-One™ qPCR Primer for MAPK3(NM_002746.2) Search again
Product ID:
HQP014855
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ERK-1, ERK1, ERT2, HS44KDAP, HUMKER1A, P44ERK1, P44MAPK, PRKM3, p44-ERK1, p44-MAPK
Gene Description:
mitogen-activated protein kinase 3
Target Gene Accession:
NM_002746.2(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 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. [provided by RefSeq].
Gene References into function
- MEK1 interacts with ERK1. This interaction is mediated via a conserved N-terminal docking site in MEK1.
- 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.
- role in acidic extracellular pH in inducing VEGF in human glioblastoma cells
- Extracellular signal-regulated kinase (ERK1 and ERK2) activation is required for GP Ibalpha-dependent endothelial cell migration.
- CD40 ligation induces macrophage IL-10 and TNF-alpha production: differential use of the PI3K and p42/44 MAPK-pathways.
- p42/44MAPK regulates baseline permeability and cGMP-induced hyperpermeability in endothelial cells
- 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
- role of activation in IGFBP-5 stimulation of growth and IGF-I secretion in intestinal smooth muscle
- Protease activity, growth factor-like and kringle domains of uPA differentially contribute to activation of p42/p44erk1,2 and p38 MAP-kinases.
- Activation of the p44 MAPK pathway contributes to the underlying mechanism of IL-12 suppression by soluble CD40 ligand.
- 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
- Eicosapentaenoic acid and docosahexaenoic acid modulate MAP kinase enzyme activity in human T-cells
- ERK1 activity ad 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 ERK1 activity and dual-phosphorylation.
- Provant Wound Closure System induces activation of p44/42 MAP kinase in normal cultured human fibroblasts
- ERK activation by cAMP does not require RAP1
- Role of ERK1 in BRCA1-induced apoptosis
- 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
- 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
- EPO induces long-lasting phosphorylation of MAPK p42/44 in vascular endothelial cells, activating signal pathways increasing the thrombogenicity of their extracellular matrices.
- expression of extracellular signal-regulated kinase, ERK1, and its relationship with clinicopathological characteristics of breast cancer
- LMP1 inhibits transforming growth factor-beta 1-mediated induction of MAPK/p21 in Epstein-barr virus infected gastric epithelial cell line GT38
- 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))
- Ubiquitylation of MEKK1 inhibits its phosphorylation of MKK1 and MKK4 and activation of the ERK1/2 and JNK pathways
- 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.
- Persistent activation of ERK1/2 by lead acetate increases nucleotide excision repair synthesis and confers anti-cytotoxicity and anti-mutagenicity.
- Helicobacter pylori-induced ERK1 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.
- NiCl2 induced that of p44/42 extracellular signal-regulated kinases, p38, and stress-activated protein kinase/c-jun N-terminal kinases.
- acute hyperglycemia-mediated mononuclear cell activation is dependent on activation of ras, p42/p44 mitogen-activated protein kinase phosphorylation, and subsequent NF-kappaB activation
- 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
- ERK1 is activated in a pathway that involves MKP1 and ubiquitin-proteasome
- 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.
- the active phosphorylated form of MAPK/ERK is aberrantly expressed in cultured and primary HD cells
- 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
- Results suggest that receptor activator of NF-kappaB ligand (RANKL) induction by high extracellular calcium might not be mediated by the G protein-coupled calcium-sensing receptor, but by the p44/42 mitogen-activated protein kinase pathway.
- Lipopolysaccharide-induced matrix metalloproteinase (MMP)-1 and MMP-9 production by monocytes is regulated by ERK1 through a mechanism involving the activation of additional MMP promoter sites via a PGE2-independent mechanism.
- ERK1 activity is regulated by p38 delta MAP kinase
- ERK1/2 signaling is regulated by B-raf in melanocytes
- Neutrophil elastase-induced PGE2 release involved activation of p44/42, but not p38, MAP kinases.
- 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.
- 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
- Alterations in MAPK pathways in part regulate peripheral microvascular dysfunction after CPB in humans.
- 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.
- agonists of PPAR alpha increased basal and insulin-stimulated PAI-1 antigen release with a mechanism involving gene transcription and requiring signaling through the ERK1/2 signaling pathway
- 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
- 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*.
- 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.
- Activities of aPKC (P<0.05) and ERK 1/2 (P=0.06), but not phosphorylation of P38 MAPK, were higher in trained than in sedentary subjects at rest.
- JCV-induced signal activates the mitogen-activated protein kinases ERK1 and ERK2 when JC virus is binding to human glial cells
- p44MAPK has a role in glucose-enhanced interleukin-6-induced VEGF165 expression
- 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
- extracellular signal-regulated kinases 1 and 2 are activated by cyclic AMP
- 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.
- ERK1 and ERK2 have roles in functional activation of estrogen receptor alpha in human tumor cells by leptin
- 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.
- The signal transduction pathway of VEGF transcription in HepG(2) cells may be through PI3K pathway, but not through p42/p44 MAPK pathway.
- 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
- LFA-1 induced the activation of src family kinases, Vav1 and p44/42 mitogen-activated protein kinase (MAPK), in human CD56+ NK cells
- The character of extracellular signal-regulated kinase 1 activation, transient or sustained, acts as a signal integrator to quantify the strength of T cell receptor engagement and direct the cellular response.
- Agonist-mediated metalloproteinase activation in C9 cells led to shedding of heparin-binding EGF (HB-EGF) and stimulation of ERK1/2 phosphorylation
- ERK1/2 is important for ER cytoplasmic localization in breast cancer cells
- 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.
- PMA-induced activations of ERK and p38 kinase are parallel events that are both required for inhibition of NO-induced death of Molt4 cells
- ERK suppresses stress-induced apoptosis downstream of mitochondrial alterations by maintaining XIAP levels and oxidants block this effect through activation of p38 and protein phosphatases
- In Helicobacter pylori-colonized gastric epithelial cells, IL-17-induced IL-8 synthesis is associated with and depends at least in part on the activation of ERK 1/2 MAP kinase.
- Activated by Trypanosoma cruzi infections in cultured human umbilical vein endothelial and vascular smooth muscle cells.
- CCL20-stimulated growth of HuH7 cells was abrogated by the inhibition of downstream signal transduction pathway mediated by p44/42 MAPK.
- 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.
- HSF1 associates with ERK1 and 14-3-3epsilon during heat shock to modulate the amplitude of the response and lead to efficient termination of HSP expression on resumption of growth conditions
- delayed and sustained ERK activation provides a survival signal to human HaCaT keratinocytes
- identified an alternatively spliced 42-kDa form of ERK1
- 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
- NF-kappaB, ERK, and GADD45beta are able to coordinate in a loop-like signaling network to defend cells against the cytotoxicity induced by ionizing radiation
- 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.
- 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
- both p38 and ERK1 are spatially regulated in different uterine regions during pregnancy/labor
- 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
- In conclusion, the ERK1/2 pathway appears to be unaffected by muscle glycogen content.
- In cholesteatoma, co-expression of p21 and pERK1/2 was prominent, whereas in retro-auricular skin there was hardly any co-expression.
- These data support ROS production and p42/44 MAP kinase phosphorylation being involved in a common strain-induced signaling pathway.
- mast cell chymase activates ERK and p38 probably through G-protein-coupled receptor, and the ERK but not p38 cascade may have a crucial role in chymase-induced migration of eosinophils
- GIT1 has a role as a scaffold for ERK1/2 activation in focal adhesions
- 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
- CBP and PCAF coactivators mediate ERK1 gene expression at both the transcriptional and post-transcriptional level
- 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
- Together, these results suggest that phosphorylation of Arix by ERK1/2 inhibits its ability to interact with target genes, and that both specificity of expression and modulation by external stimuli are monitored through the same transcription factor.
- 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
- ERK/PLD2 pathway contributes to fMLP-mediated oxidant production
- NPB and NPW (10(-6) M) stimulated tyrosine kinase (TK) and mitogen-activated PK (MAPK) p42/p44 activities in NCI-H295 cells
- 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
- Transient expression of centaurin-alpha1 in COS-7 cells results in specific activation of ERKs.
- ERK1 is capable of dimerization both in vivo and in vitro
- 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.
- 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
- Taken together, these data suggest that abnormally sustained activation of ERK in FAP may represent an early signaling cascade leading to neurodegeneration.
- MEKs regulate mitosis via all three ERK isoforms; ERK1c acts specifically in the Golgi, whereas ERK1 and 2 regulate other mitosis-related processes. Thus, ERK1c extends the specificity of the Ras-MEK cascade by activating ERK1/2-independent processes.
- 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
- 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
- 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.
- ERK1/2, JNK1/2 and p38 mapk pathways are all required for B[a]P-induced G1/S transition
- 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
- 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 results imply that ERK1 may be important for the differentiation of tubular-type cholangiocarcinoma.
- Expression and activation of ERK1 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
- Hsp90 inhibition transiently activates Src kinase and promotes Src-dependent p85 PI3K and Akt and Erk activation
- Down-regulation of MIP-1 alpha was not observed following FGFR3 inhibition in MM cells with RAS mutations implicating RAS-MAPK in MIP-1 alpha regulation
- 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
- analysis of the LLKIL motif in CXCR2, which is required for full IL-8 ligand-induced activation of Erk, Akt, and chemotaxis in HL60 cells
- 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.
- RS/MEK/ERK signal transduction cascade may provide a potential therapeutic approach in lymphomas and related malignancies that exhibit high levels of MCT-1 protein.
- 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.
- 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
- 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
- tumor samples from FMTC patients showed strong nuclear staining of phosphorylated ERK1/2 and Ser(727) STAT3; FMTC-RET mutants activate a Ras/ERK1/2/STAT3 Ser(727) pathway, which plays an important role in cell mitogenicity and transformation.
- 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.
- pneumolysin is required for up-regulation of MUC5AC mucin via TLR4-dependent activation of ERK1 in Streptococcus pneumoniae infections; IKK alpha and IKKbeta are distinctly involved in MUC5AC induction by S. pneumoniae via an ERK1-dependent mechanism
- 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.
- IL-6, via the PI3-kinase/Akt pathway leads to inhibition of the repressive kinases MAPK/pERK and GSK3beta, and this converts inactive HSF-1 to an intermediate DNA-binding form augmenting transcriptional activation in the presence of a second stressor.
- involved in ascorbic acid-induced osteoblastic differentiation during periodontic ligament cell attachment to type I collagen
- Our results suggest that the Hedgehog and ERK1/2 pathways are important for cholangiocarcinoma cell proliferation.
- 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.
- hSphK2 is phosphorylated on Ser-351 and Thr-578 by ERK1 and phosphorylation of these residues is important for EGF-stimulated migration of MDA-MB-453 cells
- 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
- 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
- In A2780 cells, 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.
- 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.
- The regulation of three major mitogen-activated protein kinases phosphorylation, ERKp44/p42, p38, and JNK, was determined. The influence of specific mitogen-activated protein kinase inhibitors on IL-1 beta protein levels during beta-endorphin stimulation
- 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.
- Proinvasive activity of BMP7 gthrough SMASD4/src -independent and ERK/Rac/JNK-dependent signaling pathways in colon cancer cells is reported.
- This review discusses the mechanisms by which activated ERK1/ERK2 regulate growth and cell cycle progression of somatic cells.
- 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.
- 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
- These results point to a pivotal role for p38 MAPK pathway during GTP-mediated erythroid differentiation of K562 cells.
- Epac1 activation in HUVEC results in ERK1/2 activation, and this protein, at least in part, mediates response to the physiologically relevant event of A(2B)AR stimulation
- ERK1/2 phosphorylation is impaired in adipocytes from patients with type 2 diabetes
- Short waves increase proliferation in human chondrocytes through activation of the ERK pathway.
- 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.
- 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
- VEGF, Ets-1, and ERK1 act synergistically in the development of diabetic retinopathy.
- Thus, the migration of human astrocytes after injury is partly initiated by activation of the MEK-ERK signalling pathway.
- IL-17 is a potent inducer of CRP expression via p38 MAPK and ERK1/2-dependent NF-kappaB and C/EBPbeta activation.
- 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.
- 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
- neuropeptide Y has a role in prostate neoplasm growth through MAP kinase/ERK 1/2 activation [review]
- 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.
- 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.
- 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.
- Hemin increased Egr-1 expression (mRNA, protein) within 30 minutes and ERK-1/2 phosphorylation and nuclear translocation within 5 minutes
- Data show that activation and nuclear translocation of ERK1/2 require Cyclophilin A.
- 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
- 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.
- Insulin-like growth factor type-I receptor-dependent phosphorylation of ERK1 can be induced by picropodophyllin.
- 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.
- Activation of protease-activated receptors but not stimulation with lipopolysaccharides leads to ERK1/2 and JNK-mediated production of IL-8.
- 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
- OSBP is able to sense both membrane cholesterol and oxidized sterols and link this information to the ERK1/2 signaling pathway.
- Our results identify a new mechanism for the disruption of architecture in epithelial acini and suggest that ERK1/2 can promote noninvasive motility in preinvasive mammary tumors.
- These data suggest that dual recruitment of FcgammaRIIIa and the IL-12R to lipid raft microdomains allows for enhanced activation of downstream signaling events that lead to IFN-gamma production.
- processing of pre-TNF alpha in LPS-stimulated macrophages is regulated by TPL2-mediated activation of ERK1 and ERK2
- [Review] ERK1 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.
- 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.
- hNUDC induced a sustained activation of the extracellular signal-regulated protein kinases-1 and -2 (ERK1/2) as well as p38 mitogen-activated kinase (p38 MAPK) pathways
- Probiotic-secretory proteins protect the intestinal epithelium from hydrogen peroxide-induced insult by a PKC beta1/epsilon- and ERK1/2-dependent mechanism.
- Tissue factor pathway inhibitor prevented ERK1 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
- 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
- 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.
- Preconditioning signaling cascade involves STAT3 activation after varepsilonPKC and ERK1/2 activation
- 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
- results suggest a novel B cell-mediated pathophysiological mechanism for the etiology of osteoporosis, which is that downregulation of ESR1 and MAPK3 in B cells regulates secretion of factors leading to altered osteoclastogenesis or osteoblastogenesis
- 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
- Rapid activation of Stat3 and ERK1/2 by nicotine modulates cell proliferation in human bladder cancer cells.
- These findings, together with observations that si-hBVR blocked activation of ERK and Elk1 by IGF1 and prevented formation of ternary complex between MEK/ERK/hBVR, define the critical role of hBVR in ERK signaling and nuclear functions of the kinase.
- 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 support a role for ERK1/2 in a postattachment step, although the precise mechanism remains under investigation.
- 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.
- 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.
- 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.
- an important interaction between BRCA1 and ERK1/2 in the regulation of cellular response after IR-induced DNA damage in MCF-7 cells.
- 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).
- These results suggest that the agonist-induced H2R internalization and ERK1/2 activation are partially dynamin-dependent. Furthermore, ERK1/2 activation via H2R is likely dependent of the endocytotic process rather than dynamin itself.
- 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
- regulation of ERK1/2 by MKP-3 is countered by the complex regulation of MKP-3 by ERK1/2.
- IL-17F may be involved in psoriasis via, in part, the activation of ERK1/2 and the induction of IL-8 in keratinocytes
- ERalpha-phospho-Ser118 may be important in leiomyoma growth and is possibly phosphorylated by phospho-p44/42 MAPK.
- HMGB1 induced the activation of p38MAPK, ERK1/2 and Akt.
- 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 characteristic structural features in both the C-helix and the activation loop likely contribute to the basal activity of the mono-phosphorylated ERK1.
- the enhanced ability of tumor-derived LMP1 to induce and stabilize the c-Fos oncogene can be localized to two amino acids in the C terminus of LMP1
- 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
- KV11 peptide (from human Apolipoprotein A) suppresses angiogenesis and tumor progression by targeting the c-Src/ERK signaling pathways in VEGF induced cells
- Specific phosphorylation events on ERK1/2 integrate differing upstream signals to induce cardiac hypertrophy.
- 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.