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Validated All-in-One™ qPCR Primer for MAP2K1(NM_002755.3) Search again
Product ID:
HQP054885
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CFC3, MAPKK1, MEK1, MEL, MKK1, PRKMK1
Gene Description:
mitogen-activated protein kinase kinase 1
Target Gene Accession:
NM_002755.3(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 dual specificity protein kinase family, which acts as a mitogen-activated protein (MAP) kinase kinase. MAP kinases, also known as extracellular signal-regulated kinases (ERKs), act as an integration point for multiple biochemical signals. This protein kinase lies upstream of MAP kinases and stimulates the enzymatic activity of MAP kinases upon wide variety of extra- and intracellular signals. As an essential component of MAP kinase signal transduction pathway, this kinase is involved in many cellular processes such as proliferation, differentiation, transcription regulation and development. [provided by RefSeq].
Gene References into function
- A-Raf interacts with MEK1 and activates MEK1 by phosphorylation.
- MEK1 interacts with B-Raf.
- c-Raf interacts with MEK1 and activates MEK1 by phosphorylation.
- MEK1 interacts with ERK1. This interaction is mediated via a conserved N-terminal docking site in MEK1.
- 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.
- Laminin-10/11 and fibronectin differentially prevent apoptosis induced by serum removal via phosphatidylinositol 3-kinase/Akt- and MEK1/ERK-dependent pathways (Laminin 10; separate entry for Laminin 11).
- PAK1 primes MEK1 for phosphorylation by Raf-1 kinase during cross-cascade activation of the ERK pathway
- MEK1 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 MEK1 activity and dual-phosphorylation.
- Activation of a Src-dependent Raf-MEK1/2-ERK signaling pathway is required for IL-1alpha-induced upregulation of beta-defensin 2 in human middle ear epithelial cells.
- MEK1 has an activation domain that forms a hydrophobic binding pocket for enzyme inhibitor PD184352
- Ubiquitylation of MEKK1 inhibits its phosphorylation of MKK1 and MKK4 and activation of the ERK1/2 and JNK pathways
- the NH(2)-terminal end of MEK is important not only for substrate interaction but also for catalytic activity
- 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.
- the dramatic activation of an endomembrane-associated MEK1 without the corresponding activation of the MEK substrate ERK during normal G(2)/M
- Inhibition of either phosphatidylinositol 3-kinase (PI3-K) or Mek1/2 signaling pathways completely abrogated the IGF-I-induced increase in VEGF secretion and promoter activity
- serum stimulation of fibroblasts in floating matrices does not result in ERK translocation to the nucleus. In addition, there was decreased serum activation of upstream members of the ERK signaling pathway, MEK and Raf
- 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.
- Inhibition of the upstream MAPK kinase inhibited the phosphorylation of ERK; modulated the levels of Bcl-2, Mcl-1, and cFLIP; and induced G2M cell-cycle arrest or apoptosis
- Distribution of total MEK1 between Alzheimer disease[AD] and age-matched control cases was similar but increased levels of activated phospho-MEK1 were specifically localized to neuronal intracytoplasmic granular structures in severe AD
- results show that p38-mediated dephosphorylation of MEK1,2 mediates initiation of apoptosis
- constituitively activated in choroidal melanoma cell lines, independent of Ras, and regulated by B-RafV599E
- RhoA binds to the amino terminus of MEKK1 and regulates its kinase activity.
- MEK1,2 response element that mediates angiotensin II-stimulated PAI-1 promoter activation and shows that activation of this element requires Sp1 and AP-1 co-activation.
- 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-.
- Glycogen synthase kinase-3beta is tyrosine-phosphorylated by mitogen-activated protein kinase kinase 1 in fibroblasts.
- Plk3 may be a key protein kinase mediating MEK1 function in the Golgi fragmentation pathway during cell division.
- in non-transformed human colonocytes, MEK activation following flagellin/TLR5 engagement is a key modulator for NFkappaB-independent, IL-8 and MIP3alpha expression.
- Has distinct ways to contribute to a regulated ERK activity and cell cycle progression.
- Molecular cross-talk between MEK1/2 and mTOR signaling during recovery of 293 cells from hypertonic stress.
- Detailed pathway analysis revealed that BM stromal cells stimulate STAT3 via the IL-6R, and MEK1/ERK1 pathways, via IL-6R-independent mechanisms
- Arsenic trioxide and inhibitors of this enzyme my be combined as anticancer agents for acute promyelocytic leukemia.
- X-ray structures of human MEK1 and MEK2, each determined as a ternary complex with MgATP and an inhibitor to a resolution of 2.4 A and 3.2 A, respectively
- Integrin alphav controls melanoma cell survival in 3D-collagen through a pathway involving p53 regulation of MEK1 signaling.
- MEK1 facilitates ligand-initiated transcriptional activation while targeting the Ah receptor for degradation
- Blockade of MEK1 by PD98059 suppresses c-Fos and Fra-1 expression and, thus, affects two counteractive signals for IL-8 mRNA.
- Selesctive inhibitors potentiate apoptosis induction by sulindac sulfide, an NSAID, suggesting a novel strategy for the prevention or treatment of colorectal cancer.
- The induction of the raf-1/MEK1 pathway blocks IGF-1-mediated intracellular neuroendocrine hormone regulation. This pathway may be a therapeutic target in gastrointestinal carcinoid tumor therapy.
- whereas MAPKK-1 signaling is required for VEGF synthesis only and PI3K activation activity was lowered in hypoxia.
- RAS-MEK-ERK1/2 signaling pathway can sensitize cells to TRAIL-induced apoptosis by up-regulating DR4 and DR5
- Cdc2 inhibits growth factor receptor-mediated ERK activation during mitosis by primarily targeting signaling proteins that are upstream of MEK1
- The ability of constitutively-active human MEK1 to stimulate ERK phosphorylation and to induce the neoplastic transformation of NIH 3T3 cells required the integrity of the D-site was found.
- results suggest that activated JNK can, in turn, activate not only jun but also raf that, in turn, activates MEK that can then cross-activate JNK in a positive feedback loop
- PP2A ABalphaC and ABdeltaC holoenzymes function as positive regulators of Raf1-MEK1/2-ERK1/2 signaling by targeting Raf1
- findings demonstrate that heterogeneous de novo missense mutations in three genes within the mitogen-activated protein kinase pathway, BRAF, MEK1 and MEK2 cause cardio-facio-cutaneous syndrome
- 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.
- REVIEW. surprises yielded by the analysis of the role of B-Raf and Raf-1 and of their downstream effectors using conditional knockouts
- A novel method of activating AtMPK proteins by fusion to a cis-acting mutant of a human MAPK kinase MEK1 was used to confirm that specific members of the AtMPK gene family can activate the RD29A stress pathway.
- Taxotere and MEK1/2 inhibitors have the potential to suppress mammary tumor growth in vivo.
- 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.
- Our data suggest that overexpression of TNFalpha leads to topical GC insensitivity by reducing GR nuclear translocation in keratinocytes.
- MEK1 exports PPARgamma from the nucleus, and this finding was supported by small interfering RNA knockdown of MEK1 and use of a cell-permeable interaction-blocking peptide, which prevented tetradecanoyl phorbol acetate-induced export of PPARgamma.
- MEK1 plays an in vivo role in Golgi reorganization, which regulates cell cycle progression.
- Further studies confirm that promoter activity correlates with protein expression by demonstrating reduced SMAD3 protein expression in A549 cells and airway smooth muscle cells after treatment with MEK1 inhibitors.
- allosteric inhibitors have a dynamic range in the type of MEK1 activation states and nucleotide complexes that they can bind.
- mutational analysis of KRAS, BRAF, and MAP2K1/2 in 56 patients with CFC syndrome; comparison of the genotype-phenotype correlation of CFC with that of Costello syndrome suggest a significant clinical overlap but not genotype overlap.
- Mek1/2 are functionally redundant in the epidermis, where they act as a linear relay in the MAPK pathway to mediate development and homeostasis.
- These results indicated that the activation of CXCR4 and its signaling pathways (MEK1/2 and Akt) are essential for CXCL12-induced cholangiocarcinoma cell invasion.
- analysis of the ATPase activity of phospho-MEK-1 uncoupled from downstream ERK phosphorylation
- WNK2 is involved in the modulation of growth factor-induced cancer cell proliferation through the MEK1/ERK1/2 pathway.
- 3 novel mutations for MEK1 (E44G, T55P, D67N) were found in cardio-facio-cutaneous syndrome. A novel mutation in exon 2 was found in Noonan syndrome.
- modulation of phosphatidylinositol 3-kinase/Akt/GSK3beta signaling cascades can be beneficial for protecting or facilitating recovery from cellular LeTx intoxication in cells that depend on basal MEK1 activity for proliferation.
- study reports data concerning the biochemical functions of novel MEK1 and MEK2 mutants found in patients with cardio-facio-cutaneous syndrome, as well as the roles of these genes in the MAPK signaling cascade
- the results of HRAS, BRAF and MAP2K1/2 mutation screening in a large cohort of patients with CS and CFC
- BRAF and MEK1/2 mutations may be more common than anticipated in ovarian cancer which could have important implications for treatment of patients with this disease and suggests potential new therapeutic avenues
- Has a role in epithelial cell proliferation and lung remodeling after toxic injury.
- Phase I trial of MEK1/2 inhibitor AZD6244 in tumor patients.
- study describes the biochemical characterization of novel BRAF and MEK germline mutations in cardio-facio-cutaneous syndrome
- 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))
- MEK1/ERK regulation of GRASP55-mediated Golgi linking is a control point in cell cycle progression
- MEK1 is the critical isoform regulating tumor cell proliferation in vitro and in vivo.
- WNK2 controls a RhoA-mediated cross-talk mechanism that regulates the efficiency with which MEK1 can activate ERK1/2 upon growth factor stimulation.
- Esophageal cells from GERD patients with Barrett's esophagus have elevated MEK1 phosphorylation and decreased MEK1/MEK2 activity.
- analysis of the MEK1 mutation in lung adenocarcinoma
- 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
- MEK1 & MEK2 isoforms have similar transforming properties & are able to induce formation of metastatic intestinal tumors in mice; results suggest MEK2 plays a more important role than MEK1 in sustaining proliferation of human colorectal cancer cells