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Validated All-in-One™ qPCR Primer for MAP3K1(NM_005921.1) Search again
Product ID:
HQP053966
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
MAPKKK1, MEKK, MEKK 1, MEKK1, SRXY6
Gene Description:
mitogen-activated protein kinase kinase kinase 1
Target Gene Accession:
NM_005921.1(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
MAP3K, or MEK kinase, is a serine/threonine kinase that occupies a pivotal role in a network of phosphorylating enzymes integrating cellular responses to a number of mitogenic and metabolic stimuli, including insulin (MIM 176730) and many growth factors.[supplied by OMIM].
Gene References into function
- Modulation of human cytomegalovirus immediate early gene enhancer and promoter activity by MEKK1 is under the control of the NFkappaB/rel sites.
- MEK kinase 1 induces mitochondrial permeability transition leading to apoptosis
- caspase cleavage of MEKK1 is a dynamic regulatory mechanism that alters the subcellular distribution of MEKK1, changing its function to pro-apoptotic signaling
- Fibroblast growth factor-2 induces translational regulation of Bcl-XL and Bcl-2 via a MEK-dependent pathway: correlation with resistance to etoposide-induced apoptosis
- Opposing roles of serine/threonine kinases MEKK1 and LOK in regulating the CD28 responsive element in T-cells
- Results suggest that the conserved AR acetylation site contributes to a pathway governing prostate cancer cellular survival, as AR acetylation mutants are defective in MEKK1-induced apoptosis.
- Results show that oncogenic ras provokes premature senescence by sequentially activating the MEK-ERK and MKK3/6-p38 pathways in normal, primary cells.
- the NOx-induced cell proliferation via activation of MEKK1 might contribute to lung tissue damage caused by NOx
- The difference of suppression in pancreatic cancer cells and non-pancreatic cancer cells suggested that the MEKK1 pathway mainly contributes to cell survival in pancreatic cancer cells
- mechanism by which the MEKK1-dependent JNK/SAPK pathway is negatively regulated by PAK through phosphorylation of serine 67
- Ubiquitylation of MEKK1 inhibits its phosphorylation of MKK1 and MKK4 and activation of the ERK1/2 and JNK pathways
- MEKK1 is activated by GSK3beta
- conclude that Ras regulates TNF-alpha-induced chemokine expression by activating the AP-1 pathway and enhancing transcriptional function of NF-kappaB, whereas MEKK1 activates both the AP-1 and NF-kappaB pathways
- Axin utilizes distinct regions for competitive MEKK1 and MEKK4 binding and JNK activation.
- subdomain VIII of MEKK1 is involved not only in binding to, but also in discrimination of, protein substrates
- coexpression of constitutive-active MEKK1 inhibited orphan receptor TR3 transcriptional activity and TR3-induced proliferation in lung cancer cells
- The G(i)-Ras-MEKK1 signaling pathway mediates lysophosphatidic acid-stimulated ovarian cancer cell migration by facilitating focal adhesion kinase redistribution to focal contacts.
- glutathione s-transferaase Mu suppresses MEKK1-mediated apoptosis and functions as a negative regulator of MEKK1.
- MEKK1 plays a key role in Bcr-Abl-induced STAT3 activation and in ES cells' capacity for LIF-independent self-renewal and may thus be involved in Bcr-Abl-mediated leukemogenesis in stem cells
- Galpha13-induced VASP phosphorylation that involves activation of RhoA and MEKK1, phosphorylation and degradation of IkappaB, release of PKA catalytic subunit from the complex with IkappaB and NF-kappaB, and subsequent phosphorylation of VASP
- Induction of Nur77 nuclear export by MEKK1 required a prolonged MEKK1 activation and was attenuated by Akt activation. Expression of constitutively active Akt prevented MEKK1-induced Nur77 nuclear export.
- Pge2 abolished the MEKK1-induced MMP-1 promoter luciferase activity.
- MEKK1 transmits wound signals, leading to the transcriptional activation of genes involved in Extracellular Matrix homeostasis, epithelial cell migration, and wound reepithelialization.
- Caspase-3 and the p38alpha MAP kinase were activated during TIMP-1-induced UT-7 cells erythroid differentiation.
- 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.
- 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
- Heterozygote carriers and minor allele homozygote carriers for SNP rs889312 in the MAP3K1 gene were less likely to be lymph node positive at breast cancer diagnosis (P = 0.044) relative to major allele homozygote carriers.
- reduction of upstream MEKK1 signals uncovers analogous but differential roles of JNK1 and JNK2 in a biological process
- MEK functions to enhance GCN2-dependent eIF2alpha phosphorylation rather than suppressing dephosphorylation
- Signaling pathways that augment or diminish beta-cell MEKK-1 activity may aid in the generation of novel therapeutic strategies in the treatment of type 1 diabetes.
- The differences in the effects of the FGFR2 and MAP3K1 SNPs between BRCA1 and BRCA2 carriers point to differences in the biology of BRCA1 and BRCA2 breast cancer tumors and confirm the distinct nature of breast cancer in BRCA1 mutation carriers.
- MEKK-1 mediates cytokine-induced JNK- and NF-kappaB activation, and this event is necessary for iNOS expression and cell death in pancreatic islet cells.
- The activation of TORC1 through MEKK1-mediated phosphorylation, is reported.
- IPS-1 requires TRAF6 and MEKK1 to activate NF-kappaB and mitogen-activated protein kinases that are critical for the optimal induction of type I interferons
- FGFR2 and MAP3K1 are involved in breast cancer susceptibility and confer their effects primarily in ER+ and PR+ tumors.