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Validated All-in-One™ qPCR Primer for MAP3K5(NM_005923.3) Search again
Product ID:
HQP011168
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ASK1, MAPKKK5, MEKK5
Gene Description:
mitogen-activated protein kinase kinase kinase 5
Target Gene Accession:
NM_005923.3(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
Mitogen-activated protein kinase (MAPK) signaling cascades include MAPK or extracellular signal-regulated kinase (ERK), MAPK kinase (MKK or MEK), and MAPK kinase kinase (MAPKKK or MEKK). MAPKK kinase/MEKK phosphorylates and activates its downstream protein kinase, MAPK kinase/MEK, which in turn activates MAPK. The kinases of these signaling cascades are highly conserved, and homologs exist in yeast, Drosophila, and mammalian cells. MAPKKK5 contains 1,374 amino acids with all 11 kinase subdomains. Northern blot analysis shows that MAPKKK5 transcript is abundantly expressed in human heart and pancreas. The MAPKKK5 protein phosphorylates and activates MKK4 (aliases SERK1, MAPKK4) in vitro, and activates c-Jun N-terminal kinase (JNK)/stress-activated protein kinase (SAPK) during transient expression in COS and 293 cells; MAPKKK5 does not activate MAPK/ERK. [provided by RefSeq].
Gene References into function
- Ask1 has a caspase-independent killing function independent of kinase activity and activable by interaction with Daxx. Induced after translocation of Daxx from the nucleus to the cytoplasm, which occurs following activation of the death receptor Fas.
- role in activating the JNK and p38 MAP kinase cascades in response to environmental stresses such as reactive oxygen species
- ASK1 binds to PKR and is involved in apoptosis signalling pathways
- Tumorigenic mutants of p53 bind to Daxx and inhibit Daxx-dependent activation of the apoptosis signal-regulating kinase 1 stress-inducible kinases and Jun NH(2)-terminal kinase.
- Type 1 insulin-like growth factor receptor (IGF-IR) signaling inhibits apoptosis through this enzyme.
- ASK1 is one of the factors involved in the caspase-independent pathway of LTbetaR-induced cell death.
- AKT2 interacts with and phosphorylates ASK1 at Ser-83 resulting in inhibition of its kinase activity and signaling down-stream of ASK1.
- These data suggest that AIP1 mediates TNF-alpha-induced ASK1 activation by facilitating dissociation of inhibitor 14-3-3 from ASK1, a novel mechanism by which TNF-alpha activates ASK1.
- glucose deprivation activates the ASK1-SEK1-JNK1-HIPK1 pathway, relocalizing Daxx from the nucleus to the cytoplasm, where Daxx binds to ASK1, and subsequently leads to ASK1 oligomerization
- results suggest that nitric oxide mediates the interferon-gamma-induced inhibition of apoptosis signal regulating kinase 1(ASK1) in L929 cells through a thiolredox mechanism
- ASK1 is regulated by reactive oxygen species through dephosphorylation at serine 967 and 14-3-3 dissociation
- apoptosis signal-regulating kinase 1 binds directly to retinoblastoma protein and has roles in apoptotic signaling and cell cycle
- ASK1 signaling is activated by PP5, which is regulated by mTOR
- apoptosis signal-regulating kinase 1 is activated by S-nitrosation of thioredoxin in the nitrogen monoxide/superoxide system
- AIP1 is a novel transducer in TNF-induced TRAF2-dependent activation of ASK1 that mediates a balance between JNK versus NF-kappaB signaling
- PP5 plays an important role in the survival of cells in a low oxygen environment by suppressing a hypoxia-induced ASK-1/MKK4/JNK signaling cascade that promotes an apoptotic response
- Taken together, our data suggested that the JNK/c-Jun signaling cascade plays a crucial role in Cd-induced neuronal cell apoptosis and provides a molecular linkage between oxidative stress and neuronal apoptosis.
- TNFalpha-induced desumoylation and cytoplasmic translocation of HIPK1 are critical in TNFalpha-induced ASK1-JNK/p38 activation
- TNFalpha-induced desumoylation and cytoplasmic translocation of HIPK1 are critical in TNFalpha-induced ASK1-JNK/p38 activation
- PKD is a critical mediator in H2O2- but not TNF-induced ASK1-JNK signaling
- Hsp90-Akt forms a complex with ASK1 and protect vascular endothelium from stress-induced apoptosis.
- ASK1 kinase is a central player upstream of p38 MAPK activation when secreted Helicobacter pylori antigen HP0175 effects induction of apopotosis in human gastric epithelial cell line AGS.
- ASK1-p38 cascade regulates the innate immunity of the skin by forming an immune barrier consisting of hBD, LL37, and TLR2 during epidermal differentiation.
- Raf-1 may mediate its anti-apoptotic function by interrupting ASK1-dependent phosphorylation of ALG-2.
- concomitant induction of E2F1 targets ASK1 and Bim by HDACIs warrants an effective activation of E2F1-dependent apoptosis in response to suberoylanilide hydroxamic acid
- E2 promoter-binding factors regulate the expression of ASK1. overexpression and RNA interference experiments support the requirement of endogenous E2F/DP (E2F dimerization partner) activity for ASK-1 expression.
- This study clearly shows the route from ROS generation by 6-OHDA to initiation of p38/JNK signalling via activation of ASK1 in the studied Parkinson disease model.
- reactive oxygen species generated by Nox4, at least in part, transmit cell survival signals through the AKT-ASK1 pathway in pancreatic cancer cells and their depletion leads to apoptosis.
- Glutathione S-transferase P1-1 attenuate TRAF2-enhanced apoptosis signal-regulating kinase 1 (ASK1) (MAP3K5)autophosphorylation
- TNF-alpha increases mitochondrial ROS and activates ASK1 in human hepaatoma cells and these TNF-alpha-induced phenomena contribute to impaired insulin signaling.
- Apoptosis signal-regulating kinase (ASK) 2 functions as a mitogen-activated protein kinase kinase kinase in a heteromeric complex with ASK1.
- TNFR2 signaling induces selective c-IAP1-dependent ASK1 ubiquitination and terminates mitogen-activated protein kinase signaling
- Current findings for the relationship between pathogenesis and ASK1-MAPK pathways.
- Binding of cyclin-dependent kinase inhibitor 1A to ASK1 requires ASK1 kinase function and may involve phosphorylation of S98
- ASK1 is activated by arsenic trioxide through reactive oxygen species accumulation and may negatively regulate apoptosis in leukemic cells without activating p38 and JNK
- TNF-induced TRAF2-RIP1-AIP1-ASK1 complex formation and for the activation of ASK1-JNK/p38 apoptotic signaling.
- These results suggest that PP2Cepsilon maintains ASK1 in an inactive state by dephosphorylation in quiescent cells, supporting the possibility that PP2Cepsilon and PP5 play different roles in H2O2-induced regulation of ASK1 activity.
- Gemin5 functions as a scaffold protein for the ASK1-JNK1 signaling module and thereby potentiates ASK1-mediated signaling events.
- ghrelin inhibits ASK1-mediated apoptosis and ASK1 activation by a mechanism involving induction of HSP70
- ASK1 expression levels can be regulated by G alpha13, at least in part via control of ASK1 ubiquitination and degradation
- These results indicate that Ask1 oxidation is required at a step subsequent to activation for signaling downstream of Ask1 after H(2)O(2) treatment.
- discusses the molecular mechanisms by which ASK1 functions in stress and immune responses and discuss the possible involvement of ASK1 in human diseases [review]
- the structure of the human ASK1 catalytic domain in complex with staurosporine
- these results indicate that activation of the ASK1/p38 MAPK/p47phox cascade plays a central role in PPD/TLR2-induced ROS generation and suggests the existence of a 'ROS/ASK1' inflammatory amplification feedback loop in monocytes/macrophages.
- present study shows that inhibition of PI3 kinase by LY294002 in THP-1 cells exposed to LPS attenuated down-regulation of ASK1 activity followed by programmed cell death
- The present study thus defines a novel role for ASK1 as a mediator of C5b-9-dependent cell injury.
- ROS-mediated activation of the ASK1-p38 MAPK pathway downstream of P2X(7) receptor is required for ATP-induced apoptosis in macrophages.
- SENP1 mediates TNF-induced desumoylation and translocation of HIPK1, leading to an enhanced ASK1-dependent apoptosis.
- PP2A and AIP1 cooperatively induce activation of ASK1-JNK signaling and vascular endothelial cell apoptosis.
- Data suggest that sequence variations of ASK1 and MAP2K6 lead to partially sex-specific changes in the levels and/or phosphorylation states of p38 and p38-regulated proteins that might contribute to the observed delaying effects in the age of onset of HD
- Data suggest that in nonapoptotic cells, endogenous ASK1 protein is normally cleaved at a number of specific sites, some of which are in the kinase domain.
- These findings suggest a negative role of Prx-1 in ASK1-induced apoptosis.
- The precursor of atrial natriuretic peptide, natriuretic peptide precursor (NPPA), physically interacts with the N-terminus of apoptosis signal-regulating kinase 1 (ASK1), negatively impacting NPPA processing and/or secretion.
- DDTD, an isoflavone derivative, induces cell apoptosis through the reactive oxygen species/apoptosis signal-regulating kinase 1 pathway in human osteosarcoma cells.
- Data show that nitric oxide derived from S-nitrosoglutathione activates ASK1 in THP-1 human myeloid macrophages, induces accumulation of HIF-1alpha protein, and induces accumulation of p53 in normal but not HIF-1alpha knockdown THP-1 cells.
- 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
- an essential role for ASK1 in cell death induced by ER stress.