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Validated All-in-One™ qPCR Primer for MAP3K7(NM_003188.3) Search again
Product ID:
HQP017891
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CSCF, FMD2, MEKK7, TAK1, TGF1a
Gene Description:
mitogen-activated protein kinase kinase kinase 7
Target Gene Accession:
NM_003188.3(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 serine/threonine protein kinase family. This kinase mediates the signaling transduction induced by TGF beta and morphogenetic protein (BMP), and controls a variety of cell functions including transcription regulation and apoptosis. In response to IL-1, this protein forms a kinase complex including TRAF6, MAP3K7P1/TAB1 and MAP3K7P2/TAB2; this complex is required for the activation of nuclear factor kappa B. This kinase can also activate MAPK8/JNK, MAP2K4/MKK4, and thus plays a role in the cell response to environmental stresses. Four alternatively spliced transcript variants encoding distinct isoforms have been reported. [provided by RefSeq].
Gene References into function
- Interleukin-1 (IL-1) receptor-associated kinase-dependent IL-1-induced signaling complexes phosphorylate TAK1 and TAB2 at the plasma membrane and activate TAK1 in the cytosol.
- TAK1-dependent activation of AP-1 and c-Jun N-terminal kinase by receptor activator of NF-kappaB.
- The TAK1-TAB1 fusion protein is a novel constitutively active mitogen-activated protein kinase kinase kinase that stimulates AP-1 and NF-kappaB signaling pathways
- TNFalpha activation of the NF-kappaB pathway is associated with the inducible binding of TAK1 to TRAF2 and both IKKalpha and IKKbeta
- TAK1- and MKK3-mediated activation of p38 are facilitated by Smad7
- Pellino2 interacts with TAK1 and activates the MAP kinase pathway.
- TAK1 has a role in TNF-alpha induced IKK phosphorylation of NF-kappaB p65
- Results indicate that dominant negative constructs of TAK1 retain the ability to intercept the TGF-beta signaling effectively.
- TAB1 participates in a SAPK2a/p38alpha-mediated feedback control of TAK1
- Tak1 has a role in Wnt signal transduction and phosphorylation and inhibition of TCF
- TAK1 protein kinase mediate IKK activation by BCL10 and MALT1. RNAi-mediated silencing of TAK1 suppressed TCR-dependent IKK activation and interleukin-2 production in T cells
- TAK1 binds with Sef, which has a role in JNK activation and apoptosis
- characterized the molecular mechanisms of cellular stress-induced TAK1 activation, focusing mainly on the phosphorylation of TAK1 at Thr-187 and Ser-192 in the activation loop; TAB1 and TAB2 were differentially involved in the phosphorylation of TAK1
- Experiments using dominant-negative Tpl2 suggest this kinase functions distal to TRAFs but proximal to the TAK1/TAB1 signaling complex, within the IKK/NFkappaB activation pathway.
- STAT3 enhances the efficiency of its own Ser-727 phosphorylation by acting as a scaffold for the TAK1-NLK kinases
- interleukin-1beta and its downstream mediator TAK1 inhibit mothers against decapentaplegic homolog 3 MAD-mediated TGFbeta target gene activation
- Arachidonic acid-mediated TAK1 activation is responsible for MAP kinase kinase 6 activation and the ensuing downstream signaling in metastatic human breast carcinoma cells
- Involvement of the TAB2/TRAF6/TAK1 signalling complex in the Edar signal transduction pathway has important implications for understanding of NF-kappaB activation and anhidrotic ectodermal dysplasia in human.
- TAK1 is recruited to the TNF-R1 complex via RIP and likely cooperates with MEKK3 to activate NF-kappaB in TNF-alpha signaling
- LMP1 utilizes two distinct pathways to activate NF-kappaB: a major one through CTAR2/TRAF6/TAK1/IKKbeta (canonical pathway) and a minor one through CTAR1/TRAF3/NIK/IKKalpha (noncanonical pathway)
- TAK1 plays a critical role in T cell activation by controlling production of IL-2.
- an LMP1-associated complex containing TRAF6, TAB2, and TAK1 plays an essential role in the activation of JNK
- A candidate gene in ectodermal dysplasia.
- TAK1 is a functional member of the Snf1/AMPK kinase family
- the TAK1-JNK pathway is activated by osmotic stress, while blocking TAK1-mediated NF-kappaB activation; TAO2 regulates TAK1 pathways
- the nuclear factor-kappaB signaling pathway is inhibed by gamma-tocopherol through inhibition of receptor-interacting protein and TAK1 leading to suppression of antiapoptotic gene products and potentiation of apoptosis
- The TAB2/TAB3 interaction with TAK1 is crucial for the activation of signaling cascades mediated by interleukin-1, tumor necrosis factor, and receptor activator of nuclear factor-kappa B ligand (RANKL).
- HspB8 overload causes melanoma growth arrest and apoptosis through TAK1 activation
- HSP27 is required for both IL-1 and TNF-induced signaling pathways for which the most upstream common signaling protein is TAK1.
- Modulates TGF-beta-dependent cellular responses by targeting SnoN/SKIL for degradation, thereby allowing the activation of TGF-beta target genes.
- TAK1 is thought to play a causative role in the determination of a finite replicative lifespan of normal and cancer cells
- Study shows that Tax functions as an intracellular stimulator of an IKK-activating kinase, Tak1; in addition, Tax physically interacts with Tak1 and mediates the recruitment of IKK to Tak1.
- IHPK2-TRAF2 binding leads to attenuation of TAK1- and NF-kappaB-mediated signaling and is partially responsible for the apoptotic activity of IHPK2.
- TAK1 as a pivotal upstream kinase and potential therapeutic target to modulate synoviocyte activation in RA.
- BY acting at the level of TAK1 (MAP3K7) activation, YopJ inhibited TLR-mediated NF-kappaB and MAP kinase activation as well as IRF3 signalling.
- p38 negatively regulated TAK1 activity through TAB1 phosphorylation.
- TAK1 contributes to TGF-beta1-mediated tumor angiogenesis and metastasis via involvement of the TAK1-NF-kappaB-MMP-9 pathway.
- These signals exert their anti-inflammatory effects by inhibiting phosphorylation of TAK1
- two independent and indispensable signaling pathways-1) JAK1-associated PI3K signaling and 2) Act1/TRAF6/TAK1-mediated NF-kappaB activation-are stimulated by IL-17A to regulate gene induction in human airway epithelial cells.
- Data provide insights into the homeostatic interactions that maintain basal NF-kappaB levels by holding the enzymes MEKK3 and TAK1 in their inactive state.
- PP2A functions as a negative regulator in TGF-beta1-induced TAK1 activation
- a TAB1:TAK1:IKK beta:NF-kappaB signaling axis forms aberrantly in breast cancer cells and, consequently, enables oncogenic signaling by TGF-beta
- suggest that Pellino 3b acts as a negative regulator for IL-1 signaling by regulating IRAK degradation through its ubiquitin protein ligase activity
- TAB4 binds TAK1 and polyubiquitin chains to promote specific sites of phosphorylation in TAK1-TAB1, which activates IKK signaling to NF-kappaB.
- Phosphorylation of Thr-178 and Thr-184 in the TAK1 T-loop is required for interleukin (IL)-1-mediated optimal NFkappaB and AP-1 activation as well as IL-6 gene expression.
- TGF-beta specifically activates TAK1 through interaction of TbetaRI with TRAF6, whereas activation of Smad2 is not dependent on TRAF6.
- These results suggest that Hsp90 is required for the folding and stability of TAK1 but is displaced and no longer required when TAK1 is complexed to TAK1-binding protein-1.