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Validated All-in-One™ qPCR Primer for TRAF6(NM_004620.3) Search again
Product ID:
HQP018237
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
MGC:3310, RNF85
Gene Description:
TNF receptor associated factor 6
Target Gene Accession:
NM_004620.3(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 TNF receptor associated factor (TRAF) protein family. TRAF proteins are associated with, and mediate signal transduction from members of the TNF receptor superfamily. This protein mediates the signaling not only from the members of the TNF receptor superfamily, but also from the members of the Toll/IL-1 family. Signals from receptors such as CD40, TNFSF11/RANCE and IL-1 have been shown to be mediated by this protein. This protein also interacts with various protein kinases including IRAK1/IRAK, SRC and PKCzeta, which provides a link between distinct signaling pathways. This protein functions as a signal transducer in the NF-kappaB pathway that activates IkappaB kinase (IKK) in response to proinflammatory cytokines. The interaction of this protein with UBE2N/UBC13, and UBE2V1/UEV1A, which are ubiquitin conjugating enzymes catalyzing the formation of polyubiquitin chains, has been found to be required for IKK activation by this protein. Two alternatively spliced transcript variants encoding identical proteins have been reported. [provided by RefSeq].
Gene References into function
- the novel zinc finger protein TIZ may play a role during osteoclast differentiation by modulating TRAF6 signaling activity.
- The C-terminal fragment of TRAF6 inhibits lipopolysaccharide-induced NF-kappa B nuclear translocation and c-Jun NH2-terminal kinase activation in endothelial cells.
- Results establish a major role of TRAF3 and -6 in X-linked ectodermal dysplasia receptor (XEDAR) signaling and in the process of ectodermal differentiation.
- Pellino 1 is required for interleukin-1-mediated signaling through its interaction with the interleukin-1 receptor-associated kinase 4-IRAK-tumor necrosis factor receptor-associated factor 6 complex
- direct endothelial-stimulatory role of lipopolysaccharides in initiating angiogenesis through activation of TRAF6-dependent signaling pathways.
- Pellino2 interacts with TRAF6 and activates the MAP kinase pathway.
- Transfection of differentiated discoidin domain receptor 1b (DDR1b)-overexpressing cells with dominant negative TRAF6 completely abrogates DDR1b-mediated p38 MAPK phosphorylation, indicating a critical role of TRAF6 in DDR1b-mediated p38 MAPK activation.
- TRAF6 interacts with TIR domain-containing adaptor inducing IFN-beta (TRIF) through the TRAF domain of TRAF6 and TRAF6-binding motifs found in the N-terminal portion of TRIF.
- In liver cells, IL-1 stimulates TRAF6 poly-ubiquitination
- STAT3/NF-kappaB p65 cross-talk activated by IL-1 via TRAF6.
- TRAF6 acts as a bifurcation point of the lipopolysaccharide-initiated death and survival signals in endothelial cells.
- TRAF6 ubiquitin ligase kinase mediates IKK activation by BCL10 and MALT1. RNAi-mediated silencing of TRAF6 suppressed TCR-dependent IKK activation and interleukin-2 production in T cells.
- identified a putative TRAF6 interaction site in Mal but not in MyD88 and we demonstrate that Mal can be co-immunoprecipitated with TRAF6
- TLR-mediated IFN-alpha induction requires the formation of a complex consisting of MyD88, TRAF6 and IRF7 as well as TRAF6-dependent ubiquitination.
- Data show that endogenous germinal center kinase is activated by agonists that require TRAF6 for c-Jun N-terminal kinase activation.
- oligomerization and polyubiquitination of TRAF6 induced by TIFA leads to the activation of TAK1 and IKK through a proteasome-independent mechanism
- IL-8-induced NF-kappaB activation proceeds through a TRAF2-independent but TRAF6-dependent pathway, followed by recruitment of IRAK and activation of IKK
- TRAF6 acts as a critical adapter of both the Src/ERK1/2 kinases and IkappaB kinase/NF-kappaB proinflammatory signaling pathways in monocytes and macrophages.
- p62 regulates nerve growth factor-induced NF-kappaB activation by influencing TRAF6 polyubiquitination
- 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.
- TRAF2-dependent CD40 signal transduction requires TRAF6 in nonhemopoietic cells
- 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)
- Rac1 facilitated the recruitment of Nox2 into the endosomal compartment and subsequent redox-dependent recruitment of TRAF6 to the MyD88/IL-1R1 complex.
- TRAF6 regulates cell fate decisions by inducing caspase 8-dependent apoptosis and the activation of NF-kappaB
- an LMP1-associated complex containing TRAF6, TAB2, and TAK1 plays an essential role in the activation of JNK
- NF-kappa B signaling is induced by the oncoprotein Tio through direct interaction with TRAF6.
- the interaction of IRF-8 with TRAF6 modulates TLR signaling and may contribute to the cross-talk between IFN-gamma and TLR signal pathways
- TGF-beta-activated kinase 1, TNF receptor-associated factor 6, and myeloid differentiation primary response gene (88) are important signal transducers in H. pylori-infected human epithelial cells
- A candidate gene in ectodermal dysplasia.
- TRAF6 is a critical adaptor linking two convergent signaling events; PKCtheta control of CARMA1 phosphorylation, and BCL10-dependent caspase-8 activation.
- knockdown of UL144, TRAF6 or NFkappaB by specific siRNA in infections with UL144-encoding HCMV prevents the activation of CCL22 expression
- An intact RING domain of TRAF6 is required for NF-kappaB activation and biological signaling.
- This study, for the first time, reveals a possible molecular mechanism that the initiation of the IL-17F/IL-17R signaling pathway requires the receptor ubiquitination by TRAF6.
- Inhibition of the MyD88 and TRAF6 adaptor proteins of the TLR pathway blocked not only B7-H1 expression induced by TLR ligands but also that mediated by IFN-gamma
- Sequencing of the promoter region and exons of the TRAF6 gene revealed three sequence variants, one of which was found in three affected members within one family with osteoporosis.
- These data establish a signaling cascade in which regulated Lys63-linked TRAF6 auto-ubiquitination is the critical upstream mediator of osteoclast differentiation.
- Results show that decrease in the ubiquitination of TRAF6 is YopJ-dependent and to prevent or is to remove the K63-polymerized ubiquitin conjugates required for signal transduction.
- These findings demonstrate that Trx, TRAF2, and TRAF6 regulate ASK1 activity by modulating N-terminal homophilic interaction of ASK1.
- IRAK-2 plays a more central role than IRAK-1 in TLR signaling to NFkappaB through TRAF6 ubiquitination
- MyD88, IRAK1 and TRAF6 proteins are crucial early mediators for the IL-1-induced MMP-13 regulation through MAPK pathways and AP-1 activity.
- 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.
- TRAF6-caspase-4 interaction, triggered by LPS, leads to NF-kappaB-dependent transcriptional up-regulation and secretion of important cytokines and chemokines in innate immune signaling in human monocytic cells.
- TRAF6 is involved but with different mechanisms in MyD88-induced and IRAK-induced activation of NF-kappaB and suggest that TRAF6 uses a distinctive mechanism to activate NF-kappaB depending on signals.
- TRAF6 is modified by small ubiquitin-related modifier-1, interacts with histone deacetylase 1, and represses c-Myb-mediated transactivation.
- Suggest that syntenin is a physiological suppressor of TRAF6 and plays an inhibitory role in IL-1R- and TLR4- mediated NF-kappaB activation pathways.
- signals from the IL-1 receptor segregate into at least two separate pathways at the level of IRAK1; one couples through TRAF6 to NFkappaB activation while a second utilizes a TRAF6-independent pathway that is responsible for mRNA stabilization
- In this study, the lysine selection process for TRAF6/p62 ubiquitination was examined.
- The RING domain and first zinc finger of TRAF6 coordinate signaling by interleukin-1, lipopolysaccharide, and RANKL
- the HSV U(L)37 virion structural protein can activate NF-kappaB through TRAF6.
- TRAF6 and its E3 ligase activity are required for LMP1-stimulated IRF7 ubiquitination.
- TGF-beta specifically activates TAK1 through interaction of TbetaRI with TRAF6, whereas activation of Smad2 is not dependent on TRAF6.
- Through nuclear magnetic resonance spectroscopy it has been determined that the RING domain of TRAF6 is rigid at the protein core, consistent with the functional requirement that RING domains form a binding scaffold for E2 ubiquitin conjugation enzymes.
- pneumolysin selectively induced expression of MKP1 via a TLR4-dependent MyD88-TRAF6-ERK pathway, which inhibited the PAK4-JNK signaling pathway,leading to up-regulation of MUC5AC mucin production
- These results indicate that TGF-beta activates JNK and p38 through a mechanism similar to that operating in the interleukin-1beta/Toll-like receptor pathway.
- 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
- TRAF6 and interleukin receptor-associated kinase 2 are novel binding partners for PS1, and IL-1R1 is a new substrate for presenilin-dependent gamma-secretase cleavage
- analysis of TRAF6 autoubiquitination-independent activation of the NFkappaB and MAPK pathways in response to IL-1 and RANKL