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Validated All-in-One™ qPCR Primer for IRAK1(NM_001569.3) Search again
Product ID:
HQP009773
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
IRAK, pelle
Gene Description:
interleukin 1 receptor associated kinase 1
Target Gene Accession:
NM_001569.3(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
This gene encodes the interleukin-1 receptor-associated kinase 1, one of two putative serine/threonine kinases that become associated with the interleukin-1 receptor (IL1R) upon stimulation.
Gene References into function
- proximal signaling molecules involved in LPS-induced NF-kappa B activation have a requisite involvement in LPS-induced apoptosis and that the pathways leading to NF-kappa B activation and apoptosis diverge downstream of IRAK-1.
- Gram-negative flagellin-induced self-tolerance is associated with a block in interleukin-1 receptor-associated kinase release from toll-like receptor 5.
- Down-regulation of the common Toll-like receptor intracellular signaling factor IRAK in vitro will lead to a state of cross-tolerance and decreased IL-1 beta and TNF-alpha production upon subsequent challenge with multiple microbial toxins.
- Identification of threonine 66 as a functionally critical residue of the protein
- In lipopolysaccharide (LPS)-tolerant monocytes IRAK-1 is not activated in response to LPS restimulation, although protein and mRNA levels remain normal or slightly up-regulated.
- association of a haplotype (196Phe/532Ser) in the interleukin-1-receptor-associated kinase (IRAK1) gene with low radial bone mineral density in two independent populations
- phosphorylates Stat1 on serine 727 in response to interleukin-1 and affects gene expression
- Pellino2 interacts with kinase-active as well as kinase-inactive IRAK1 and IRAK4
- IRAK-1 regulates its own availability as an adapter molecule by sequential autophosphorylation
- IRAK-1 is the central kinase involved in the activation of the macrophage at distant sites during septic shock
- Involvement of CD14/TLR4, CR3, and phosphatidylinositol 3-kinase in the degradation of IL-1 receptor-associated kinase in response to LPS.
- IRAK1 is essential for lipopolysaccharide-induced interleukin-10 gene expression
- study shows that PBMCs of patients with advanced gastric cancer show poor production of TNF and IL-12p40 in response to stimulation with tumor cells in vitro & this unresponsiveness is associated in some patients with diminished IRAK-1 expression in vivo
- the Hsp90.Cdc37 molecular chaperone module has a central role in interleukin-1 receptor-associated-kinase-dependent signaling by toll-like receptors
- Only LPS, not taxol, caused a dramatic decrease in IRAK1 protein levels.
- Presence of a regulated, alternative splice variant of IRAK1 that functions as a kinase-dead, dominant-negative protein adds further complexity to the variety of mechanisms that regulate Toll/IL-1 receptor signaling and subsequent inflammatory response.
- following stimulation by exogenous CD26, Tollip and IRAK-1 dissociate from caveolin-1, and IRAK-1 is then phosphorylated in the cytosol, leading to the upregulation of CD86 via activation of NF-kappaB
- Monarch-1 associates with IRAK-1 but not MyD88, resulting in the blockage of IRAK-1 hyperphosphorylation
- The critical IRAK1 role in LMP1-induced NF-kappaB activation is in mediating p65/RelA S536 phosphorylation through an effect on p38 or other p65 S536 kinases.
- Data show that IRAK-1 acts as the essential upstream adaptor that recruits BCL10 to the TLR4 signaling complex and mediates signaling to NF-kappaB through the BCL10-MALT1-TRAF6-TAK1 cascade.
- ozLDL inhibited NF-kappaB and IRAK-1-associated signaling which may impair immune function and promote apoptosis
- Death domain of IRAK-1 is a multimerization domain which mediates association towards MyD88, Tollip, Irak-4 & Irak-1.
- variation in the IRAK1 gene is associated with C-reactive protein concentration in Caucasian women in the Diabetes Heart Study
- ST2825 interfered with recruitment of IRAK1 and IRAK4 by MyD88, causing inhibition of IL-1beta-mediated activation of NF-kappaB transcriptional activity.
- kinase-inactive IRAK proteins can associate with Pellino proteins, thus excluding the possibility that their inability to regulate Pellino degradation is due to lack of association with the Pellino proteins
- Variant IRAK-1 is associated with alterations in multiple intracellular events that are likely to contribute to increased NF-kappa B activation and inflammatory responses in individuals with this commonly occurring IRAK-1 variant haplotype.
- 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.
- Constitutive association of MyD88 with IRAK1 was observed in all three of HTLV-I-transformed T cells, but not in HTLV-I-negative T cells
- Pellino isoforms may be the E3 ubiquitin ligases that mediate the IL-1-stimulated formation of K63-pUb-IRAK1 in cells, which may contribute to activation of IKKbeta and transcription factor NF-kappaB, as well as signalling pathways dependent on IRAK1/4
- SELP and IRAK1 were identified as novel SLE-associated genes with a high degree of significance, suggesting new directions in understanding the pathogenesis of systemic lupus erythematosus.
- TRAF6 is involved but with different mechanisms of IRAK-1-induced activation of NF-kappaB.
- These results suggested that the expression of IRAK-4 alone is sufficient to cause the degradation of IRAK-1; the autophosphorylation of IRAK-1 is not necessary to terminate the TLR-induced activation of NF-kappaB.
- Both cytosolic and nuclear actions of IRAK-1 participate in the activation of NF-kappaB-dependent transcriptional events.
- The sites of IRAK-1 ubiquitination were mapped to Lys134 and Lys180, and arginine substitution of these residues impaired IL-1R/TLR-mediated IRAK-1 ubiquitination.
- 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
- Significant & strong 2- & 3-locus interactions between SNPs in TOLLIP (rs4963060), TLR4 (rs6478317) & IRAK1 (rs1059703)were associated with the response to whole-cell vaccine pertussis vaccination in 490 1-yr-old children.
- TLR-ligands can render DCs tolerant with respect to TNF gene expression by a mechanism that likely involves blockade of signal transduction at the level of IRAK-1.