Human IRAK2 blocking peptide (CDBP1615)

Synthetic Human IRAK2 blocking peptide for BL

Product Overview
IRAK2 peptide ( human )
Species Reactivity
Application Notes
Stable for one year.
0.2 mg/ml
50 μg
Preservative: 0.02% Sodium Azide; Constituents: 0.1% BSA, PBS. pH 7.2
0.02% Sodium Azide
Upon Receipt - Keep as concentrated solution. Aliquot and store at -20℃ or below. Avoid freeze-thaw cycles.
UniProt ID
Antigen Description
IRAK2 encodes the interleukin-1 receptor-associated kinase 2, one of two putative serine/threonine kinases that become associated with the interleukin-1 receptor (IL1R) upon stimulation. IRAK2 is reported to participate in the IL1-induced upregulation of NF-kappaB. [provided by RefSeq, Jul 2008]
ATP binding; nucleotide binding; protein binding; protein heterodimerization activity; protein homodimerization activity; protein kinase activity; transferase activity, transferring phosphorus-containing groups;
IRAK2; interleukin-1 receptor-associated kinase 2; interleukin-1 receptor-associated kinase-like 2; interleukin-1 receptor associated kinase-2; IRAK-2; MGC150550;


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Microbial cell components induced tolerance to flagellin-stimulated inflammation through Toll-like receptor pathways in intestinal epithelial cells


Authors: Li, Nan; Quidgley, Maria C.; Kobeissy, Firas H.; Joseph, Jessica; Neu, Josef

In the intestine, bacterial components activate innate responses that protect the host. We hypothesize that bacterial components reduce Interleukin-8 (IL-8) production in intestinal epithelial cells stimulated by flagellin via the Toll-like receptor (TLR) signaling pathway. Caco-2 cells were pretreated with various doses of lipopolysaccharide (LPS), lipoteichoic acid (LTA), or low-dose flagellin (LDFL) for 24 h. Cells were then treated with flagellin (FL) 500 ng/ml (HDFL) for another 48 h. IL-8 production was measured in the cell culture medium by ELISA. Eighty-four genes in the TLR pathway were evaluated by RT Profiler PCR Array. Pathway Studio 8.0 software was used for altered pathway analysis. HDFL induced IL-8 production by 19-fold (p < 0.01). Pretreatment with LDFL at 20, 10 or 1 ng/ml reduced HDFL-induced IL-8 production by 61%, 52% and 40%, respectively (p < 0.05). LPS at 50 mu g/ml decreased HDFL-induced IL-8 production by 38% (p < 0.05). HDFL up-regulated CXCL10, IL1B, IL-8, IRAK2, NF-kappa B1 and I-kappa B (all p < 0.05). Pathway Studio analysis showed that HDFL induced cell processes including inflammation, cell death and apoptosis. Pretreatment with LDFL at 10 ng/ml down-regulated FADD, FOS, MAP4K4. MyD88, TLR2, TLR3 and TNFERSF1A compared to HDFL (all p < 0.05). These down-regulated genes are integral for numerous cell functions including inflammatory response, cell death, apoptosis and infection. These results demonstrate that LPS and LDFL provoke tolerance to HDFL-induced IL-8 production. This tolerance effect was accompanied by a complex interaction of multiple genes related to inflammatory as well as other responses in the TLR pathway rather than a single gene alteration. (C) 2012 Elsevier Ltd. All rights reserved.

Notch-RBP-J signaling regulates the transcription factor IRF8 to promote inflammatory macrophage polarization


Authors: Xu, Haixia; Zhu, Jimmy; Smith, Sinead; Foldi, Julia; Zhao, Baohong; Chung, Allen Y.; Outtz, Hasina; Kitajewski, Jan; Shi, Chao; Weber, Silvio; Saftig, Paul; Li, Yueming; Ozato, Keiko; Blobel, Carl P.; Ivashkiv, Lionel B.; Hu, Xiaoyu

Emerging concepts suggest that the functional phenotype of macrophages is regulated by transcription factors that define alternative activation states. We found that RBP-J, the main nuclear transducer of signaling via Notch receptors, augmented Toll-like receptor 4 (TLR4)-induced expression of key mediators of classically activated M1 macrophages and thus of innate immune responses to Listeria monocytogenes. Notch-RBP-J signaling controlled expression of the transcription factor IRF8 that induced downstream M1 macrophage-associated genes. RBP-J promoted the synthesis of IRF8 protein by selectively augmenting kinase IRAK2-dependent signaling via TLR4 to the kinase MNK1 and downstream translation-initiation control through eIF4E. Our results define a signaling network in which signaling via Notch-RBP-J and TLRs is integrated at the level of synthesis of IRF8 protein and identify a mechanism by which heterologous signaling pathways can regulate the TLR-induced inflammatory polarization of macrophages.

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