Human IRAK2 blocking peptide (CDBP1615)

Synthetic Human IRAK2 blocking peptide for BL

Product Overview
IRAK2 peptide ( human )
Target
IRAK2
Nature
Synthetic
Species Reactivity
Human
Tag/Conjugate
Unconjugated
Application Notes
Stable for one year.
Procedure
None
Concentration
0.2 mg/ml
Size
50 μg
Buffer
Preservative: 0.02% Sodium Azide; Constituents: 0.1% BSA, PBS. pH 7.2
Preservative
0.02% Sodium Azide
Storage
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]
Function
ATP binding; nucleotide binding; protein binding; protein heterodimerization activity; protein homodimerization activity; protein kinase activity; transferase activity, transferring phosphorus-containing groups;
Synonyms
IRAK2; interleukin-1 receptor-associated kinase 2; interleukin-1 receptor-associated kinase-like 2; interleukin-1 receptor associated kinase-2; IRAK-2; MGC150550;

Citations


Have you cited CDBP1615 in a publication? Let us know and earn a reward for your research.

Related Products


Customer Reviews


Write a review, share your experiences with others and get rewarded !
Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket
Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket

References


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

CYTOKINE

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

NATURE IMMUNOLOGY

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.

Online Inquiry

Name:
Phone: *
E-mail Address: *
Technology Interest:
Type of Organization:
Service & Products Interested: *
Project Description:
Verification code
Click image to refresh the verification code.

Online Inquiry

  Interested in larger quantities ? request a quote!
  Protocol may be improved. Please feel free to contact us to obtain the latest version.!

Ordering Information

Payment methods we support:
Invoice / Purchase Order
Credit card

OUR PROMISE TO YOU Guaranteed product quality expert customer support

Inquiry Basket