Product Name: KinSub1RILSP
Product Number: PE-01AHR95
Size: | 200 µg | | Price: | 99.00 |
| | | $US | |
Peptide Name: KinSub1RILSP
Product Use: For assaying the phosphotransferase activity of nterleukin-1 receptor-associated kinase 3 (IRAK3, UniProt ID Q9Y616). The KinSub1RILSP peptide demonstrated low phosphotransferase activity with IRAK3, and exhibited very high specificity when assayed with over 200 other protein kinases. A listing of other kinases that show appreciable phosphotransferase activity towards this peptide are listed in Table 1.
Peptide Production Method: Solid-phase peptide synthesis
Peptide Origin: KinSub1RILSP was originally identified using a microarray with peptides that were predicted as optimal substrates for 500 human protein kinases with a proprietary algorithm developed at Kinexus with our academic partners.
Peptide Sequence: GGRSRILSPRGGGGY
Peptide Modifications N Terminus: Free amino
Peptide Modifications C Terminus: Amide
Peptide Molecular Mass Calculated: 1488.7 Da
Peptide Purity Percent after Synthesis and Purification: >95
Peptide Appearance: White powder
Peptide Form: Solid
Storage Conditions: -20°C
Peptide Recommended Enzyme: IRAK3
Scientific Background: IRAK3 is one of several protein kinases that can phosphorylate KinSub1RILSP. Human IRAK3 is a protein-serine/threonine kinase of 596 amino acid length, with a predicted molecular mass of 67,753 Da. It is a member of the TKL group of protein kinases in the IRAK family. IRAK3 is primarily expressed in monocytes and macrophages and functions as a negative regulator of Toll-like receptor signaling (1). IRAKM mediates critical aspects of innate immunity that result in an immunocompromised state during sepsis (2). Mutations in IRAK3 are associated with a susceptibility to asthma.
References[1] del Fresno C, Otero K, Gómez-García L, González-León MC, Soler-Ranger L, Fuentes-Prior P, Escoll P, Baos R, Caveda L, García F, Arnalich F, López-Collazo E. Tumor cells deactivate human monocytes by up-regulating IL-1 receptor associated kinase-M expression via CD44 and TLR4. J Immunol. 2005 Mar 1;174(5):3032-40. PMID: 15728517.[2] Deng JC, Cheng G, Newstead MW, Zeng X, Kobayashi K, Flavell RA, Standiford TJ. Sepsis-induced suppression of lung innate immunity is mediated by IRAK-M. J Clin Invest. 2006 Sep;116(9):2532-42. PMID: 16917541.