Product Name: KinSub2RPLSP
Product Number: PE-01AJZ95
Size: 200 µg      Price:99.00
      $US
Peptide Name: KinSub2RPLSP

Product Use: For assaying the phosphotransferase activity of Osaka thyroid oncogene protein-serine kinase (Tpl2); Mitogen-activated protein kinase kinase kinase 8 (COT, UniProt ID P41279). The KinSub2RPLSP peptide demonstrated high phosphotransferase activity with COT, 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: KinSub2RPLSP 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: GGRGRPLSPGKKGGG

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

Peptide Molecular Mass Calculated: 1379.6 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Peptide Recommended Enzyme: Cot (Tpl2)

Scientific Background: COT and CDK2 are one of the few protein kinases that can phosphorylate KinSub2RPLSP. Human Cot is a protein-serine/threonine kinase of 467 amino acid length, with a predicted molecular mass of 52,925 Da. It is a member of the STE group of protein kinases in the STE-Unique family. This kinase is highly expressed in most tested human tissues, but many known tissues have not apparently been tested. Orthologues of Cot are highly conserved in mammals and birds. Cot is activated by phosphorylation at S62 and T290 by IKKb. Cot is an oncogene that can activate both the MAP kinase and JNK kinase pathways, for example in response to IL1. CoT activates IkappaB kinases and induces the nuclear production of NF-kappaB. The C-terminal catalytic domain of Ksr2 associates with Cot, and Ksr2 can negatively regulates the kinase activity of Cot in vitro. Co-transfection of KSR2 with Cot in cells lead to reduced Cot-mediated ERK1/2 activation and Cot-induced IL8 production in a dose-dependent manner (1). Blockage of expression of Cot results in failure of IL1 to induce an increase in IL8 and MIP-1beta mRNA levels (2). Cot has been linked with the development of breast cancers.