Product Name: KinSub2DDNYV
Product Number: PE-01AJX95
Size: 200 µg      Price:99.00
      $US
Peptide Name: KinSub2DDNYV

Product Use: For assaying the phosphotransferase activity of Ephrin type-A receptor 2 protein-tyrosine kinase (EphA2, UniProt ID P29317). The KinSub2DDNYV peptide demonstrated very high phosphotransferase activity with Brk, and exhibited 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: KinSub2DDNYV 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: GGGEDDNYVGGGGHG

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

Peptide Molecular Mass Calculated: 1346.3 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Peptide Recommended Enzyme: Brk

Scientific Background: EphA2 is one of several protein kinases that can phosphorylate KinSub2DDNYV. Human EphA2 is a receptor protein-tyrosine kinase of 976 amino acid length, with a predicted molecular mass of 108266 Da. It is a member of the TK group of protein kinases in the Eph family. This kinase is moderate to highly expressed in most tested human tissues. Orthologues of EphA2 are highly conserved in vertebrates, including amphibians. EphA2 is activated by binding ephrin-A1, A2, A3, A4 or A5. Phosphorylation of Y735 increases phosphotranserase activity and interaction with PIK3R1. EphA2 is a member of the ephrin receptor subfamily of protein-tyrosine kinases that bind the ephrin-A ligand and have diverse cellular functions. EphA2 has been linked with the development of cataract -cortical age-related type 2 (ARCC2), as well as diverse cancers of the breast, cervical, gastric, lung, ovary and cervix. .EphA2 is overexpressed in several human cancer types and promotes malignancy through a mechanism involving RhoA-dependent destabilization of adherens junctions (1). EphA2 overexpression induces a FAK-dependent increase in MMP-2 expression and invasiveness and this process that can be reversed by ligation of EphA2 (2).
References

[1] Fang WB, Ireton RC, Zhuang G, Takahashi T, Reynolds A, Chen J. Overexpression of EphA2 receptor destabilizes adherens junctions via a RhoA-dependent mechanism. J Cell Sci. 2008 Feb 1;121(Pt 3):358-68. Epub 2008 Jan 15. PMID: 18198190

[2] Duxbury MS, Ito H, Zinner MJ, Ashley SW, Whang EE. Ligation of EphA2 by Ephrin A1-Fc inhibits pancreatic adenocarcinoma cellular invasiveness. Biochem Biophys Res Commun. 2004 Aug 6;320(4):1096-102. PMID: 15249202