Product Name: KinSub3DDLYY
Product Number: PE-01AKL95
Size: 200 µg      Price:99.00
      $US
Peptide Name: KinSub3DDLYY

Product Use: For assaying the phosphotransferase activity of Fyn proto-oncogene-encoded protein-tyrosine kinase (UniProt ID P06241). The KinSub3DDLYY peptide demonstrated high phosphotransferase activity with IRR, and exhibited low 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: KinSub3DDLYY 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: GGGEDDLYYNPCGGY

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

Peptide Molecular Mass Calculated: 1578.6 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Peptide Recommended Enzyme: IRR

Scientific Background: Fyn is one of several protein kinases that can phosphorylate KinSub3DDLYY. Human Fyn is a protein-tyrosine kinase of 537 amino acid length, with a predicted molecular mass of 60,762 Da. It is a member of the TK group of protein kinases in the Src family. This kinase is highly expressed and widely distributed in most tested human tissues. Orthologues of Fyn are highly conserved in vertebrates and insects. Fyn is inhibited by phosphorylation at Y531. Fyn has been shown to phosphorylate Dab1, an intracellular adaptor protein that interacts with amyloid precursor protein (APP) and apoE receptor 2 (apoEr2) (1). The interaction of Fyn and Dab1 regulates the phosphorylation, trafficking, and processing of APP and apoEr2. Fyn can interact with Fyn-binding protein and the p85 subunit of PI3K (2). It has been shown to be part of a protein complex involving DCC and FAK, which is downstream of Netrin-1, a pathway important in promoting both axonal outgrowth and axonal guidance in path finding (3). Fyn expression has been shown to be significantly increased in Chronic Myelogenous Leukemia (CML) (4). Knockdown of Fyn with shRNA slows leukemia cell growth, inhibits clonogenicity, and leads to increased sensitivity to imatinib. Fyn has also been linked with the development of lung squamous cell carcinomas (LSCC), melanomas (metastatic) and epilepsy.