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.
References[1] Hoe HS, Minami SS, Makarova A, Lee J, Hyman BT, Matsuoka Y, Rebeck GW. Fyn modulation of Dab1 effects on amyloid precursor protein and ApoE receptor 2 processing. J Biol Chem. 2008 Mar 7;283(10):6288-99. Epub 2007 Dec 18. PMID: 18089558[2] Semba K, Nishizawa M, Miyajima N, Yoshida MC, Sukegawa J, Yamanashi Y, Sasaki M, Yamamoto T, Toyoshima K. yes-related protooncogene, syn, belongs to the protein-tyrosine kinase family. Proc Natl Acad Sci U S A. 1986 Aug;83(15):5459-63. PMID: 3526330[3] Li W, Lee J, Vikis HG, Lee SH, Liu G, Aurandt J, Shen TL, Fearon ER, Guan JL, Han M, Rao Y, Hong K, Guan KL. Activation of FAK and Src are receptor-proximal events required for netrin signaling. Nat Neurosci. 2004 Nov;7(11):1213-21. Epub 2004 Oct 17. PMID: 15494734 [4] Ban K, Gao Y, Amin HM, Howard A, Miller C, Lin Q, Leng X, Munsell M, Bar-Eli M, Arlinghaus RB, Chandra J. BCR-ABL1 mediates up-regulation of Fyn in chronic myelogenous leukemia. Blood. 2008 Mar 1;111(5):2904-8. Epub 2008 Jan 7. PMID: 18180382