Product Name: KinSub1FDDYY
Product Number: PE-01AHC95
Size: 200 µg      Price:99.00
      $US
Peptide Name: KinSub1FDDYY

Product Use: For assaying the phosphotransferase activity of Proto-oncogene tyrosine-protein kinase receptor Ret (Ret, UniProt ID P07949). The KinSub1FDDYY peptide demonstrated high phosphotransferase activity with Brk, and exhibited medium 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: KinSub1FDDYY 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: GGGNFDDYYGPGGGG

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

Peptide Molecular Mass Calculated: 1388.4 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: Ret is one of several protein kinases that can phosphorylate KinSub1FDDYY. Human Ret is a receptor protein-tyrosine kinase of 1114 amino acid length, with a predicted molecular mass of 124,319 Da. It is a member of the TK group of protein kinases in the Ret family. It is highly expressed and widely distributed in most tested human tissues. Orthologues are highly conserved in vertebrates, including amphibians. Ret is activated by binding one of four structurally ligands (i.e. GDNF, neurturin, artemin and persephin (1)). Autophosphorylation of S696, Y806, Y809, Y864, Y900, Y905, Y928, Y952, Y981 and Y1062 of Ret increases kinase activity. Protein interactions are induced with phosphorylation of Y981 (with Src), Y1062 (with Crk, Dok6, FRS2, Gab1, IRS1, PIK3R1, RapGEF1, Shc1 & Shc3), and Y1096 (with Grb2 & PIK3R1). Phosphorylation of Y1015 inhibits kinase activity. Ret orchestrates intestine organogenesis (2). Germline mutations of Ret cause a dominantly inherited dysgenesis of the enteric nervous system known as Hirschsprung's disease. Ret can undergo oncogenic activation by cytogenetic rearrangement (3). It is constitutively activated by point mutations in hereditary medullary thyroid carcinomas (MTCs). Multiple endocrine neoplasia type 2A (MEN 2A) is associated with two mutations of Ret (4). Ret has also been linked with congenital central hypoventilation syndrome, bladder carcinomas, and colorectal adenocarcinomas.