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.
References[1] Geneste O, Bidaud C, De Vita G, Hofstra RM, Tartare-Deckert S, Buys CH, Lenoir GM, Santoro M, Billaud M. Two distinct mutations of the Ret receptor causing Hirschsprung's disease impair the binding of signalling effectors to a multifunctional docking site. Hum Mol Genet. 1999 Oct;8(11):1989-99. PMID:10484767[2] Veiga-Fernandes H, Coles MC, Foster KE, Patel A, Williams A, Natarajan D, Barlow A, Pachnis V, Kioussis D. Tyrosine kinase receptor Ret is a key regulator of Peyer's patch organogenesis. Nature. 2007 Mar 29;446(7135):547-51. Epub 2007 Feb 25. PMID: 17322904[3] Grieco M, Santoro M, Berlingieri MT, Melillo RM, Donghi R, Bongarzone I, Pierotti MA, Della Porta G, Fusco A, Vecchio G. PTC is a novel rearranged form of the Ret proto-oncogene and is frequently detected in vivo in human thyroid papillary carcinomas. Cell. 1990 Feb 23;60(4):557-63. PMID: 2406025