Product Name: KinSub1DPGYF
Product Number: PE-01AHA95
Size: 200 µg      Price:99.00
      $US
Peptide Name: KinSub1DPGYF

Product Use: For assaying the phosphotransferase activity of Insulin receptor (InsR, UniProt ID P06213). The KinSub1DPGYF peptide demonstrated very 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: KinSub1DPGYF 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: GGGGDPGYFCVGGGW

Peptide Modifications N Terminus: Free amino
Peptide Modifications C Terminus: Amide

Peptide Molecular Mass Calculated: 1384.5 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: InsR is one of several protein kinases that can phosphorylate KinSub1DPGYF. Human InsR is a receptor protein-tyrosine kinase of 1382 amino acid length, with a predicted molecular mass of 156,319 Da. It is a member of the TK group of protein kinases in the InsR family. It is highly expressed and widely distributed in most tested human tissues. Orthologues are highly conserved in vertebrates and insects. Insulin binds to InsR to trigger autophosphorylation at many sites, including Y999, S1001, Y1185, Y1189, Y1190, S1332, S1333, Y1355, Y1361 and T1375, which increases its kinase activity. Protein interactions are induced with phosphorylation of Y999 (with SOCS3) and Y1185, Y1189 and Y1190 (with IRS2 and PTP1B). Binding of insulin to the InsR stimulates glucose uptake (1). Insulin receptor signalling helps to maintain fuel homeostasis and prevent diabetes. InsR signaling also increases the regeneration of adult beta-cells and the central control of nutrient homeostasis (2). InsR has also been linked with the development of insulin resistance, familial hyperinsulinemic hypoglycemia Type 5 (HHF5), and gastric adenocarcinomas.
References

[1] Okamoto H, Nakae J, Kitamura T, Park BC, Dragatsis I, Accili D. Transgenic rescue of insulin receptor-deficient mice. J Clin Invest. 2004 Jul;114(2):214-23. PMID:15254588

[2] Lin X, Taguchi A, Park S, Kushner JA, Li F, Li Y, White MF. Dysregulation of insulin receptor substrate 2 in beta cells and brain causes obesity and diabetes. J Clin Invest. 2004 Oct;114(7):908-16. PMID: 15467829