Product Name: KinSub1RRMYV
Product Number: PE-01AJM95
Size: 200 µg      Price:99.00
      $US
Peptide Name: KinSub1RRMYV

Product Use: For assaying the phosphotransferase activity of ErbB2 (Neu) receptor-tyrosine kinase (UniProt ID P04626). The KinSub1RRMYV peptide demonstrated high phosphotransferase activity with TXK, and exhibited very 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: KinSub1RRMYV 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: GGRSRRMYVCPGGGG

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

Peptide Molecular Mass Calculated: 1508.8 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Peptide Recommended Enzyme: TXK

Scientific Background: ErbB2 is one of several protein kinases that can phosphorylate KinSub1RRMYV. Human ErbB2 (also known as HER2 and Neu) is a receptor protein-tyrosine kinase of 1255 amino acid length, with a predicted molecular mass of 137,910 Da. It is a member of the TK group of protein kinases in the EGFR family. It is highly expressed and widely distributed in most tested human tissues except in the brain and spinal cord, where it is more moderately expressed. Orthologues are highly conserved in vertebrates, including amphibians. ErbB2 is activated by heregulin (HRG), which induces heterodimerization with other ErbB receptors. Protein interaction is induced with phosphorylation of Y1139 (with Grb2, Grb7 & Src), Y1196 (with Crk), and Y1222 (with CGI-27, Grb2 & Shc1). Phosphorylation of Y1112 induces interaction with Cbl, which promotes ErbB2 degradation. Overexpression of unaltered ErbB2 coding sequences in NIH-3T3 cells results in cellular transformation and tumorigenesis (1). ErbB2 is amplified in about 30% of primary human breast malignancies and overexpression of ErbB2 is associated with the most aggressive tumours that show uncontrolled proliferation, resistance to apoptosis and increased motility (2). ErbB2 has also been linked with the development of ovarian cancer, gastric and lung adenocarcinomas, and glioblastomas.