Product Name: KinSub2RRGSP
Product Number: PE-01AKD95
Size: 200 µg      Price:99.00
      $US
Peptide Name: KinSub2RRGSP

Product Use: For assaying the phosphotransferase activity of Tyrosine-protein kinase ITK/TSK (UniProt ID Q08881). The KinSub2RRGSP peptide demonstrated medium phosphotransferase activity with Brk, 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: KinSub2RRGSP 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: GGRGRRGSPYVGGYY

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

Peptide Molecular Mass Calculated: 1600.8 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: ITK is one of several protein kinases that can phosphorylate KinSub2RRGSP. Human ITK is a non-receptor, protein-tyrosine kinase of 620 amino acid length, with a predicted molecular mass of 71,831 Da. It is a member of the TK group of protein kinases in the Tec family. This kinase is widely distributed from moderate to high levels in most human tissues with highest expression in bladder, lung, lymph node, spleen, stomach, thymus, tonsils and uterus. Orthologues of ITK are highly conserved in mammals and birds. Ligation of CD2, TCR or CD28 induces activation and tyrosine phosphorylation of ITK at Y512. ITK is expressed in T-cells and is important for T-cell development and activation through the antigen receptor. ITK require prior activation of Lck, ZAP70 and PI3-kinase for efficient activation (1). ITK knockout mice show multiple effects on T cell development, cytokine production and T-helper cell differentiation. T cells that lack or express mutant versions of ITK show impaired TCR-induced actin polymerization, cell polarization and regulation of the signaling events involved in cytoskeletal reorganization (2). ITK has been linked with the development of gastric adenocarcinomas, melanoma (metastatic) and lymphoproliferative syndrome ebv-associated autosomal type 1 (LPSA1).