Product Name: KinSub1RRDSG
Product Number: PE-01AHY95
Size: 200 µg      Price:99.00
      $US
Peptide Name: KinSub1RRDSG

Product Use: For assaying the phosphotransferase activity of Protein-serine kinase C zeta (PKCz, UniProt ID Q05513). The KinSub1RRDSG peptide demonstrated medium 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: KinSub1RRDSG 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: GFLSRRDSGYGSGGG

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

Peptide Molecular Mass Calculated: 1471.6 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: PKCz is one of several protein kinases that can phosphorylate KinSub1RRDSG. Human PKCz is a protein-serine/threonine kinase of 592 amino acid length, with a predicted molecular mass of 67,660 Da. It is a member of the AGC group of protein kinases in the PKC family, and Iota subfamily. It is moderate to highly expressed in most tested human tissues. Orthologues are highly conserved in vertebrates, including amphibians. PI 3,4,5-trisphosphate activates PKCz. Phosphorylation at Y356, T410 and T560 increases PKCz kinase activity. Phosphorylation of Y356 induces interaction with 14-3-3 to increase PKCz kinase activity and facilitate its complex formation with Raf1 to activate it. Phosphorylation of S113, S148, T179, S186, S217, S218, S262, and S520 induces interaction with 14-3-3 beta and Raf1. PKCz is found in both particulate and soluble fractions and is not activated by phorbol ester. However, overexpression of PKCz and subsequent phorbol ester treatment abolished phorbol ester-induced reduction in cell proliferation (1). Overexpression of PKCz also potentiates phorbol ester-induced mitogen-activated protein (MAP) kinase activation in a PKC-dependent manner. PKCz is an upstream modulator of p70S6K, an important regulator of cell proliferation (2). PKCz has been linked with the development of colorectal adenocarcinomas.