Product Name: KinSub3RRGSP
Product Number: PE-01AKQ95
Size: 200 µg      Price:99.00
      $US
Peptide Name: KinSub3RRGSP

Product Use: For assaying the phosphotransferase activity of Mitogen-activated protein-serine kinase p38 gamma; Mitogen-activated protein kinase 12 (p38g, UniProt ID P53778). The KinSub3RRGSP peptide demonstrated high phosphotransferase activity with CDK2, and exhibited high 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: KinSub3RRGSP 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: HGRGRRGSPGVRGHW

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

Peptide Molecular Mass Calculated: 1670.9 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Peptide Recommended Enzyme: CDK2

Scientific Background: p38g is one of several protein kinases that can phosphorylate KinSub3RRGSP. Human p38g (also known as MAPK12) is a protein-serine/threonine kinase of 367 amino acid length, with a predicted molecular mass of 41,940 Da. It is a member of the CMGC group of protein kinases in the MAPK family, and p38 subfamily. This kinase is moderate to highly expressed in most tested human tissues except in the pituitary, spinal cord and vagina, where it is notably absent. Orthologues of p38g are highly conserved in animals and plants. p38g is activated by phosphorylation at Y185 and probably T183. p38g has been linked with the development of inflammation, autoimmunity , diabetes and cancer. p38g is activated in response to stress (1). p38g was mapped to 22q13.3 and functions as a signal transducer during differentiation of myoblasts to myotubes. Enforced localization of p38g in the nucleus or cytoplasm markedly attenuates the ability of the kinase to induce cell cycle arrest in fibroblasts. p38g increases basal glucose uptake and decreases DNP- and contraction-stimulated glucose uptake, partially by affecting levels of glucose transporter expression in skeletal muscle (2).