Product Name: KinSub1RLLSP
Product Number: PE-01AHS95
Size: 200 µg      Price:99.00
      $US
Peptide Name: KinSub1RLLSP

Product Use: For assaying the phosphotransferase activity of Serine/threonine protein kinase NLK (UniProt ID Q9UBE8). The KinSub1RLLSP peptide demonstrated moderate phosphotransferase activity with NLK, 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: KinSub1RLLSP 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: GGRSRLLSPCGGGYG

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

Peptide Molecular Mass Calculated: 1435.6 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Peptide Recommended Enzyme: NLK

Scientific Background: NLK is one of several protein kinases that can phosphorylate KinSub1RLLSP. Human NLK is a protein-serine/threonine kinase of 527 amino acid length, with a predicted molecular mass of 58,283 Da. It is a member of the CMGC group of protein kinases in the MAPK family, and nmo subfamily. This kinase is highly expressed and widely distributed in most tested human tissues. Orthologues of NLK are highly conserved in vertebrates and insects. NLK is activated by phosphorylation at tyrosine and threonine. NLK plays a role in cell fate determination and is required for the differentiation of bone marrow stromal cells. NLK also suppresses a wide range of transcription factors such as CREB by phosphorylation of the co-activator CREBBP. NLK expression increases the number of apoptotic cells but does not induce obvious cell cycle arrest (1). NLK suppresses Notch signalling by interfering with formation of the Notch active transcriptional complex (2). NLK has been linked with the development of glioblastoma multiforme (GM).