Product Name: KinSub3DDDYG
Product Number: PE-01AKJ95
Size: 200 µg      Price:99.00
      $US
Peptide Name: KinSub3DDDYG

Product Use: For assaying the phosphotransferase activity of Nerve growth factor (NGF) receptor-tyrosine kinase; High affinity nerve growth factor receptor (TrkA, UniProt ID P04629). The KinSub3DDDYG peptide demonstrated very high phosphotransferase activity with Blk, 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: KinSub3DDDYG 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: GGGEDDDYGCGGGGG

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

Peptide Molecular Mass Calculated: 1271.2 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Peptide Recommended Enzyme: Blk

Scientific Background: TrkA is one of several protein kinases that can phosphorylate KinSub3DDDYG. Human TrkA is a receptor protein-tyrosine kinase of 796 amino acid length, with a predicted molecular mass of 87,497 Da. It is a member of the TK group of protein kinases in the Trk family. It appears to have a very restricted human tissue expression with the highest levels detected in lung. Orthologues are highly conserved in mammals and birds. TrkA is activated by binding of nerve growth factor (NGF). Autophosphorylation of Y496, Y757 and Y791 increases phosphotransferase activity. Phosphorylation of Y496 also promotes interaction with FRS2 and Shc1, and phosphorylation at Y791 induces interaction with PLCg1. Phosphorylation of Y701 inhibits phosphotransferase activity and induces TrkA interaction with CLTC and LAMP1. NGF elicits the rapid phosphorylation of TrkA on tyrosine residues leading to increased c-Fos expression, DNA synthesis and morphologic transformation (1). A decreased expression of TrkA on the striatal cholinergic neurons has been observed which may contribute, when it reaches a crucial threshold, to the death of cholinergic neurons observed in Alzheimer disease (2). TrkA has been linked with the development of congenital insensitivity to pain with anhidrosis, ovarian serous and papillary thyroid carcinomas, and breast cancer.
References

[1] Kaplan DR, Hempstead BL, Martin-Zanca D, Chao MV, Parada LF. The trk proto-oncogene product: a signal transducing receptor for nerve growth factor. Science. 1991 Apr 26;252(5005):554-8. PMID:1850549

[2] Boissière F, Lehéricy S, Strada O, Agid Y, Hirsch EC. Neurotrophin receptors and selective loss of cholinergic neurons in Alzheimer disease. Mol Chem Neuropathol. 1996 May-Aug;28(1-3):219-23. PMID: 8871962