Product Name: AurA (122-135)
Product Number: PE-01ASI95
Size: 200 µg      Price:48.00
1 mg      $US96.00
5 mg      210.00
Peptide Name: AurA (122-135)

Product Use: Services as a blocking peptide for use with the AurKA rabbit polyclonal antibody (Cat. No.: AB-NK008-4P) that is also available from Kinexus.

Peptide Production Method: Solid-phase peptide synthesis

Peptide Origin: Homo sapiens

Peptide Sequence: CESKKRQWALEDFEI

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

Peptide Molecular Mass Calculated: 1881.1 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Related Product 1: AurA pan-specific antibody (Cat. No.: AB-NK008-4P)

Scientific Background: AurA (AurKA, AIK) is a protein-serine/threonine kinase of the Other group and AUR family. It regulates cell cycle progression, and it mediates chromosomal segregation during mitosis. AurA phosphotransferase activity is greatest during mitosis. It is activated by phosphorylation at S284, T287, T288 and S342. AurA appears to be a tumour requiring protein (TRP). The active form of the protein kinase normally acts to promote tumour cell proliferation. Although AurA is not an oncoprotein, it is required for upstream oncoproteins to promote tumour formation. Its low rate of mutation and down-regulation in human cancers supports it identification as a TRP, and as a target for cancer drug development. However, the overexpression of AURA has been well documented in many malignant cancers including breast, ovarian, colon, prostate and neuroblastomas. Overexpression of AURA appears to override checkpoints in cell cycle progression leading to increased cell division and proliferation. Its phosphotransferase activity is decreased 10-fold with G198N (which also induces abnormal binding to INCENP and BIRC5), or increased with T288D. Phosphatase type I interactions could be decreased with F165A, and F346A mutations, while ubiquitination could be reduced with R205A. Autophosphorylation is inhibited with D274N, and TPX2 interactions are interrupted with a T287E mutation.