Polyclonal Anti-AURKA

Price

200.00 USD

Size

100ug/vial

Reactivities

Mouse, Rat

Format

Each vial contains 5mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg Thimerosal, 0.05mg NaN3.

References

1. Bischoff, J. R., Plowman, G. D. The Aurora/lpl 1p kinase family: regulators of chromosome \nsegregation and cytokinesis. Trends Cell Biol. 9: 454-459, 1999.\n2. Hutterer, A., Berdnik, D., Wirtz-Peitz, F., Zigman, M., Schleiffer, A., Knoblich, J. A. Mitotic activation \nof the kinase Aurora-A requires its binding partner Bora. Dev. Cell 11: 147-157, 2006.\n3. Seki, A., Coppinger, J. A., Jang, C.-Y., Yates, J. R., III, Fang, G. Bora and the kinase Aurora A \ncooperatively activate the kinase Plk1 and control mitotic entry. Science 320: 1655-1658, 2008.

Storage Temp

At -20 degree C for one year. After reconstitution, at 4 degree C for one month. It can also be aliquotted and stored frozen at -20 degree C for a longer time.Avoid repeated freezing and thawing.

Scientific Background

AURKA(aurora kinase A), also called ARK1, AurA, AIK , AURORA2 ,BTAK, PPP1R47, STK7, STK15,\nSTK6, is a mitotic centrosomal protein kinase. The main role of AURKA in tumor development is in \ncontrolling chromosome segregation during mitosis . Aurora A is a member of a family of mitotic \nserine/threonine kinases. Cell cycle and Northern blot analyses showed that peak expression \nof AURKA occurs during the G2/M phase and then decreases. By fluorescence in situ \nhybridization, AURKA gene is represented by 2 signals in chromosome bands 20q13.2-q13.3 and \n1q41-q42. The AURKA gene is overexpressed in many human cancers. Ectopic overexpression of \nAurora kinase A in mammalian cells induces centrosome amplification, chromosome instability, and \noncogenic transformation, a phenotype characteristic of loss-of-function mutations of p53. Depletion of \nAjuba prevented activation of AURKA at centrosomes in late G2 phase and inhibited mitotic entry. \nActivation of AURKA was independently sufficient to induce rapid ciliary resorption, and AURKA acted in \nthis process through phosphorylation of HDAC6, leading to HDAC6-dependent tubulin deacetylation \nand destabilization of the ciliary axoneme. Small molecule inhibitors of AURKA and HDAC6 reduced \nregulated disassembly of cilia.