title: Aurora kinase-C-T191D is constitutively active mutant.
abstract: BACKGROUND
  Aurora kinases (Aurora-A, B and C) belong to a family of conserved serine/threonine kinases which are key regulators of cell cycle progression. Aurora-A and Aurora-B are expressed in somatic cells and involved in cell cycle regulation while aurora-C is meiotic chromosome passenger protein. As Aurora kinase C is rarely expressed in normal somatic cells and has been found over expressed in many cancer lines. It is suggested that Aurora-C-T191D is not hyperactive mutant.
  
  
  RESULTS
  Aurora-C-T191D variant form was investigated and compared with wild type. The overexpression of Aurora-C-T191D was observed that it behaves like Aurora-C wild type (aurC-WT). Both Aurora-C-T191D and aurC-WT induce abnormal cell division resulting in centrosome amplification and multinucleation in transiently transfected cells as well as in stable cell lines. Similarly, Aurora-C-T191D and aurC-WT formed foci of colonies when grown on soft agar, indicating that a gain of Aurora-C activity is sufficient to transform cells. Furthermore, we reported that NIH-3 T3 stable cell lines overexpressing Aurora-C-T191D and its wild type partner induced tumour formation when injected into nude mice, demonstrating the oncogenic activity of enzymatically active Aurora kinase C. Interestingly enough tumour aggressiveness was positively correlated with the rate of kinase activity, making Aurora-C a potential anti-cancer therapeutic target.
  
  
  CONCLUSIONS
  These findings proved that Aurora C-T191D is not hyperactive but is constitutively active mutant.
authors.affiliation: Department of Biological Sciences, Gomal University Dera Ismail Khan, Dera Ismail Khan, Pakistan.
authors.forename: Jabbar
authors.initials: J
authors.lastname: Khan
authors.forename: Sanaullah
authors.initials: S
authors.lastname: Khan
authors.forename: Sobia
authors.initials: S
authors.lastname: Attaullah
authors.forename: Ijaz
authors.initials: I
authors.lastname: Ali
authors.forename: Shahid Niaz
authors.initials: SN
authors.lastname: Khan
mesh_terms: D000818:Animals; D064096:Aurora Kinase A; D064107:Aurora Kinase B; D064108:Aurora Kinase C; D064127:Aurora Kinases; D002455:Cell Division / Q000502:physiology; D002460:Cell Line; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000378:metabolism*; D018385:Centrosome / Q000502:physiology; D005260:Female; D006801:Humans; D051379:Mice; D008819:Mice, Nude; D050505:Mutant Proteins / Q000378:metabolism*; D009154:Mutation / Q000235:genetics; D010766:Phosphorylation / Q000502:physiology; D017346:Protein Serine-Threonine Kinases / Q000235:genetics* / Q000378:metabolism*
chemical_list: D050505:Mutant Proteins; C576921:AURKB protein, human; C576927:AURKC protein, human; C576918:Aurka protein, mouse; C576924:Aurkb protein, mouse; C576928:Aurkc protein, mouse; D064096:Aurora Kinase A; D064107:Aurora Kinase B; D064108:Aurora Kinase C; D064127:Aurora Kinases; D017346:Protein Serine-Threonine Kinases