ライフサイエンスコーパス: Aurora kinase A

1 nvestigational, oral, selective inhibitor of aurora kinase A.

2 crease in its expression and deregulation of Aurora Kinase A.

3 f Cyclin B1 and decreased phosphorylation of Aurora kinase A.

4 educed Ser315 phosphorylation in response to aurora kinase A.

5 sive network of cell-cycle factors linked to aurora kinase A.

6 nduced apoptosis, and elevated expression of aurora kinase A abolishes this response.

7 a convergence of LIN28B and RAN signaling on Aurora kinase A activity.

8 Aurora kinase A (also called STK15 and BTAK) is overexpr

9 with decreased survival, and a reduction in aurora kinase A and aurora kinase B expression inhibits

10 finitively test the clinical benefit of dual Aurora kinase A and B inhibition.

11 lso interacted with a selective inhibitor of aurora kinase A and B to potentiate apoptosis without mo

12 multiple microtubule organizing centers with Aurora kinase A and gamma-tubulin.

13 al stabilization of the CDH1 targets such as Aurora kinase A and Polo-like kinase 1.

14 6a as a moderately potent dual inhibitor of aurora kinases -A and -B.

15 polyploid cells caused by the suppression of Aurora kinases A and B (AURKA/B), which are critical med

16 Finally, we show that down-regulation of Aurora kinases A and B and chromatin licensing and DNA r

17 ive mesotheliomas expressed higher levels of Aurora kinases A and B and functionally related genes in

18 Overexpression and hyperactivation of aurora kinases A and B have major roles in tumorigenesis

19 Here, we demonstrate that Aurora kinases A and B phosphorylate a conserved residue

20 Aurora kinases A and B, both of which were highly expres

21 1) signalling pathway and down-modulation of Aurora kinases A and B, cyclin B1 and CDC25C.

22 uced cyclin-dependent kinase 2 (Cdk2), Cdk4, Aurora kinase A, and Aurora kinase B expression.

23 Cells depleted of aurora kinase A are more sensitive to cisplatin-induced

24 beta-catenin and Aurora kinase A are present in most MM but not in normal

25 ion and the phosphorylation of its substrate Aurora kinase A (AurA).

26 by loss of VHL and associated with increased Aurora kinase A (AURKA) and histone deacetylase 6 (HDAC6

27 and overexpression of the mitotic regulator Aurora kinase A (AURKA) drives tumor aneuploidy and chro

28 Centrosome-localized mitotic Aurora kinase A (AURKA) facilitates G2/M events.

29 The aurora kinase A (AURKA) gene is frequently amplified and

30 Recently, we reported a novel role of Aurora kinase A (AURKA) in BCSCs, as a transactivating c

31 We investigated the role of Aurora kinase A (AURKA) in regulating p73-dependent apop

32 We find that Aurora kinase A (AURKA) is a novel, hypoxia-independent

33 Aurora kinase A (AURKA) is a therapeutic target in acute

34 Aurora kinase A (AURKA) is located at 20q13, a region th

35 Our previous analyses suggested that Aurora kinase A (AURKA) is regulated by androgens in pro

36 Aurora kinase A (AURKA) localizes to centrosomes and mit

37 rough pharmacologic and genetic studies that aurora kinase A (AURKA) represents a new therapeutic tar

38 Depletion of one such molecule, aurora kinase A (Aurka), resulted in compromised self-re

39 Here, we report that LKB1 undergoes Aurora kinase A (AURKA)-mediated phosphorylation, which

40 ning revealed that a major target of diMF is Aurora kinase A (AURKA).

41 of a high degree of mitotic genes including Aurora Kinase A (Aurora A, STK6).

42 tically, CRAF, but not BRAF, associates with Aurora kinase A (Aurora-A) and Polo-like kinase 1 (Plk1)

43 Aurora kinase A (Aurora-A) belongs to a highly conserved

44 screening, we showed PTTG1 interacting with Aurora kinase A (Aurora-A), and confirmed the interactio

45 Aurora kinase-A (Aurora-A) promotes timely entry into mi

46 cyclin-dependent kinases (CDK1 and CDK4) and Aurora kinases A, B, and C, were found to be hyperactiva

47 ations were found to affect SRC, SMAD genes, aurora kinase A, epidermal growth factor receptor, heat

48 Elevated Aurora kinase-A expression is correlated with abrogation

49 monstrate regulation of a novel target gene, Aurora kinase A, implicating beta-catenin in G2/M regula

50 Ectopic overexpression of aurora kinase A in mammalian cells induces centrosome am

51 oughput datasets that particularly implicate aurora kinase A in the pathogenesis of squamous-cell car

52 data provide a promising rationale for using Aurora kinase A inhibition as a therapeutic modality of

53 Moreover, treatment with a specific Aurora kinase A inhibitor blocks cell proliferation by i

54 fied neuroblastomas, we demonstrate that the Aurora Kinase A inhibitor MLN8237 combines with ABT-199

55 We conclude that aurora kinase A is a key regulatory component of the p53

56 Destabilization of p53 by aurora kinase A is abrogated in the presence of mutant M

57 omas of the head and neck, overexpression of aurora kinase A is associated with decreased survival, a

58 e demonstrate by gene expression arrays that Aurora kinase A is one of the highly overexpressed genes

59 f the p53 pathway and that overexpression of aurora kinase A leads to increased degradation of p53, c

60 is not degraded in the presence of inactive aurora kinase A or ubiquitination-defective Mdm2.

61 Here we show that aurora kinase A phosphorylates p53 at Ser315, leading to

62 ed of glandular atypia, P53 abnormality, and Aurora kinase A positivity, and the interaction of age,

63 Silencing of aurora kinase A results in less phosphorylation of p53 a

64 nvolved in cell cycle progression, including Aurora Kinase A, that has previously been implicated in

65 ng three protein biomarkers (P53, c-Myc, and Aurora kinase A), two methylation markers (MYOD1 and RUN

66 vel functional link between beta-catenin and Aurora kinase A, underscoring a critical role of these p

67 s with wild-type p53, elevated expression of aurora kinase A was correlated with low p53 concentratio

68 f several known oncogenes, such as ErbB2 and Aurora Kinase A, was increased in tumor samples.

69 p-regulated protein (HURP) is a substrate of Aurora kinase A, which plays a crucial role in the stabi