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 -regulating proteins, polo-like kinase 1 and Aurora kinase A.

7 s TNBC cells more sensitive to inhibitors of Aurora Kinase A, a protein facilitating mitosis.

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

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

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

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

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

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

14 These findings show that Aurora kinase A and Bcl-2 family proteins are potential

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

16 ugh the proteasomal-dependent degradation of aurora kinase A and induces premature senescence in huma

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

18 6a as a moderately potent dual inhibitor of aurora kinases -A and -B.

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

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

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

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

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

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

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

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

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

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

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

30 ance in response to EGFR inhibitors requires Aurora kinase A (AURKA) activity.

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

32 of KRAS signaling and overexpression of the aurora kinase A (AURKA) are often detected in luminal ga

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

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

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

36 Aurora kinase A (AURKA) has emerged as a drug target for

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

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

39 954) of zebrafish Par-3 is phosphorylated by Aurora kinase A (AurkA) in vitro.

40 NEPC tumor growth, increased the efficacy of aurora kinase A (AURKA) inhibitors, and limited the expr

41 was associated with increased sensitivity to Aurora kinase A (AURKA) inhibitors.

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

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

44 Aurora kinase A (AURKA) is an established oncogenic fact

45 Aurora Kinase A (AURKA) is an oncogenic kinase with majo

46 Aurora kinase A (AURKA) is frequently overexpressed in s

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

48 Aurora kinase A (AURKA) is necessary for proper primary

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

50 von Hippel Lindau (VHL) arise from elevated Aurora Kinase A (AURKA) levels.

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

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

53 In this article, we report that Aurora kinase A (AURKA) responsive WNT signaling activat

54 Aurora kinase A (AURKA), a critical cell cycle regulator

55 e why translation is increased, we evaluated aurora kinase A (AURKA), a kinase that activates CPEB1 i

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

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

58 n with Aurora kinase B (AURKB), but not with Aurora kinase A (AURKA).

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

60 gulated oncogenes, including SRSF1, MYC, and Aurora kinase A (AURKA).

61 ownstream of PKA: RAS/MAPK components and an Aurora Kinase A (AURKA)/glycogen synthase kinase (GSK3)

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

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

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

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

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

67 eening, we further investigated the roles of Aurora kinases A, B, and C and Nuak kinases 1 and 2.

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

69 Many aurora kinase A/B (AURKA/B) pathway genes are repressed

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

71 Elevated Aurora kinase-A expression is correlated with abrogation

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

73 pregulation of Polo-like kinase 1 (Plk1) and Aurora kinase A, important mitotic kinases involved in c

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

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

76 ion and degradation of the mitosis-promoting Aurora kinase A in the S and G2 phases of the cell cycle

77 ecruitment and recovery of GFP-tagged AIR-1 (Aurora kinase A) in early C. elegans embryos, enabling p

78 Aurora kinase A inhibition also destabilized MYCN, which

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

80 ting mutations in TP53 were sensitive to the Aurora kinase A inhibitor alisertib.

81 Combined treatment with an Aurora kinase A inhibitor and navitoclax in FP-RMS cell

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

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

84 ase, while rendering TNBC cells sensitive to Aurora kinase A inhibitors and decreasing cell viability

85 Potential therapeutic strategies, including aurora kinase A inhibitors, polyadenosine diphosphate-ri

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

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

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

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

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

91 This revealed that inhibition of Aurora kinase A most efficiently negatively affected PAX

92 teins instrumental in driving NEPC including Aurora Kinase A, N-Myc, E2F1 and STAT3.

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

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

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

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

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

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

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

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

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

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

103 s identify a novel functional interaction of Aurora kinase A with both PAX3-FOXO1 and its effector MY