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Validated All-in-One™ qPCR Primer for AURKA(NM_198436.3) Search again
Product ID:
HQP161459
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AIK, ARK1, AURA, BTAK, PPP1R47, STK15, STK6, STK7
Gene Description:
aurora kinase A
Target Gene Accession:
NM_198436.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
The protein encoded by this gene is a cell cycle-regulated kinase that appears to be involved in microtubule formation and/or stabilization at the spindle pole during chromosome segregation.
Gene References into function
- Cell-cycle-dependent regulation of human aurora A transcription is mediated by periodic repression of E4TF1
- overexpression shows tetraploidization as a mjor route to centrosome amplification in p53-/- cells
- Aurora-A binds to TPX2, a prominent component of the spindle apparatus
- The suppression of STK15 oncogenic activity by p53 might be explained by the finding that p53 inhibited STK15 kinase activity via direct interaction with the latter's Aurora box. This revealed a novel mechanism for the tumor suppressor function of p53.
- crystal structure of Aurora-2 kinase in complex with adenosine
- Results describe the identification of a novel negative regulator of Aurora-A, named AIP (Aurora-A kinase Interacting Protein).
- role in phosphorylating and associating with MBD3
- elevated Aurora-A expression causes resistance to apoptosis in human cancer cell line
- results show that STK15 is overexpressed in pancreatic tumors and carcinoma cell lines and suggest that overexpression of STK15 may play a role in pancreatic carcinogenesis
- BTAK may play a critical role in development of ovarian cancer
- Overexpression of STK15 gene in laryngeal carcinoma was discovered the first time, it may caused chromosomal instability through abnormal centrosome, therefore having some effect during the occurrence and development of laryngeal carcinoma.
- likely prognostic indicator for patients with breast tumors
- a candidate skin tumor susceptibility gene
- amplification of the STK15 gene may be a non-random genetic alteration in human gliomas playing a role in the genetic pathways of tumorigenesis
- Aurora A protein kinase has a role in G2/M progression [introduction]
- phosphorylation of CENP-A on Ser-7 by Aurora-A in prophase is essential for kinetochore function.
- STK15 expression associated with nuclear grade in breast carcinoma
- induces telomerase activity and hTERT by up-regulation of c-Myc
- BRCA1 phosphorylation by Aurora-A plays a role in G(2) to M transition of cell cycle
- overexpressed frequently in hepatocellular carcinoma and correlated with high grade and high stage
- immunohistochemistry of tissues taken directly from patients demonstrated an overexpression of Aurora-2 in 26 of 28 pancreatic cancers compared with 18 normal pancreas samples
- STK15 polymorphism is a genetic susceptibility factor for the occurrence and aggression of esophageal squamous cell carcinoma.
- Phosphorylation of CDC25B by AURA at the centrosome contributes to the G2-M transition.
- Aurora-A induces phosphorylation of Lats2 and this phosphorylation plays a role of the centrosomal localization of Lats2
- protein phosphatase inhibitor-2 is a bifunctional signaling protein with separate domains to inhibit PP1 and directly stimulate Aurora-A kinase
- Taken together, our study suggests that Plk3 and Aurora A kinases may lie in the same regulatory pathway and that Plk3 and Aurora A as well as BubR1 may play an important role in polyploidization and megakaryocytic differentiation.
- STK15 may represent a low penetrance type breast cancer susceptibility gene.
- Aurora-A may have a role in differentiated type gastric carcinogenesis
- phosphorylation of p53 at Ser-215 by Aurora-A is a major mechanism to inactivate p53
- Aurora A may have a role in ESCC occurrence and progression
- analysis of sequences required for human Aurora-A kinase destruction
- Aurora-A gene amplification and overexpression play a role in human carcinogenesis, largely due to the effect of Aurora-A on oncogenic cell growth, rather than a loss of maintenance of centrosomal or chromosomal integrity
- Breast cancer development is driven by genomic instability associated with variant Aurora-A
- PML3 has a direct role in the control of centrosome duplication through suppression of Aurora A activation to prevent centrosome reduplication
- Over-expression of Aurora-A is present in some normal and the majority of high-grade prostatic intraepithelial neoplasia lesions indicating that this may be an early event that leads to the genetic instability seen in prostate carcinogenesis
- STK15 T+91A variant is a low penetrance cancer susceptibility allele affecting multiple cancer types.
- overexpression of STK15 significantly correlates with nude mice tumorigenicity and chromosomal aneuploidy in human ovarian cancer cells grown in vitro
- AURKA amplification contributes to pancreatic carcinogenesis by increasing chromosome instability and centrosome abnormality.
- Amplification and overexpression of AURKA is a common and significant event during immortalization of ovarian epithelial cells.
- Data indicate that the highly increased level of STK15 protein in breast cancer cell line MCF7 cannot be explained by gene amplification alone.
- Aurora-A phosphorylates HURP in vitro and in vivo.
- results support the role of AURKA Ile31 as a low penetrance colorectal cancer susceptibility factor; study shows for the first time that the preferential amplification of 91A is observed more frequently in familial colorectal cancer
- findings indicate that Aurora-A and hMPS1 aberrations are uncommon in aggressive lymphomas but Aurora-A overexpression may contribute to numerical chromosomal alterations in occasional mantle cell lymphomas
- Aurora-A-mediated phosphorylation of CDC25B at the centrosome is an important step contributing to the earliest events inducing mitosis, upstream of CDK1-cyclin B1 activation
- AurA plays a key role upstream of CDK1. A model depicting the possible role of AurA at the onset of mitosis and upon DNA damage is presented
- Activation of AurA by TPX2 is essential for Ran-stimulated spindle assembly in the presence or absence of centrosomes.
- Detection of STK15 overexpression in laryngeal carcinoma has led us to propose that the above may be one of the mechanisms underlying laryngeal carcinogenesis
- the 169G>A polymorphism in AURKA is associated with progression of gastric cancer by affecting relative kinase activities of AURKA variants
- Overexpression of Aurora-kinase A is associated with Esophageal Neoplasms
- TRAP220/MED1 plays a novel coregulatory role in facilitating the recruitment of TRAP/Mediator to specific target genes involved in growth and cell cycle progression via GABP
- Results suggest that STK15 gene amplification contributes to its mRNA and protein overexpression through affecting the exact replication of centrosome and separation of chromosomes.
- Gadd45a interacts with aurora-A and inhibits its kinase activity
- Aurora-A amplification studied by FISH was significantly more common in breast tumours from BRCA2 mutation carriers.
- Aurora-A activates Akt and induces chemoresistance in a p53-dependent manner and that inhibition of Akt may be an effective means of overcoming Aurora-A-associated chemoresistance in ovarian cancer cells expressing wild-type p53.
- Data show that small molecule-mediated inhibition of Aurora A and Aurora B yields distinct phenotypes, suggesting that the Auroras may present two avenues for anti-cancer drug discovery.
- The up-regulation of AURKA mRNA may play a critical role in the tumor progression of HNSCC and provides useful information as a prognostic factor for HNSCC patients.
- Data provide no support for the hypothesis that sequence variation in STK15 defined by SNP F31I per se confers an elevated risk of colorectal cancer.
- N-terminal domain of Aurora-A Phe-31 variant exhibits an intrinsic ubiquitin ligase activity
- Aurora-A-mediated phosphorylation of NDEL1 is essential for centrosomal separation and centrosomal maturation and for mitotic entry
- IKKalpha was found to be associated with Aurora A in the centrosome and regulate Aurora A phosphorylation at threonine residue 288, a site which is important in modulating its kinase activity.
- results show a statistically significant increased risk of sporadic breast cancer for individuals that are homozygous for the 91A allele but no effect in carriers of BRCA mutations
- AURKA and MDM2 were identified as interesting novel amplified genes in juvenile angiofibromas
- influence of Aurora-A, 91T-to-A (F31I) and 169G-to-A (V57I) polymorphisms on age of onset of hereditary nonpolyposis colorectal cancer
- protein phosphatase PP2A controls Aurora-A degradation by dephosphorylating serine 51 in the A box of the human enzyme
- Aurora-A was a sensitive marker to predict tumor recurrence in bladder carcinoma with statistical significant correlation between immunohistochemical staining and clinical outcome.
- Aurora-A is amplified and overexpressed in esophageal squamous cancer.
- Here, we report an intramolecular inhibitory regulation in Aurora-A between its N-terminal regulatory domain (aa 1-128, Nt) and the C-terminal catalytic domain (aa 129-403, Cd).
- AURAK was inhibited by MLN8054 and caused spindle pole and chromosome congression defects leading to aneuploidy.
- We propose that AURKAIP1 might function upstream of the Az1 by enhancing the binding affinity of Az1 to Aurora-A to promote recognition, targeting to proteasome and subsequent degradation.
- Aurora-A amplification was strongly associated with a high fractional allelic loss score (p = 0.0001), but not with microsatellite instability, nor with the promoter methylation phenotype in colorectal cancer.
- Patients with urothelial cell carcinoma and elevated levels of STK15 mRNA generally showed a more adverse disease course than patients with low levels
- These results identify a GEF-H1-dependent mechanism to modulate localized RhoA activation during cytokinesis under the control of mitotic kinases.
- Aurora-A-mediated phosphorylation of RASSF1A is a novel mechanism that regulates the ability of this tumor suppressor to interact with microtubules and modulate M-phase cell cycle progression.
- due to low number of cases, we are not able to state that statistically significant quantitative differences in Aurora-A mRNA expression exist between columnar-lined oesophagus & Barrett's oesophagus with & without dysplasia & p53-positive immunostaining
- Our study demonstrates that STK15 F31I SNP is associated with an increased risk for uterine cancer.
- Here, we show that interactions between the prometastatic scaffolding protein HEF1/Cas-L/NEDD9 and the oncogenic Aurora A (AurA) kinase at the basal body of cilia causes phosphorylation and activation of HDAC6, promoting ciliary disassembly.
- AURKA polymorphism and over expression is associated with breast tumors
- These results suggest that Rho GTPases function in G2/M transition of mammalian cells by mediating multiple signaling pathways converging to centrosomal activation of Aurora-A.
- New light on AURKA expression and regulation in epithelial cancers in vivo and shows its value as a clinically relevant marker and as a potential therapeutic target per se.
- Aurora-A kinase is overexpressed by a substantial proportion of ovarian cancers and is associated with centrosome amplification and poor prognosis andsurvival.
- Higher BTAK expression was found in ovarian cancer cells compared to ovaries without cancer but with known BRCA1/2 mutation or strong family history.
- ectopically BRCA2-expressing cells have different intracellular levels of Aurora A, Aurora B, p21, E2F-1, and pRb, suggesting a BRCA2-mediated suppression of polyploidy via stabilization of the checkpoint proteins levels
- TPX2 binding decreases the size and accessibility of a hydrophobic pocket, adjacent to the ATP site, to inhibitors.
- High level of STK15 amplification is associated with bladder cancer
- There may be an association between the AURKA Ile31 allele and an altered transcriptome in normal non-neoplastic prostates.
- Aurora-A and TACC3 interaction is important to control the mitotic spindle organization required for proper chromosome segregation.
- Study demonstrates that AurA-mediated phosphorylation of ASAP is essential to spindle formation and mitosis.
- c-Fos may undergo cell cycle dependent phosphorylation, in which some kinases including Aurora-A play a role in catalyzing the post translational modification of c-Fos.
- Aurora-A kinase-inhibition enhances the efficacy of chemotherapeutic agents and reverses acquired resistance resulting from the activation of NF-kappaB.
- AURKA phosphorylation of AIP and stabilization of the enzyme-substrate complex are reported.
- Study found that Aur-A increases cell migration and this novel function was correlated with Akt1 activation.
- Aurora A activity is inhibited by MK615, from ume, a variety of Japanese apricot in hepatocellular carcinoma cells
- polymorphic variant of Aurora A does not appear to be associated with variation in colorectal cancer risk in HNPCC
- Perimembrane Aurora-A status was a significant factor to predict a poor prognosis in correction with enhanced proliferative activity in non-small cell lung cancer.
- In colorectal adenocarcinoma, the expression of aurora kinase protein was found to be related to the distal location, grade of tumor, p16 expression, and telomerase activity.
- Frequent overexpression of AURKA transcript in upper gastrointestinal adenocarcinomas was detected compared with normal samples (47%; P= .001). Overexpression of AURKA led to a remarkable reduction in the transcription activity of p53.
- AURKA overexpression, which is regulated at the DNA level, is a novel predictive marker for a subgroup of patients with stage III ovarian carcinomas.
- Phosphorylation of HURP by Aurora A provides a regulatory mechanism for the control of spindle assembly and function.
- The association of Id1 and Cdh1 is dependent on the canonical destruction box motif of Id1, the increased binding of which may compete with the interaction between Cdh1 and Aurora A, leading to stabilization of Aurora A in Id1-overexpressing cells.
- Astrin acts upstream of Aurora-A to regulate its mitotic spindle localization.
- p53 and p16 are critical in preventing mammary gland tumorigenesis in the human Aurora A overexpression mouse model
- GSK-3beta modulates the early mitotic Aurora-A level through binding and phosphorylating AIP.
- This study evaluated the role of genetic polymorphisms of Aurora-A gene in the lung cancer in the Turkish population.
- The upregulation of Aurora-A by estrogen in short-term in vitro cultures is an indirect consequence of estrogen-induced cell proliferation.
- Aurora-A gene expression is already strongly deregulated in early stages of urothelial carcinoma with abnormal expression, and might be considered a biomarker of tumor aggression
- tumor hypoxia may trigger overexpression of STK15 observed in various tumors
- study reports that the synergistic action of Bora & the kinase Aurora A controls G2-M transition; Bora accumulates in G2 phase & promotes Aur-A-mediated activation of Polo-like kinase 1, leading to activation of cyclin-dependent kinase 1 & mitotic entry
- data demonstrate that the initial activation of PLK1 is a primary function of aurora A
- Aurora A expression defines a population of breast cancer patients with decreased survival.
- RASSF1A may function as a scaffold to bring together Aurora-A and its activator(s).
- Chromosome nucleation is involved in spindle pole separation and setting spindle length. A second Aurora A-independent function of TPX2 is required to bipolarize spindles.
- A novel function of Aurora-A, the regulation of ch-TOG and MCAK localization, in a common pathway in control of spindle pole integrity.
- Aur-A acted through a downstream MAP kinase pathway to promote epithelial-mesenchymal transition and invasiveness in nasopharyngeal tumorigenesis.
- Aurora-A transcriptional silencing seems to confer cancer cells a greater sensitivity to chemotherapy by vincristine, indicating Aurora-A as a possible gene target in cancer therapy
- These antibodies specifically recognize endogenous Aurora-A in both immunoblotting and immunofluroscence experiments.
- AURA is a novel target of transcriptional regulation by histone deacetylase inhibitors in non-small cell lung cancer.
- The findings provide the first evidence of Aurora-A, in association with INCENP and TPX2, being a key regulator of kinetochore/chromatin associated microtubule formation in human cells.
- E2F3 modulates Aurora-A mRNA expression during the cell cycle.
- analysis of the negative feedback regulation of Aurora-A via phosphorylation of Fas-associated factor-1
- The two investigated single nucleotide polymorphisms in AURKA were not found to be associated with prostate cancer risk.
- the downregulation of STK15 expression led to cell arrest in the G(2)/M phase and finally apoptosis induction of HepG2 cells.
- Overexpression of AURKA can cause aneuploidy in urothelial cells, and the AURKA gene copy number is a promising biomarker for detection of bladder cancer.
- Pdx-1-driven overexpression of aurora a kinase induces mild ductal dysplasia of pancreatic ducts near islets in transgenic mice.
- Aurora-A kinase overexpression in chronic lymphocytic leukemia may be involved in the genesis of chromosomal abnormalities and is a potential target for therapeutic intervention.
- identified DNA copy number gains at 20q13.2-q13.3 (AURKA locus) and determined that overexpression of AURKA accompanied dysregulation of DNA Damage Response genes in high risk tumors
- overexpression of Aurora-A may stabilize Cyclin B1 through inhibiting its degradation
- Aurora kinases A and B overexpression is a relatively early phenomenon in the genesis of malignant epithelial neoplasm tumorigenesis.
- the mitotic kinases Aurora A and Aurora B are regulated by EWS-Fli1 fusion protein in Ewing sarcoma cells
- Aurora A interacts with both N-Myc and the SCF(Fbxw7) ubiquitin ligase that ubiquitinates N-Myc and counteracts degradation of N-Myc, thereby uncoupling N-Myc stability from growth factor-dependent signals