Atlas of Genetics and Cytogenetics in Oncology and Haematology

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Taking over the Atlas
Dear Colleagues,
The Atlas, once more, is in great danger, and I will have to proceed to a collective economic lay-off of all the team involved in the Atlas before the begining of April 2015 (a foundation having suddenly withdrawn its commitment to support the Atlas). I ask you herein if any Scientific Society (a Society of Cytogenetics, of Clinical Genetics, of Hematology, or a Cancer Society, or any other...), any University and/or Hospital, any Charity, or any database would be interested in taking over the Atlas, in whole or in part. If taking charge of the whole lot is too big, a consortium of various actors could be the solution (I am myself trying to find partners). Could you please spread the information, contact the relevant authorities, and find partners.
Survival of the Atlas will be critically dependant upon your ability to find solutions (and urgently!).
Kind regards.
Jean-Loup Huret jlhuret@AtlasGeneticsOncology.org
Donations are also welcome
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Don't let the Atlas imminent demise
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AURKA (aurora kinase A)

Identity

Other namesAurora A
ARK1
AURA
Aurora2
BTAK
MGC34538
STK15
STK6
STK7
HGNC (Hugo) AURKA
LocusID (NCBI) 6790
Location 20q13.2
Location_base_pair Starts at 54944445 and ends at 54967351 bp from pter ( according to hg19-Feb_2009)  [Mapping]

DNA/RNA

Description The gene encompasses 22,8 kb of DNA; 9 Exons.
Transcription 2253 bp mRNA.

Protein

 
Description 403 amino acids, 46kDa protein. At the amino terminal domain, three putative conserved Aurora boxes (A-boxI, A-boxII and A-boxIII) can be identified. The functional significance of these boxes are not yet clearly known and there is suggestive evidence in the literature that these may be involved in subcellular localization or substrate recognition for the proteins. One of the serine residues in the A-boxII of Aurora-A kinase has recently been shown to be involved in the degradation of the protein. One activation motif and a destruction box in C-terminal. AURKA is regulated by phosphorylation in a cell cycle dependent manner. This phosphorylation occurs on a conserved residue, threonine 288, within the activation loop of the catalytic domain of the kinase and results in a significant increase in the enzymatic activity.
AURKA protein is able to physically associate with multiple important cellular proteins such as p53, BRCA1, and TACC1. The interactions of AURKA with those critical molecules have been shown to disrupt/alter their physiological functions and may play roles in tumorigenesis.
Expression Widely expressed, AURKA mRNA and protein expression levels are low during G1 and S phase and peak during the G2/M phase of the cell cycle. Kinase activity of the protein is also cell cycle regulated and the highest activity coincides with the most elevated expression level of the protein during mitosis.
Localisation AURKA localizes next to the centrosome late in the G1 phase and early in the S phase. As the cell cycle progresses, concentration of AURKA increases and the kinase associates with the mitotic poles and the adjacent spindle microtubules. AURKA remains associated with the spindles through telophase.
Function Serine/threonine kinase identified as key regulator of the mitotic cell division process. Known to be involved in the regulation of centrosome function, bipolar spindle assembly and chromosome segregation processes. AURKA is critical for proper formation of mitotic spindle. It is required for the recruitment of several different proteins important to the spindle formation. Among these target proteins are TACC, a microtubule-associated protein that stabilizes centrosomal microtubules and Kinesin 5, a motor protein involved in the formation of the bipolar mitotic spindle. Two upstream regulators of AURKA, Ajuba and targeting protein for Xklp2 ( TPX2 ) are known. TPX2 is a MT-binding protein involved in spindle pole formation and is the best characterized RanGTP-dependent spindle activator. TPX2 is required for AURKA binding to spindle MTs and its binding to AURKA holds the latter in an active conformation. Ajuba and AURKA interact in mitotic cells and become phosphorylated. In vitro analyses revealed that Ajuba induces the autophosphorylation and consequent activation of AURKA. Depletion of Ajuba prevented activation of AURKA at centrosomes in late G2 phase and inhibited mitotic entry.
AURKA induces p53 degradation by phosphorylation of Ser-315. It was demonstrated that DNA binding and transactivation activity of p53 was abrogated by AURKA. AURKA phosphorylates p53 at Ser-215 in vitro and in vivo. The inhibition of p53 DNA binding and transactivation activity by AURKA depends on phosphorylation of Ser-215 but not Ser-315. Further, AURKA phosphorylation of Ser-215 of p53 is associated with AURKA -regulated cell cycle progression, cell survival, and transformation. The p53 is a physiological substrate of AURKA and that AURKA exerts its function through phosphorylation of Ser-215 of p53.
Homology Aurora related kinases, AURKA and AURKB are present in Drosophila,C.elegans and X. laevis. Among mammals, three members of the family, AURKA, -B and -C have so far been identified. The three members of the mammalian kinases of varying peptide lengths share similar catalytic domains located in the carboxyl terminus but their amino terminal extensions are of variable length and display little or no similarity. By examination of the AURKA cDNA sequence the threonine at residue 288 in the catalytic domain was found to be highly conserved in all Aurora family members as well as in various other serine/threonine kinases.

Mutations

Germinal No germline mutations have been reported.
Somatic Recent studies have demonstrated the overexpression and amplification of AURKA in many malignant human cancers and cell lines including breast, ovarian, colon, prostate, and neuroblastoma cancer cell lines. AURKA overexpression induces supernumerary centrosomes aneuploidy and cells transformation. It has been also reported that ectopic overexpression of AURKA in NIH3T3 and immortalized Rat1 induces cells transformation that generates tumor when implanted in nude mice. Elevated AURKA expression amplification overrides the checkpoint mechanism that monitors mitotic spindle assembly, inducing resistance to the chemotherapeutic agent paclitaxel. Cells overexpressing Aurora-A inappropriately enter anaphase despite defective spindle formation, and the persistence of MAD2 at the kinetochores, marking continued activation of the spindle assembly checkpoint. These findings suggest that enhanced AURKA expression causes resistence to apoptosis induced by mitotic inhibitors in human cancer cells.

Implicated in

Entity Breast cancer
Disease Breast cancer is the most common cause of cancer in women and the second most common cause of cancer death in women. Some of the patients are hereditary, with a large proportion characterized by mutation in BRCA1 and/or BRCA2 genes.
Oncogenesis The protein level of AURKA is increased at the G2 to M phase transition in normal cells, where AURKA is specifically localised at centrosomes and mitotic spindles. By contrast, analysis of tumour cells of the breast for AURKA expression patterns shows that overexpression of AURKA was present in 94% of the cases, regardless of their cell-cycle phases, and is diffusely detected in the cytoplasm. Amplification of AURKA has been detected at higher frequency in tumors from BRCA1 and BRCA2 mutation carriers than in sporadic breast tumors, suggesting that overexpression of AURKA and inactivation of BRCA1 and BRCA2 cooperate during tumor development and progression. The F31I polymorphism in AURKA has been associated with breast cancer risk in the homozygous state in prior studies. Studies have demonstrated that AURKA overexpression contributes to genetic instability and tumourigenesis by disrupting the proper assembly of the mitotic checkpoint complex and occurs in a high proportion of breast cancers.
  
Entity Pancreatic cancer
Disease Pancreatic ductal adenocarcinoma is one of the most fatal malignancies. Intensive investigation of molecular pathogenesis might lead to identifying useful molecules for diagnosis and treatment of the disease.
Oncogenesis Pancreatic ductal adenocarcinoma harbors complicated aberrations of alleles including losses of 1p, 6q, 9p, 12q, 17p, 18q, and 21q, and gains of 8q and 20q. Pancreatic cancer is usually initiated by mutation of KRAS and aberrant expression of SHH. Overexpression of AURKA mapping on 20q13.2 may significantly enhance overt tumorigenesity. AURKA was a direct downstream target of MAPK1, suggesting that the overexpression of AURKA without gene amplification may be induced by constitutive activation of MAPK1 in cancer cells. The constitutive activation of MAPK1 is frequently observed in pancreatic cancer.
  
Entity Ovarian cancer
Disease Ovarian cancer is the most lethal gynecologic malignancy in developed countries. The exact cause is usually unknown. The risk of developing ovarian cancer appears to be affected by several factors.
Oncogenesis Recent studies have shown that DNA gains of the chromosomal region 20q13 and overexpression of the centrosomal kinase AURKA, the gene of which is found within the 20q13 region, are hallmarks of ovarian cancer. Amplification of AURKA has been reported in ovarian tumors, suggesting a role in ovarian cancer pathology. AURKA is polymorphic with two single nucleotide substitutions (449t/a and 527g/a) in evolutionarily conserved regions causing amino acid changes (F31I and V57I). Two other nucleotide substitutions (287c/g and 1891g/c) of unknown significance are in 5' and 3' untranslated regions (UTR), respectively. AURKA overexpression represented a survival factor for tumor cells and a negative prognostic molecular marker.
  
Entity Human esophageal squamous cell carcinoma
Disease Human esophageal squamous cell carcinoma (ESCC) is one of the most frequent malignancies worldwide and occurs at a very high frequency in the People's Republic of China, South Africa, France, and Italy. A number of epidemiological investigations have shown that esophageal carcinogenesis and the malignant development of esophageal cancers are complex and associated with multiple etiologic factors, including genetic backgrounds, environmental stimuli, nutritional conditions, and cultural habits.
Oncogenesis Despite some epidemiological observations, the biological mechanism(s) that is involved in ESCC occurrence and progression remains to be elucidated. It has been shown that point mutations of the tumor suppressor gene p53 are detected in 40% of human esophageal cancers. The Rb gene is also frequently mutated in ESCC. Amplification of the cellular protooncogenes Myc, EGFR, HST1, INT2, and cyclin D1 are often found in this malignant disease. A recent demonstration indicates that AURKA polymorphisms are associated with advanced disease status of ESCC, and there are strong evidence that AURKA is overexpressed in human ESCC and may play a role in carcinogenesis and malignancy development of ESCC.
  
Entity Human Bladder Cancer
Disease Bladder tumors are among the most common human cancers, with approximately 55 000 new cases detected each year in the United States. Bladder cancers, which represent a group of tumors with diverse morphologic and clinical behavior, exhibit one of the strongest relationships seen in any cancer between clinical aggressiveness and degree of aneuploidy.
Oncogenesis Bladder cancers arise from at least two distinct, albeit sometimes overlapping, pathways that lead to the development of papillary and solid or nonpapillary tumors. Most superficially growing, low-grade papillary lesions are diploid or near-diploid. Although they often recur, they are unlikely to invade the bladder wall and metastasize. By contrast, virtually all nonpapillary tumors are highly aneuploid and have a strong propensity to invade the stroma and metastasize. Superficial bladder tumors that are aneuploid are also likely to progress to invasive clinically aggressive carcinomas, which may metastasize. AURKA amplification is frequently overexpressed in bladder tumors tested by FISH and the strong association of the gene amplification and overexpression levels with the degree of aneuploidy suggests that AURKA may play an important role in bladder carcinogenesis by contributing to the development of aneuploid cell populations with aggressive phenotypes.
  
Entity Human colon cancer
Disease It is the third most common form of cancer and the second leading cause of cancer-related death in the Western world. Colorectal cancer causes 655,000 deaths worldwide per year, including about 16,000 in the UK, where it is the second most common site (after lung) to cause cancer death. The most common colon cancer cell type is adenocarcinoma which accounts for 95% of cases. Other, rarer types include lymphoma and squamous cell carcinoma. Adenocarcinoma is a malignant epithelial tumor, originating from glandular epithelium of the colorectal mucosa. It invades the wall, infiltrating the muscularis mucosae, the submucosa and thence the muscularis propria.
Oncogenesis Colorectal cancer is a disease originating from the epithelial cells lining the gastrointestinal tract. Hereditary or somatic mutations in specific DNA sequences, among which are included DNA replication or DNA repair genes and also the APC, K-Ras, NOD2 and p53 genes, lead to unrestricted cell division. Furthermore, genetic instability is expressed in colon cancer by an increased rate of a number of different genetic alterations. These different manifestations of genetic instability are classified into two major categories. The first one involves subtle changes in DNA sequences typically represented by microsatellite instability (MIN). The second one is characterized by gains and losses of whole or parts of chromosomes, named chromosomal instability (CIN), and it is considered a driving force for tumourigenesis. MIN occurs in approximately 15% of colon cancers and results from inactivation of the mismatch repair (MMR) system by either MMR gene mutations or hypermethylation of the MLH1 promoter. The mechanisms inducing CIN in cancer and more specifically in colon cancer are only partly understood. At least two possible causes, not mutually exclusive, could be responsible for CIN: mutations in genes encoding mitotic regulators, such as spindle checkpoint proteins, and defects in genes controlling centrosome homeostasis. The presence of mutations of the mitotic checkpoint regulators BUB1 and BUBR1 and amplification of AURKA in a subset of human colon cancers have suggested that CIN results primarily from deregulation of DNA replication and mitotic-spindle checkpoints.
  
Entity Human Multiple myeloma
Disease Multiple myeloma (also known as MM, myeloma, plasma cell myeloma, or as Kahler's disease after Otto Kahler) is a type of cancer of plasma cells which are immune system cells in bone marrow that produce antibodies. Myeloma is regarded as incurable, but remissions may be induced with steroids, chemotherapy, thalidomide and stem cell transplants. Myeloma is part of the broad group of diseases called hematological malignancies. Multiple myeloma (MM) is a malignancy characterized by genetic instability, suggesting a disruption of checkpoints that arrest cells at G2M when injury to the mitotic machinery occurs.
Oncogenesis The expression of RHAMM and other centrosome-associated genes are known to correlate with the extent of centrosome amplification in multiple myeloma, and with poor prognosis. RHAMM has a significant interaction with TPX2, a protein which regulates the localization and action of AURKA at the spindle poles. AURKA is expressed ubiquitously in myeloma, to varying degrees. Aurora kinase inhibitor VE-465 also induces apoptosis and death in myeloma cell lines and primary myeloma plasma cells. The combination of VE-465 and dexamethasone improves cell killing compared with the use of either agent alone, even in cells resistant to the single agents.
  
Entity Human hepatocellular carcinoma
Disease Hepatocellular carcinoma (HCC, also called hepatoma) is a primary malignancy (cancer) of the liver. Most cases of HCC are secondary to either a viral hepatitide infection (hepatitis B or C) or cirrhosis (alcoholism being the most common cause of hepatic cirrhosis). In countries where hepatitis is not endemic, most malignant cancers in the liver are not primary HCC but metastasis (spread) of cancer from elsewhere in the body, e.g. the colon. Treatment options of HCC and prognosis are dependent on many factors but especially on tumor size and staging.
Oncogenesis AURKA is overexpressed frequently in HCC, and correlated with high grade and high stage, indicating that overexpression of AURKA plays a role in the development and progression of HCC. Furthermore in HCC is frequently associated the homozygous deletion of p15E2 ( MTS2/INK4b/CDKN2B ) and p16E2 ( MTS1/INK4a/CDKN2A ) with overexpression of AURKA gene, this association may play a role in the oncogenesis and malignant progression of HCC.
  
Entity Human Upper gastrointestinal adenocarcinomas
Disease Upper gastrointestinal adenocarcinomas are the second most common cause of cancer-related death in the world. and are characterized by complex molecular changes. Several epidemiological studies have indicated that the incidence of proximal adenocarcinomas of the gastroesophageal junction and lower esophagus is rising faster than ever before in the Western world. The incidence of adenocarcinoma of the cardia, gastroesophageal junction, and lower esophagus has been rapidly rising, 5-fold to 6-fold in the past few decades, especially in patients younger than 50 years of age.
Oncogenesis Overexpression of AURKA is frequent in upper gastrointestinal adenocarcinomas and in recently works it was identified the AURKA/AKT axis as an important mechanism that provides cancer cells with potent antiapoptotic properties through regulating p53-dependent apoptosis. Frequent overexpression of AURKA at the mRNA and protein levels in upper gastrointestinal adenocarcinomas, and interestingly, this overexpression was more prevalent in gastroesophageal junction adenocarcinomas andlower esophageal, Barrett-related adenocarcinomas (BAs) than in antrum and body gastric adenocarcinomas. There are not an association between AURKA overexpression and histopathological paramters such as tumor grade, TNM classification, and lymph-node metastasis.
  

Other Leukemias implicated (Data extracted from papers in the Atlas)

Leukemias 11q23ChildAMLID1615

Other Solid tumors implicated (Data extracted from papers in the Atlas)

Solid Tumors AmeloblastomID5945

External links

Nomenclature
HGNC (Hugo)AURKA   11393
Cards
AtlasAURKAID730ch20q13
Entrez_Gene (NCBI)AURKA  6790  aurora kinase A
GeneCards (Weizmann)AURKA
Ensembl hg19 (Hinxton)ENSG00000087586 [Gene_View]  chr20:54944445-54967351 [Contig_View]  AURKA [Vega]
Ensembl hg38 (Hinxton)ENSG00000087586 [Gene_View]  chr20:54944445-54967351 [Contig_View]  AURKA [Vega]
ICGC DataPortalENSG00000087586
cBioPortalAURKA
AceView (NCBI)AURKA
Genatlas (Paris)AURKA
WikiGenes6790
SOURCE (Princeton)AURKA
Genomic and cartography
GoldenPath hg19 (UCSC)AURKA  -     chr20:54944445-54967351 -  20q13   [Description]    (hg19-Feb_2009)
GoldenPath hg38 (UCSC)AURKA  -     20q13   [Description]    (hg38-Dec_2013)
EnsemblAURKA - 20q13 [CytoView hg19]  AURKA - 20q13 [CytoView hg38]
Mapping of homologs : NCBIAURKA [Mapview hg19]  AURKA [Mapview hg38]
OMIM603072   
Gene and transcription
Genbank (Entrez)AF008551 AF011468 AK301769 AK312776 AL711075
RefSeq transcript (Entrez)NM_003600 NM_198433 NM_198434 NM_198435 NM_198436 NM_198437
RefSeq genomic (Entrez)AC_000152 NC_000020 NC_018931 NG_012133 NT_011362 NW_001838666 NW_004929418
Consensus coding sequences : CCDS (NCBI)AURKA
Cluster EST : UnigeneHs.250822 [ NCBI ]
CGAP (NCI)Hs.250822
Alternative Splicing : Fast-db (Paris)GSHG0019276
Alternative Splicing GalleryENSG00000087586
Gene ExpressionAURKA [ NCBI-GEO ]     AURKA [ SEEK ]   AURKA [ MEM ]
SOURCE (Princeton)Expression in : [Normal Tissue Atlas]  [carcinoma Classsification]  [NCI60]
Protein : pattern, domain, 3D structure
UniProt/SwissProtO14965 (Uniprot)
NextProtO14965  [Medical]
With graphics : InterProO14965
Splice isoforms : SwissVarO14965 (Swissvar)
Catalytic activity : Enzyme2.7.11.1 [ Enzyme-Expasy ]   2.7.11.12.7.11.1 [ IntEnz-EBI ]   2.7.11.1 [ BRENDA ]   2.7.11.1 [ KEGG ]   
Domaine pattern : Prosite (Expaxy)PROTEIN_KINASE_ATP (PS00107)    PROTEIN_KINASE_DOM (PS50011)    PROTEIN_KINASE_ST (PS00108)   
Domains : Interpro (EBI)Kinase-like_dom    Prot_kinase_dom    Protein_kinase_ATP_BS    Ser/Thr_dual-sp_kinase_dom    Ser/Thr_kinase_AS   
Related proteins : CluSTrO14965
Domain families : Pfam (Sanger)Pkinase (PF00069)   
Domain families : Pfam (NCBI)pfam00069   
Domain families : Smart (EMBL)S_TKc (SM00220)  
DMDM Disease mutations6790
Blocks (Seattle)O14965
PDB (SRS)1MQ4    1MUO    1OL5    1OL6    1OL7    2BMC    2C6D    2C6E    2DWB    2J4Z    2J50    2NP8    2W1C    2W1D    2W1E    2W1F    2W1G    2WQE    2WTV    2WTW    2X6D    2X6E    2X81    2XNE    2XNG    2XRU    3COH    3E5A    3EFW    3FDN    3H0Y    3H0Z    3H10    3HA6    3K5U    3LAU    3M11    3MYG    3NRM    3O50    3O51    3P9J    3QBN    3R21    3R22    3UNZ    3UO4    3UO5    3UO6    3UOD    3UOH    3UOJ    3UOK    3UOL    3UP2    3UP7    3VAP    3W10    3W16    3W18    3W2C    4B0G    4BN1    4BYI    4BYJ    4DEA    4DEB    4DED    4DEE    4DHF    4JAI    4JAJ    4JBO    4JBP    4JBQ   
PDB (PDBSum)1MQ4    1MUO    1OL5    1OL6    1OL7    2BMC    2C6D    2C6E    2DWB    2J4Z    2J50    2NP8    2W1C    2W1D    2W1E    2W1F    2W1G    2WQE    2WTV    2WTW    2X6D    2X6E    2X81    2XNE    2XNG    2XRU    3COH    3E5A    3EFW    3FDN    3H0Y    3H0Z    3H10    3HA6    3K5U    3LAU    3M11    3MYG    3NRM    3O50    3O51    3P9J    3QBN    3R21    3R22    3UNZ    3UO4    3UO5    3UO6    3UOD    3UOH    3UOJ    3UOK    3UOL    3UP2    3UP7    3VAP    3W10    3W16    3W18    3W2C    4B0G    4BN1    4BYI    4BYJ    4DEA    4DEB    4DED    4DEE    4DHF    4JAI    4JAJ    4JBO    4JBP    4JBQ   
PDB (IMB)1MQ4    1MUO    1OL5    1OL6    1OL7    2BMC    2C6D    2C6E    2DWB    2J4Z    2J50    2NP8    2W1C    2W1D    2W1E    2W1F    2W1G    2WQE    2WTV    2WTW    2X6D    2X6E    2X81    2XNE    2XNG    2XRU    3COH    3E5A    3EFW    3FDN    3H0Y    3H0Z    3H10    3HA6    3K5U    3LAU    3M11    3MYG    3NRM    3O50    3O51    3P9J    3QBN    3R21    3R22    3UNZ    3UO4    3UO5    3UO6    3UOD    3UOH    3UOJ    3UOK    3UOL    3UP2    3UP7    3VAP    3W10    3W16    3W18    3W2C    4B0G    4BN1    4BYI    4BYJ    4DEA    4DEB    4DED    4DEE    4DHF    4JAI    4JAJ    4JBO    4JBP    4JBQ   
PDB (RSDB)1MQ4    1MUO    1OL5    1OL6    1OL7    2BMC    2C6D    2C6E    2DWB    2J4Z    2J50    2NP8    2W1C    2W1D    2W1E    2W1F    2W1G    2WQE    2WTV    2WTW    2X6D    2X6E    2X81    2XNE    2XNG    2XRU    3COH    3E5A    3EFW    3FDN    3H0Y    3H0Z    3H10    3HA6    3K5U    3LAU    3M11    3MYG    3NRM    3O50    3O51    3P9J    3QBN    3R21    3R22    3UNZ    3UO4    3UO5    3UO6    3UOD    3UOH    3UOJ    3UOK    3UOL    3UP2    3UP7    3VAP    3W10    3W16    3W18    3W2C    4B0G    4BN1    4BYI    4BYJ    4DEA    4DEB    4DED    4DEE    4DHF    4JAI    4JAJ    4JBO    4JBP    4JBQ   
Human Protein AtlasENSG00000087586
Peptide AtlasO14965
HPRD04066
IPIIPI00298940   IPI00790518   IPI00646206   IPI00640695   IPI00641685   IPI00646759   IPI00796387   
Protein Interaction databases
DIP (DOE-UCLA)O14965
IntAct (EBI)O14965
FunCoupENSG00000087586
BioGRIDAURKA
IntegromeDBAURKA
STRING (EMBL)AURKA
Ontologies - Pathways
QuickGOO14965
Ontology : AmiGOG2/M transition of mitotic cell cycle  mitotic cell cycle  protein kinase activity  protein serine/threonine kinase activity  protein serine/threonine/tyrosine kinase activity  protein binding  ATP binding  nucleus  centrosome  centrosome  spindle  cytosol  spindle microtubule  protein phosphorylation  cell cycle  spindle organization  mitotic nuclear division  microtubule cytoskeleton  protein kinase binding  cell projection organization  midbody  anaphase-promoting complex-dependent proteasomal ubiquitin-dependent protein catabolic process  spindle pole centrosome  ubiquitin protein ligase binding  regulation of protein stability  negative regulation of protein binding  spindle stabilization  positive regulation of mitosis  regulation of centrosome cycle  protein autophosphorylation  phosphatidylinositol-mediated signaling  perinuclear region of cytoplasm  
Ontology : EGO-EBIG2/M transition of mitotic cell cycle  mitotic cell cycle  protein kinase activity  protein serine/threonine kinase activity  protein serine/threonine/tyrosine kinase activity  protein binding  ATP binding  nucleus  centrosome  centrosome  spindle  cytosol  spindle microtubule  protein phosphorylation  cell cycle  spindle organization  mitotic nuclear division  microtubule cytoskeleton  protein kinase binding  cell projection organization  midbody  anaphase-promoting complex-dependent proteasomal ubiquitin-dependent protein catabolic process  spindle pole centrosome  ubiquitin protein ligase binding  regulation of protein stability  negative regulation of protein binding  spindle stabilization  positive regulation of mitosis  regulation of centrosome cycle  protein autophosphorylation  phosphatidylinositol-mediated signaling  perinuclear region of cytoplasm  
Pathways : BIOCARTARole of Ran in mitotic spindle regulation [Genes]   
Pathways : KEGGOocyte meiosis   
Protein Interaction DatabaseAURKA
DoCM (Curated mutations)AURKA
Wikipedia pathwaysAURKA
Gene fusion - rearrangements
Polymorphisms : SNP, variants
NCBI Variation ViewerAURKA [hg38]
dbSNP Single Nucleotide Polymorphism (NCBI)AURKA
dbVarAURKA
ClinVarAURKA
1000_GenomesAURKA 
Exome Variant ServerAURKA
SNP (GeneSNP Utah)AURKA
SNP : HGBaseAURKA
Genetic variants : HAPMAPAURKA
Genomic Variants (DGV)AURKA [DGVbeta]
Mutations
ICGC Data PortalENSG00000087586 
Somatic Mutations in Cancer : COSMICAURKA 
CONAN: Copy Number AnalysisAURKA 
LOVD (Leiden Open Variation Database)Whole genome datasets
LOVD (Leiden Open Variation Database)LOVD - Leiden Open Variation Database
LOVD (Leiden Open Variation Database)LOVD 3.0 shared installation
Impact of mutations[PolyPhen2] [SIFT Human Coding SNP] [Buck Institute : MutDB] [Mutation Assessor] 
Diseases
DECIPHER (Syndromes)20:54944445-54967351
Mutations and Diseases : HGMDAURKA
OMIM603072   
MedgenAURKA
NextProtO14965 [Medical]
GENETestsAURKA
Disease Genetic AssociationAURKA
Huge Navigator AURKA [HugePedia]  AURKA [HugeCancerGEM]
snp3D : Map Gene to Disease6790
DGIdb (Drug Gene Interaction db)AURKA
General knowledge
Homologs : HomoloGeneAURKA
Homology/Alignments : Family Browser (UCSC)AURKA
Phylogenetic Trees/Animal Genes : TreeFamAURKA
Chemical/Protein Interactions : CTD6790
Chemical/Pharm GKB GenePA36201
Clinical trialAURKA
Cancer Resource (Charite)ENSG00000087586
Other databases
Probes
Litterature
PubMed423 Pubmed reference(s) in Entrez
CoreMineAURKA
GoPubMedAURKA
iHOPAURKA

Bibliography

A homologue of Drosophila aurora kinase is oncogenic and amplified in human colorectal cancers.
Bischoff JR, Anderson L, Zhu Y, Mossie K, Ng L, Souza B, Schryver B, Flanagan P, Clairvoyant F, Ginther C, Chan CS, Novotny M, Slamon DJ, Plowman GD.
EMBO J. 1998 Jun 1;17(11):3052-65.
PMID 9606188
 
Identification of phosphorylated residues that affect the activity of the mitotic kinase Aurora-A.
Littlepage LE, Wu H, Andresson T, Deanehan JK, Amundadottir LT, Ruderman JV.
Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15440-5.
PMID 12422018
 
Amplification/Overexpression of a Mitotic Kinase Gene in Human Bladder Cancer.
Sen S, Zhou H, Zhang RD, Yoon DS, Vakar-Lopez F, Ito S, Jiang F, Johnston D, Grossman HB, Ruifrok AC, Katz RL, Brinkley W, Czerniak B.
J Natl Cancer Inst. 2002 Sep 4;94(17):1320-9.
PMID 12208897
 
Aurora-A and an interacting activator, the LIM protein Ajuba, are required for mitotic commitment in human cells.
Hirota T, Kunitoku N, Sasayama T, Marumoto T, Zhang D, Nitta M, Hatakeyama K, Saya H.
Cell. 2003 Sep 5;114(5):585-98.
PMID 13678582
 
The Aurora kinases: role in cell transformation and tumorigenesis.
Katayama H, Brinkley WR, Sen S.
Cancer Metastasis Rev. 2003 Dec; 22(4): 451-64. (Review).
PMID 12884918
 
STK15 polymorphisms and association with risk of invasive ovarian cancer.
Dicioccio RA, Song H, Waterfall C, Kimura MT, Nagase H, McGuire V, Hogdall E, Shah MN, Luben RN, Easton DF, Jacobs IJ, Ponder BA, Whittemore AS, Gayther SA, Pharoah PD, Kruger-Kjaer S.
Cancer Epidemiol Biomarkers Prev. 2004 Oct;13(10):1589-94.
PMID 15466974
 
Overexpression and amplification of Aurora-A in hepatocellular carcinoma.
Jeng YM, Peng SY, Lin CY, Hsu HC.
Clin Cancer Res. 2004 Mar 15;10(6):2065-71.
PMID 15041727
 
Aurora-A abrogation of p53 DNA binding and transactivation activity by phosphorylation of serine 215.
Liu Q, Kaneko S, Yang L, Feldman RI, Nicosia SV, Chen J, Cheng JQ.
J Biol Chem. 2004 Dec 10;279(50):52175-82. Epub 2004 Oct 6.
PMID 15469940
 
Overexpression of Aurora-A Contributes to Malignant Development of Human Esophageal Squamous Cell Carcinoma.
Tong T, Zhong Y, Kong J, Dong L, Song Y, Fu M, Liu Z, Wang M, Guo L, Lu S, Wu M, Zhan Q.
Clin Cancer Res. 2004 Nov 1;10(21):7304-10.
PMID 15534106
 
Two functional coding single nucleotide polymorphisms in STK15 (Aurora-A) coordinately increase esophageal cancer risk.
Kimura MT, Mori T, Conroy J, Nowak NJ, Satomi S, Tamai K, Nagase H.
Cancer Res. 2005 May 1;65(9):3548-54.
PMID 15867347
 
A functional interplay between Aurora-A, Plk1 and TPX2 at spindle poles: Plk1 controls centrosomal localization of Aurora-A and TPX2 spindle association.
De Luca M, Lavia P, Guarguaglini G.
Cell Cycle. 2006 Feb;5(3):296-303. Epub 2006 Feb 7.
PMID 16418575
 
AURKA is one of the downstream targets of MAPK1/ERK2 in pancreatic cancer.
Furukawa T, Kanai N, Shiwaku HO, Soga N, Uehara A, Horii A.
Oncogene. 2006 Aug 10;25(35):4831-9.
PMID 16532023
 
Aurora-A and p16 polymorphisms contribute to an earlier age at diagnosis of pancreatic cancer in Caucasians.
Chen J, Li D, Wei C, Sen S, Killary AM, Amos CI, Evans DB, Abbruzzese JL, Frazier ML.
Clin Cancer Res. 2007 May 15;13(10):3100-4.
PMID 17505013
 
Consortium analysis of 7 candidate SNPs for ovarian cancer.
Couch FJ, Sinilnikova O, Vierkant RA, Pankratz VS, Fredericksen ZS, Stoppa-Lyonnet D, Coupier I, Hughes D, Hardouin A, Berthet P, Peock S, Cook M, Baynes C, Hodgson S, Morrison PJ, Porteous ME, Jakubowska A, Lubinski J, Gronwald J, Spurdle AB; kConFab, Schmutzler R, Versmold B, Engel C, Meindl A, Sutter C, Horst J, Schaefer D, Offit K, Kirchhoff T, Andrulis IL, Ilyushik E, Glendon G, Devilee P, Vreeswijk MP, Vasen HF, Borg A, Backenhorn K, Struewing JP, Greene MH, Neuhausen SL, Rebbeck TR, Nathanson K, Domchek S, Wagner T, Garber JE, Szabo C, Zikan M, Foretova L, Olson JE, Sellers TA, Lindor N, Nevanlinna H, Tommiska J, Aittomaki K, Hamann U, Rashid MU, Torres D, Simard J, Durocher F, Guenard F, Lynch HT, Isaacs C, Weitzel J, Olopade OI, Narod S, Daly MB, Godwin AK, Tomlinson G, Easton DF, Chenevix-Trench G, Antoniou AC; Consortium of Investigators of Modifiers of BRCA1/2.
Cancer Epidemiol Biomarkers Prev. 2007 Jul;16(7):1416-21.
PMID 17627006
 
Simultaneous Aurora-A/STK15 overexpression and centrosome amplification induce chromosomal instability in tumour cells with a MIN phenotype.
Lentini L, Amato A, Schillaci T, Di Leonardo A.
BMC Cancer. 2007 Nov 13;7:212.
PMID 17999753
 
Aurora A kinase RNAi and small molecule inhibition of Aurora kinases with VE-465 induce apoptotic death in multiple myeloma cells.
Evans R, Naber C, Steffler T, Checkland T, Keats J, Maxwell C, Perry T, Chau H, Belch A, Pilarski L, Reiman T.
Leuk Lymphoma. 2008 Mar;49(3):559-69.
PMID 18297535
 
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Written05-2008Laura Lentini, Aldo Di Leonardo
Department of Cellular and Developmental Biology A, Monroy, University of Palermo, viale delle Scienze, Palermo, Italy

Citation

This paper should be referenced as such :
Lentini, L ; Di, Leonardo A
AURKA (aurora kinase A)
Atlas Genet Cytogenet Oncol Haematol. 2009;13(4):253-257.
Free journal version : [ pdf ]   [ DOI ]
URL : http://AtlasGeneticsOncology.org/Genes/AURKAID730ch20q13.html

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