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AURKA (aurora kinase A)

Written2008-05Laura Lentini, Aldo Di Leonardo
Department of Cellular, Developmental Biology A, Monroy, University of Palermo, viale delle Scienze, Palermo, Italy

(Note : for Links provided by Atlas : click)

Identity

Alias_namesSTK15
STK6
serine/threonine kinase 15
serine/threonine kinase 6
Alias_symbol (synonym)BTAK
AurA
STK7
ARK1
PPP1R47
AIK
Other aliasAurora A
AURA
Aurora2
MGC34538
HGNC (Hugo) AURKA
LocusID (NCBI) 6790
Atlas_Id 730
Location 20q13.2  [Link to chromosome band 20q13]
Location_base_pair Starts at 56369389 and ends at 56392337 bp from pter ( according to hg19-Feb_2009)  [Mapping AURKA.png]
Fusion genes
(updated 2017)		Data from Atlas, Mitelman, Cosmic Fusion, Fusion Cancer, TCGA fusion databases with official HUGO symbols (see references in chromosomal bands)
AURKA (20q13.2) / PCK1 (20q13.31)BCAS4 (20q13.13) / AURKA (20q13.2)

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

Note
  
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.
  

Bibliography

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Aurora-A and p16 polymorphisms contribute to an earlier age at diagnosis of pancreatic cancer in Caucasians.
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Consortium analysis of 7 candidate SNPs for ovarian cancer.
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STK15 polymorphisms and association with risk of invasive ovarian cancer.
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Aurora A kinase RNAi and small molecule inhibition of Aurora kinases with VE-465 induce apoptotic death in multiple myeloma cells.
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Identification of phosphorylated residues that affect the activity of the mitotic kinase Aurora-A.
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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 ]
On line version : http://AtlasGeneticsOncology.org/Genes/AURKAID730ch20q13.html

Other Leukemias implicated (Data extracted from papers in the Atlas) [ 1 ]
  inv(16)(p13q24) CBFA2T3/GLIS2

Other Solid tumors implicated (Data extracted from papers in the Atlas) [ 4 ]
  Thyroid: Anaplastic (undifferentiated) carcinoma
Male breast cancer
AURKA/PCK1 (20q13)
BCAS4/AURKA (20q13)

External links

Nomenclature
HGNC (Hugo)AURKA   11393
Cards
AtlasAURKAID730ch20q13
Entrez_Gene (NCBI)AURKA  6790  aurora kinase A
AliasesAIK; ARK1; AURA; BTAK; 
PPP1R47; STK15; STK6; STK7
GeneCards (Weizmann)AURKA
Ensembl hg19 (Hinxton)ENSG00000087586 [Gene_View]
Ensembl hg38 (Hinxton)ENSG00000087586 [Gene_View]  ENSG00000087586 [Sequence]  chr20:56369389-56392337 [Contig_View]  AURKA [Vega]
ICGC DataPortalENSG00000087586
TCGA cBioPortalAURKA
AceView (NCBI)AURKA
Genatlas (Paris)AURKA
WikiGenes6790
SOURCE (Princeton)AURKA
Genetics Home Reference (NIH)AURKA
Genomic and cartography
GoldenPath hg38 (UCSC)AURKA  -     chr20:56369389-56392337 -  20q13.2   [Description]    (hg38-Dec_2013)
GoldenPath hg19 (UCSC)AURKA  -     20q13.2   [Description]    (hg19-Feb_2009)
EnsemblAURKA - 20q13.2 [CytoView hg19]  AURKA - 20q13.2 [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_001323303 NM_001323304 NM_001323305 NM_003600 NM_198433 NM_198434 NM_198435 NM_198436 NM_198437
RefSeq genomic (Entrez)
Consensus coding sequences : CCDS (NCBI)AURKA
Cluster EST : UnigeneHs.250822 [ NCBI ]
CGAP (NCI)Hs.250822
Alternative Splicing GalleryENSG00000087586
Gene ExpressionAURKA [ NCBI-GEO ]   AURKA [ EBI - ARRAY_EXPRESS ]   AURKA [ SEEK ]   AURKA [ MEM ]
Gene Expression Viewer (FireBrowse)AURKA [ Firebrowse - Broad ]
SOURCE (Princeton)Expression in : [Datasets]   [Normal Tissue Atlas]  [carcinoma Classsification]  [NCI60]
GenevestigatorExpression in : [tissues]  [cell-lines]  [cancer]  [perturbations]  
BioGPS (Tissue expression)6790
GTEX Portal (Tissue expression)AURKA
Human Protein AtlasENSG00000087586-AURKA [pathology]   [cell]   [tissue]
Protein : pattern, domain, 3D structure
UniProt/SwissProtO14965   [function]  [subcellular_location]  [family_and_domains]  [pathology_and_biotech]  [ptm_processing]  [expression]  [interaction]
NextProtO14965  [Sequence]  [Exons]  [Medical]  [Publications]
With graphics : InterProO14965
Splice isoforms : SwissVarO14965
PhosPhoSitePlusO14965
Domaine pattern : Prosite (Expaxy)PROTEIN_KINASE_ATP (PS00107)    PROTEIN_KINASE_DOM (PS50011)    PROTEIN_KINASE_ST (PS00108)   
Domains : Interpro (EBI)Aur    AURKA    Kinase-like_dom_sf    Prot_kinase_dom    Protein_kinase_ATP_BS    Ser/Thr_kinase_AS   
Domain families : Pfam (Sanger)Pkinase (PF00069)   
Domain families : Pfam (NCBI)pfam00069   
Domain families : Smart (EMBL)S_TKc (SM00220)  
Conserved Domain (NCBI)AURKA
DMDM Disease mutations6790
Blocks (Seattle)AURKA
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    4C3P    4C3R    4CEG    4DEA    4DEB    4DED    4DEE    4DHF    4J8M    4J8N    4JAI    4JAJ    4JBO    4JBP    4JBQ    4O0S    4O0U    4O0W    4PRJ    4UTD    4UYN    4UZD    4UZH    4ZS0    4ZTQ    4ZTR    4ZTS    5AAD    5AAE    5AAF    5AAG    5DN3    5DNR    5DOS    5DPV    5DR2    5DR6    5DR9    5DRD    5DT0    5DT3    5DT4    5EW9    5G15    5G1X    5L8J    5L8K    5L8L    5LXM    5OBJ    5OBR    5ODT    5ONE    5ORL    5ORN    5ORO    5ORP    5ORR    5ORS    5ORT    5ORV    5ORW    5ORX    5ORY    5ORZ    5OS0    5OS1    5OS2    5OS3    5OS4    5OS5    5OS6    5OSD    5OSE    5OSF   
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    4C3P    4C3R    4CEG    4DEA    4DEB    4DED    4DEE    4DHF    4J8M    4J8N    4JAI    4JAJ    4JBO    4JBP    4JBQ    4O0S    4O0U    4O0W    4PRJ    4UTD    4UYN    4UZD    4UZH    4ZS0    4ZTQ    4ZTR    4ZTS    5AAD    5AAE    5AAF    5AAG    5DN3    5DNR    5DOS    5DPV    5DR2    5DR6    5DR9    5DRD    5DT0    5DT3    5DT4    5EW9    5G15    5G1X    5L8J    5L8K    5L8L    5LXM    5OBJ    5OBR    5ODT    5ONE    5ORL    5ORN    5ORO    5ORP    5ORR    5ORS    5ORT    5ORV    5ORW    5ORX    5ORY    5ORZ    5OS0    5OS1    5OS2    5OS3    5OS4    5OS5    5OS6    5OSD    5OSE    5OSF   
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    4C3P    4C3R    4CEG    4DEA    4DEB    4DED    4DEE    4DHF    4J8M    4J8N    4JAI    4JAJ    4JBO    4JBP    4JBQ    4O0S    4O0U    4O0W    4PRJ    4UTD    4UYN    4UZD    4UZH    4ZS0    4ZTQ    4ZTR    4ZTS    5AAD    5AAE    5AAF    5AAG    5DN3    5DNR    5DOS    5DPV    5DR2    5DR6    5DR9    5DRD    5DT0    5DT3    5DT4    5EW9    5G15    5G1X    5L8J    5L8K    5L8L    5LXM    5OBJ    5OBR    5ODT    5ONE    5ORL    5ORN    5ORO    5ORP    5ORR    5ORS    5ORT    5ORV    5ORW    5ORX    5ORY    5ORZ    5OS0    5OS1    5OS2    5OS3    5OS4    5OS5    5OS6    5OSD    5OSE    5OSF   
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    4C3P    4C3R    4CEG    4DEA    4DEB    4DED    4DEE    4DHF    4J8M    4J8N    4JAI    4JAJ    4JBO    4JBP    4JBQ    4O0S    4O0U    4O0W    4PRJ    4UTD    4UYN    4UZD    4UZH    4ZS0    4ZTQ    4ZTR    4ZTS    5AAD    5AAE    5AAF    5AAG    5DN3    5DNR    5DOS    5DPV    5DR2    5DR6    5DR9    5DRD    5DT0    5DT3    5DT4    5EW9    5G15    5G1X    5L8J    5L8K    5L8L    5LXM    5OBJ    5OBR    5ODT    5ONE    5ORL    5ORN    5ORO    5ORP    5ORR    5ORS    5ORT    5ORV    5ORW    5ORX    5ORY    5ORZ    5OS0    5OS1    5OS2    5OS3    5OS4    5OS5    5OS6    5OSD    5OSE    5OSF   
Structural Biology KnowledgeBase1MQ4    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    4C3P    4C3R    4CEG    4DEA    4DEB    4DED    4DEE    4DHF    4J8M    4J8N    4JAI    4JAJ    4JBO    4JBP    4JBQ    4O0S    4O0U    4O0W    4PRJ    4UTD    4UYN    4UZD    4UZH    4ZS0    4ZTQ    4ZTR    4ZTS    5AAD    5AAE    5AAF    5AAG    5DN3    5DNR    5DOS    5DPV    5DR2    5DR6    5DR9    5DRD    5DT0    5DT3    5DT4    5EW9    5G15    5G1X    5L8J    5L8K    5L8L    5LXM    5OBJ    5OBR    5ODT    5ONE    5ORL    5ORN    5ORO    5ORP    5ORR    5ORS    5ORT    5ORV    5ORW    5ORX    5ORY    5ORZ    5OS0    5OS1    5OS2    5OS3    5OS4    5OS5    5OS6    5OSD    5OSE    5OSF   
SCOP (Structural Classification of Proteins)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    4C3P    4C3R    4CEG    4DEA    4DEB    4DED    4DEE    4DHF    4J8M    4J8N    4JAI    4JAJ    4JBO    4JBP    4JBQ    4O0S    4O0U    4O0W    4PRJ    4UTD    4UYN    4UZD    4UZH    4ZS0    4ZTQ    4ZTR    4ZTS    5AAD    5AAE    5AAF    5AAG    5DN3    5DNR    5DOS    5DPV    5DR2    5DR6    5DR9    5DRD    5DT0    5DT3    5DT4    5EW9    5G15    5G1X    5L8J    5L8K    5L8L    5LXM    5OBJ    5OBR    5ODT    5ONE    5ORL    5ORN    5ORO    5ORP    5ORR    5ORS    5ORT    5ORV    5ORW    5ORX    5ORY    5ORZ    5OS0    5OS1    5OS2    5OS3    5OS4    5OS5    5OS6    5OSD    5OSE    5OSF   
CATH (Classification of proteins structures)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    4C3P    4C3R    4CEG    4DEA    4DEB    4DED    4DEE    4DHF    4J8M    4J8N    4JAI    4JAJ    4JBO    4JBP    4JBQ    4O0S    4O0U    4O0W    4PRJ    4UTD    4UYN    4UZD    4UZH    4ZS0    4ZTQ    4ZTR    4ZTS    5AAD    5AAE    5AAF    5AAG    5DN3    5DNR    5DOS    5DPV    5DR2    5DR6    5DR9    5DRD    5DT0    5DT3    5DT4    5EW9    5G15    5G1X    5L8J    5L8K    5L8L    5LXM    5OBJ    5OBR    5ODT    5ONE    5ORL    5ORN    5ORO    5ORP    5ORR    5ORS    5ORT    5ORV    5ORW    5ORX    5ORY    5ORZ    5OS0    5OS1    5OS2    5OS3    5OS4    5OS5    5OS6    5OSD    5OSE    5OSF   
SuperfamilyO14965
Human Protein Atlas [tissue]ENSG00000087586-AURKA [tissue]
Peptide AtlasO14965
HPRD04066
IPIIPI00298940   IPI00790518   IPI00646206   IPI00640695   IPI00641685   IPI00646759   IPI00796387   
Protein Interaction databases
DIP (DOE-UCLA)O14965
IntAct (EBI)O14965
FunCoupENSG00000087586
BioGRIDAURKA
STRING (EMBL)AURKA
ZODIACAURKA
Ontologies - Pathways
QuickGOO14965
Ontology : AmiGOG2/M transition of mitotic cell cycle  mitotic cell cycle  condensed nuclear chromosome, centromeric region  protein kinase activity  protein serine/threonine kinase activity  protein serine/threonine kinase activity  protein serine/threonine/tyrosine kinase activity  protein binding  ATP binding  nucleus  nucleoplasm  centrosome  centrosome  centriole  spindle  cytosol  cytosol  spindle microtubule  spindle microtubule  cilium  protein phosphorylation  DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest  spindle organization  mitotic spindle organization  spindle assembly involved in female meiosis I  mitotic centrosome separation  response to wounding  anterior/posterior axis specification  regulation of G2/M transition of mitotic cell cycle  negative regulation of G2/M transition of mitotic cell cycle  microtubule cytoskeleton  protein kinase binding  midbody  anaphase-promoting complex-dependent catabolic process  spindle pole centrosome  spindle pole centrosome  ubiquitin protein ligase binding  regulation of protein stability  negative regulation of protein binding  chromosome passenger complex  positive regulation of proteasomal ubiquitin-dependent protein catabolic process  regulation of cytokinesis  histone serine kinase activity  histone-serine phosphorylation  germinal vesicle  negative regulation of apoptotic process  axon hillock  pronucleus  positive regulation of mitotic nuclear division  regulation of centrosome cycle  protein autophosphorylation  protein heterodimerization activity  perinuclear region of cytoplasm  spindle midzone  cell division  centrosome localization  protein localization to centrosome  meiotic spindle  liver regeneration  mitotic spindle pole  positive regulation of oocyte maturation  regulation of signal transduction by p53 class mediator  neuron projection extension  
Ontology : EGO-EBIG2/M transition of mitotic cell cycle  mitotic cell cycle  condensed nuclear chromosome, centromeric region  protein kinase activity  protein serine/threonine kinase activity  protein serine/threonine kinase activity  protein serine/threonine/tyrosine kinase activity  protein binding  ATP binding  nucleus  nucleoplasm  centrosome  centrosome  centriole  spindle  cytosol  cytosol  spindle microtubule  spindle microtubule  cilium  protein phosphorylation  DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest  spindle organization  mitotic spindle organization  spindle assembly involved in female meiosis I  mitotic centrosome separation  response to wounding  anterior/posterior axis specification  regulation of G2/M transition of mitotic cell cycle  negative regulation of G2/M transition of mitotic cell cycle  microtubule cytoskeleton  protein kinase binding  midbody  anaphase-promoting complex-dependent catabolic process  spindle pole centrosome  spindle pole centrosome  ubiquitin protein ligase binding  regulation of protein stability  negative regulation of protein binding  chromosome passenger complex  positive regulation of proteasomal ubiquitin-dependent protein catabolic process  regulation of cytokinesis  histone serine kinase activity  histone-serine phosphorylation  germinal vesicle  negative regulation of apoptotic process  axon hillock  pronucleus  positive regulation of mitotic nuclear division  regulation of centrosome cycle  protein autophosphorylation  protein heterodimerization activity  perinuclear region of cytoplasm  spindle midzone  cell division  centrosome localization  protein localization to centrosome  meiotic spindle  liver regeneration  mitotic spindle pole  positive regulation of oocyte maturation  regulation of signal transduction by p53 class mediator  neuron projection extension  
Pathways : KEGGOocyte meiosis   
NDEx NetworkAURKA
Atlas of Cancer Signalling NetworkAURKA
Wikipedia pathwaysAURKA
Orthology - Evolution
OrthoDB6790
GeneTree (enSembl)ENSG00000087586
Phylogenetic Trees/Animal Genes : TreeFamAURKA
HOVERGENO14965
HOGENOMO14965
Homologs : HomoloGeneAURKA
Homology/Alignments : Family Browser (UCSC)AURKA
Gene fusions - Rearrangements
Fusion : MitelmanAURKA/PCK1 [20q13.2/20q13.31]  
Fusion : MitelmanBCAS4/AURKA [20q13.13/20q13.2]  [t(20;20)(q13;q13)]  
Fusion PortalAURKA 20q13.2 PCK1 20q13.31 BRCA
Fusion : QuiverAURKA
Polymorphisms : SNP and Copy number variants
NCBI Variation ViewerAURKA [hg38]
dbSNP Single Nucleotide Polymorphism (NCBI)AURKA
dbVarAURKA
ClinVarAURKA
1000_GenomesAURKA 
Exome Variant ServerAURKA
ExAC (Exome Aggregation Consortium)ENSG00000087586
GNOMAD BrowserENSG00000087586
Varsome BrowserAURKA
Genetic variants : HAPMAP6790
Genomic Variants (DGV)AURKA [DGVbeta]
DECIPHERAURKA [patients]   [syndromes]   [variants]   [genes]  
CONAN: Copy Number AnalysisAURKA 
Mutations
ICGC Data PortalAURKA 
TCGA Data PortalAURKA 
Broad Tumor PortalAURKA
OASIS PortalAURKA [ Somatic mutations - Copy number]
Somatic Mutations in Cancer : COSMICAURKA  [overview]  [genome browser]  [tissue]  [distribution]  
Mutations and Diseases : HGMDAURKA
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
BioMutasearch AURKA
DgiDB (Drug Gene Interaction Database)AURKA
DoCM (Curated mutations)AURKA (select the gene name)
CIViC (Clinical Interpretations of Variants in Cancer)AURKA (select a term)
intoGenAURKA
NCG5 (London)AURKA
Cancer3DAURKA(select the gene name)
Impact of mutations[PolyPhen2] [Provean] [Buck Institute : MutDB] [Mutation Assessor] [Mutanalyser]
Diseases
OMIM603072   
Orphanet
DisGeNETAURKA
MedgenAURKA
Genetic Testing Registry AURKA
NextProtO14965 [Medical]
TSGene6790
GENETestsAURKA
Target ValidationAURKA
Huge Navigator AURKA [HugePedia]
snp3D : Map Gene to Disease6790
BioCentury BCIQAURKA
ClinGenAURKA
Clinical trials, drugs, therapy
Chemical/Protein Interactions : CTD6790
Chemical/Pharm GKB GenePA36201
Clinical trialAURKA
Miscellaneous
canSAR (ICR)AURKA (select the gene name)
Probes
Litterature
PubMed499 Pubmed reference(s) in Entrez
GeneRIFsGene References Into Functions (Entrez)
CoreMineAURKA
EVEXAURKA
GoPubMedAURKA
iHOPAURKA
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed

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