Atlas Image
Exons are represented by solid dark rectangles.


The CCNA1 gene is located at chromosome 13q12.3-q13 (Yang et al., 1997) and made up of 9 exons and 8 introns that extend over ~ 13 kb (Müller et al., 1999).


2,1 kb mRNA; coding region is from 130 to 1527 bp (Yang et al., 1997). The cyclin A1 promoter does not possess a TATA box, whereas the region upstream of the transcriptional start site region contains four GC boxes, with multiple Sp1-binding sites important for the regulation of cyclin A1 expression (Müller et al., 1999). Three different transcript variants exist: isoform "a" is the longest transcript and encodes the longest isoform; isoform "b" has an alternate in-frame splice site in the 5 coding region resulting in a protein that is 1 amino acid shorter than isoform "a"; isoform "c" contains a distinct 5 UTR and lacks an in-frame portion of the 5 coding region, resulting in a 44 aa shorter N-terminus compared to isoform "a".


None described.


Atlas Image
Schematic diagram of human cyclin A1. The positions of the cyclin box (with the two cyclin box folds) and the polyalanine sequence are shown. Numbers represent the amino acids positions.


MW: 52 kDa. Amino acids (aa): 465 full-length isoform a (464 aa isoform b; 421 aa isoform c). Cyclin A1 is a member of the highly conserved cyclin family whose members are able to control the progression of cells through the cell cycle by activating cyclin-dependent kinases (CDKs). Within the protein the cyclin box is a region of protein sequence homology that is common to all members of the cyclin family and is required for interaction with the CDK partner.


Cyclin A1 expression is tissue-specific and high levels of expression are restricted to testis; a lower expression is reported in other human cell lines and in healthy brain. Cyclin A1 is also expressed in several myeloid leukemia cell lines and various other tumour types (Yang et al., 1997; Wegiel et al., 2008). Cyclin A1 is expressed at low levels in G0 phase and increases in early G1, S and G2/M phases (Yang et al., 1997; Yang et al., 1999).


Mammalian cyclin A1 is primarily localized in the nuclei of spermatocytes in mouse and human (Liu et al., 1998; Liao et al., 2004). Cyclin A1 has an important role in the development of acute myeloid leukemia (AML): its localization in normal hematopoietic cells is nuclear, whereas in leukemic cells from AML patients and cell lines, it is predominantly cytoplasmic (Ekberg et al., 2004).


Cyclin A1 belongs to the A-type cyclin family of proteins originally identified as 60 kDa polypeptides associated to CDK2 and interacting with viral proteins (Giordano et al., 1989; Giordano et al., 1991). Cyclin A family members are characterized by a typical periodicity in protein abundance through the cell division cycle functioning as activating subunits of enzymatic complexes, together with cyclin-dependent kinases (CDKs) (Lapenna and Giordano, 2009). Cyclin A2, also known as cyclin A, is the major A-type cyclin in mammals. Cyclin A1 primarily functions in the meiotic cell cycle, but it also seems to contribute to G1/S cell cycle progression in somatic cells (Ji et al., 2005). Human cyclin A1 interacts with CDK2 in vitro and in vivo (Yang et al., 1997) and the resulting complex is essential for spermatogenesis and contributes to leukemogenesis, although its molecular functions remain largely unclear. Male knockout mice lacking cyclin A1 are infertile owing to a cell cycle arrest before the first meiotic division (Liu et al., 1998). Cyclin A1 interacts also with E2F1 and the retinoblastoma protein (Yang et al., 1999), with GPS2 (Diederichs et al., 2004), binds to and activates B-MYB in leukemic blasts (Müller-Tidow et al., 2001). Moreover the cyclin A1-CDK2 complex regulates DNA double-strand break repair following radiation damage (Müller-Tidow et al., 2004) by competing with CDK2-cyclin A2 for the binding to Ku70, a pivotal player in the non-homologous end-joining double strand break repair pathway, and inhibiting apoptosis through modulating RB functions in leukemia cells (Ji et al., 2007). Consistently, cyclin A1 knockout mice and Xenopus embryos show defects in the DNA repair process and are more prone to undergo apoptosis (Müller-Tidow et al., 2004; Cho et al., 2006). Finally, following exposure to DNA damaging agents, cyclin A1 is strongly upregulated and localizes to the nucleus. Inhibition of this upregulation, through roscovitine treatment, resulted in a significant decrease of DNA repair and an increase of DNA damage over time (Federico et al., 2010).


The percentage of identity below represents identity over an aligned protein region using pairwise alignment function of ClustalW software:
Bos taurus: 87%
Rattus norvegicus: 85%
Mus musculus: 84%
Xenopus tropicalis: 60%
Xenopus laevis: 59%
Danio rerio: 53%





Some mutations in the CCNA1 gene have been found in several tumor types. No insertions, nonsense substitutions or deletions have been described, whereas, some substitutions leading to missense (P50L in skin; A429V in stomach; C452Y in ovary) or silent mutations (Y107Y in stomach; L122L in lung; A391A in ovary) have been reported and were obtained from the Sanger Institute Catalogue Of Somatic Mutations In Cancer web site (Bamford et al., 2004).

Implicated in

Entity name
Cyclin A1 is expressed in the majority of myeloid and undifferentiated hematological malignancies as well as in normal hematopoietic progenitor cells (Krämer et al., 1998). It has an important role in the development of acute myeloid leukemia (AML): overexpression of murine cyclin A1 in the myeloid lineage of transgenic mice leads to abnormal myelopoiesis in the first months after birth and to the development of AML at a low frequency over the course of 7-14 months. This indicates that cyclin A1 overexpression results in abnormal myelopoiesis and is necessary to induce transformation thus contributing to leukemogenesis (Liao et al., 2001). Cyclin A1 expression is an independent prognostic factor in predicting overall survival and disease-free survival in AML patients (Ekberg et al., 2005) and high expression levels of both cyclin A2 and A1 are associated with good prognosis in the same patients (Nakamaki et al., 2003). Its localization in normal hematopoietic cells is nuclear, whereas in leukemic cells from AML patients and cell lines, it is predominantly cytoplasmic (Ekberg et al., 2004). The frequency of cyclin A1 overexpression is also high in acute promyelocytic leukemia (APL) as a consequence of the APL-associated aberrant fusion proteins (PML-retinoic acid receptor alpha [PML-RAR alpha] or PLZF-RAR alpha) (Müller et al., 2000). Cyclin A1 is highly expressed in lymphoblastic leukemic cell lines and in childhood acute lymphoblastic leukemia (ALL) patients and its expression correlates with patient age and with a poorer event-free survival (Holm et al., 2006). Interestingly, in human promyelocytic leukemia cells HL60, cyclin A1 expression is regulated by a miR34b-CREB axis, which seems to be crucial for myeloid transformation (Pigazzi et al., 2009).
AML is a relatively rare cancer of the myeloid line of blood cells, characterized by the rapid growth of abnormal white blood cells that accumulate in the bone marrow and do not mature, thereby interfering with the production of normal blood cells. APL is a subtype of AML characterized by a chromosomal translocation involving the retinoic acid receptor alpha (RARα or RARA) gene and is unique, compared to other forms of AML, in its responsiveness to all trans retinoic acid (ATRA) therapy. In ALL, malignant, immature white blood cells continuously multiply and are overproduced in the bone marrow. ALL causes damage and death by crowding out normal cells in the bone marrow, and by spreading to other organs.
Entity name
Prostate cancer
Cyclin A1 promotes cell survival in response to growth factors through PI3K/Akt signaling (Wegiel et al., 2008). Also, cyclin A1 mediates VEGF expression in cooperation with Rb- and androgen-dependent pathways (Wegiel et al., 2005). In particular, cyclin A1, by interacting with AR, binds to VEGF and MMP2 promoters and increases their expression, thus contributing to prostate cancer invasion (Wegiel et al., 2008).
Prostate cancer is a slow-growing cancer that develops in the prostate. Cancer cells can metastasize from the prostate to secondary sites, particularly the bones and lymph nodes. Treatment options are primarily surgery, radiation therapy, stereotactic radiosurgery and proton therapy.
Many prostate cancers are successfully cured and most patients will ultimately die from causes other than the disease itself.
Entity name
Testicular cancer
Cyclin A1 is highly expressed in aggressive testicular germ cell tumors (Müller-Tidow et al., 2003). Among the different histological subtypes of testicular tumors, embryonal cell carcinomas and immature teratomas expressed the highest levels of cyclin A1, whereas intermediate levels were expressed in seminomas and yolk sac tumors. Cyclin A1 expression was very low in mature teratomas.
Testicular cancer is a common cancer in males that develops in testicles. If it is diagnosed early, in the great majority of cases it can be treated by surgery, radiation and/or chemotherapy.
Entity name
Cervical cancer
Ectopic expression of miR-372 suppresses cell growth and induces arrest in the S/G2 phases of cell cycle in HeLa cells by targeting CDK2 and cyclin A1 (Tian et al., 2011). Also, it seems that in invasive cervical cancer the integrated form of HPV might affect CCNA1 promoter methylation (Yanatatsaneejit et al., 2011). In human cervical cancer cells, down-regulation of pSrcY416 inhibits cell proliferation by increasing the cell population in the G0-G1 phase and causes the up-regulation of p21Cip1 and p27Kip1 and the decrease of cyclin A1, cyclin E, and CDK-6, cyclin B and CDK-2 (Kong et al., 2011). Also, overexpressed Notch1 results in significant growth inhibition of human cervical carcinoma cells, which is related to a decrease of cyclin A1, cyclin E and pRb protein expression (Wang et al., 2007). The CCNA1 gene is never methylated in normal cervices and rarely in low-grade squamous intraepithelial lesions, whereas its methylation frequency increases with the severity of cervical lesions (Yang et al., 2010). In human papillomavirus-associated cervical cancer, promoter hypermethylation is also specific to the invasive phenotype in comparison with other histopathological stages during multistep carcinogenesis (Kitkumthorn et al., 2006).
Cervical cancer is a malignant neoplasm of the cervix. In almost all cases, human papillomavirus (HPV) infection is a necessary factor in the development of this cancer. Treatment includes surgery in early stages and chemotherapy and radiotherapy in advanced stages of the disease.
It is usually a slow-growing cancer, in some cases there might be no obvious symptoms until the cancer is in its advanced stages.
Entity name
Head and neck squamous cell carcinoma (HNSCC)
Methylation of CCNA1 is an important risk factors for HNSCC development since the cyclin A1 promoter is methylated in salivary rinses from HNSCC patients (Sun et al., 2012). The CCNA1 promoter is methylated in 45% of tumours but in none of the normal tissues and this methylation is inversely related to p53 mutational status in primary tumors (Tokumaru et al., 2004). In another study, cyclin A1 promoter methylation is associated with human papillomavirus 16 induced HNSCC, independently of p53 mutation (Weiss et al., 2011).
HNSCC refers to the squamous cell carcinomas of the oral cavity, pharynx and larynx. The major risk factor for head and neck cancer is chronic exposure of epithelia to tobacco smoke and alcohol, UV light, some chemicals and human papillomavirus.
HNSCC are frequently aggressive; patients are at a higher risk of developing another cancer in the head and neck area. These cancers are highly curable if detected early, surgery and radiotherapy are the main modality of treatment. Chemotherapy, acting as a radio-sensitizer, increases survival in locally advanced disease. Recently, inhibition of epidermal growth factor receptor (EGFR) has proved a successful therapeutic strategy.
Entity name
Bladder cancer
The CCNA1 promoter has been found hypermethylated in urine sediments from bladder cancer patients (Yu et al., 2007). Also, in another study, the CCNA1 gene displays high frequency of methylation in bladder cancer samples and no methylation in normal uroepithelium, indicating a potential role of cyclin A1 in the pathogenesis and spread of bladder cancer (Brait et al., 2008). Interestingly, the deubiquitinating enzyme USP2a can bind cyclin A1 and consequently blocks its ubiquitination and degradation. Enforced expression of USP2a resulted in cyclin A1 accumulation and increased cell proliferation in bladder cancer cells (Kim et al., 2012).
Bladder cancer is a cancer of the urothelium. Treatment options for people with bladder cancer are surgery, chemotherapy, biological therapy, and radiation therapy.
Entity name
Breast cancer
Six1 overexpression in mammary cells induces genomic instability and malignant transformation that is dependent on upregulation of its transcriptional target cyclin A1 (Coletta et al., 2004). Consistently, in another study, the tumor suppressor miR-185, by inhibiting the expression of Six1 and consequently of its transcriptional targets c-myc and Cyclin A1, sensitizes cancer cells to apoptosis (Imam et al., 2010). Also, in the malignant breast cancer cell line MDA-MB-231, the dysregulation of activating transcription factor-3 by TGFβ1 activates cyclin A1 and MMP-13 leading to cell invasion and metastasis (Kwok et al., 2009). The histone demethylase JMJD2B is regulated by both ERalpha and HIF-1alpha driving breast cancer cell proliferation in normoxia and hypoxia, and epigenetically regulates the expression of cell cycle genes such as CCND1, CCNA1, and WEE1 (Yang et al., 2010). On the contrary, the dietary supplement BreastDefend inhibits proliferation and invasive behavior of the highly metastatic MDA-MB-231 cell line by downregulating the expression of CCNA1 and CDK6 genes (Jiang et al., 2011). Bisphenol A promotes mammary carcinogenesis by stimulating the DNA methylation of genes related to development of most or all tumor types, including the CCNA1 gene (Qin et al., 2012).
Breast cancer is a type of cancer originating from breast tissue. The size, stage, rate of growth and other characteristics of the tumor determine the kinds of treatment which may include surgery, hormonal, therapy and chemotherapy, radiation and/or immunotherapy.
Entity name
Other cancers
Some studies indicate a potential tumor suppressor role for cyclin A1 in nasopharyngeal carcinomas, colon carcinomas, oral carcinomas, melanomas, and hepatocellular carcinomas (Yanatatsaneejit et al., 2008; Xu et al., 2004; Shaw et al., 2006; Garrido et al., 2012; Yu et al., 2003). Also, Cyclin A1 mediates apoptosis, G2/M arrest, and mitotic catastrophe in renal, ovarian, and lung carcinoma cells through an inappropriate activation of CDK1 (Rivera et al., 2006). Other studies show that cyclin A1 is overexpressed in human hepatocellular carcinoma (Studach et al., 2012) and correlates with a poor outcome in ependymomas (Lukashova-v Zangen et al., 2007).
The information contained herein was partially compiled using Proteinquest, a software able to automatically parse the scientific literature to extract relevant data.


Pubmed IDLast YearTitleAuthors
151880092004The COSMIC (Catalogue of Somatic Mutations in Cancer) database and website.Bamford S et al
188430242008Aberrant promoter methylation of multiple genes during pathogenesis of bladder cancer.Brait M et al
169843812006Induction of cell apoptosis in non-small cell lung cancer cells by cyclin A1 small interfering RNA.Cho NH et al
151238402004The Six1 homeoprotein stimulates tumorigenesis by reactivation of cyclin A1.Coletta RD et al
151594022004Identification of interaction partners and substrates of the cyclin A1-CDK2 complex.Diederichs S et al
160046072005Expression of cyclin A1 and cell cycle proteins in hematopoietic cells and acute myeloid leukemia and links to patient outcome.Ekberg J et al
154898992004Regulation of the cyclin A1 protein is associated with its differential subcellular localization in hematopoietic and leukemic cells.Ekberg J et al
206847762010R-Roscovitine (Seliciclib) prevents DNA damage-induced cyclin A1 upregulation and hinders non-homologous end-joining (NHEJ) DNA repair.Federico M et al
222191782012MHC class I molecules act as tumor suppressor genes regulating the cell cycle gene expression, invasion and intrinsic tumorigenicity of melanoma cells.Garrido C et al
16539691991Cell cycle regulation of histone H1 kinase activity associated with the adenoviral protein E1A.Giordano A et al
161823642006Cyclin A1 expression and associations with disease characteristics in childhood acute lymphoblastic leukemia.Holm C et al
206036202010MicroRNA-185 suppresses tumor growth and progression by targeting the Six1 oncogene in human cancers.Imam JS et al
158299812005Cyclin A1, the alternative A-type cyclin, contributes to G1/S cell cycle progression in somatic cells.Ji P et al
174552442007DNA damage response involves modulation of Ku70 and Rb functions by cyclin A1 in leukemia cells.Ji P et al
209267362011Suppression of proliferation and invasive behavior of human metastatic breast cancer cells by dietary supplement BreastDefend.Jiang J et al
223704832012The ubiquitin-specific protease USP2a enhances tumor progression by targeting cyclin A1 in bladder cancer.Kim J et al
165244602006Cyclin A1 promoter hypermethylation in human papillomavirus-associated cervical cancer.Kitkumthorn N et al
205326782011Down-regulation of phospho-non-receptor Src tyrosine kinases contributes to growth inhibition of cervical cancer cells.Kong L et al
96394171998Cyclin A1 is predominantly expressed in hematological malignancies with myeloid differentiation.Krämer A et al
195827872009Transforming growth factor-beta1 regulation of ATF-3 and identification of ATF-3 target genes in breast cancer cells.Kwok S et al
195682822009Cell cycle kinases as therapeutic targets for cancer.Lapenna S et al
146960912004Elevated levels and distinct patterns of expression of A-type cyclins and their associated cyclin-dependent kinases in male germ cell tumors.Liao C et al
113811402001Altered myelopoiesis and the development of acute myeloid leukemia in transgenic mice overexpressing cyclin A1.Liao C et al
98432121998Cyclin A1 is required for meiosis in the male mouse.Liu D et al
172650492007Ependymoma gene expression profiles associated with histological subtype, proliferation, and patient survival.Lukashova-v Zangen I et al
110900752000The aberrant fusion proteins PML-RAR alpha and PLZF-RAR alpha contribute to the overexpression of cyclin A1 in acute promyelocytic leukemia.Müller C et al
154568662004The cyclin A1-CDK2 complex regulates DNA double-strand break repair.Müller-Tidow C et al
145109452003Elevated levels of cyclin A1 and A (A2) mRNA in acute myeloid leukaemia are associated with increased survival.Nakamaki T et al
192584992009miR-34b targets cyclic AMP-responsive element binding protein in acute myeloid leukemia.Pigazzi M et al
222580362012Effects of bisphenol A exposure on the proliferation and senescence of normal human mammary epithelial cells.Qin XY et al
167998732006Cyclin A1 is a p53-induced gene that mediates apoptosis, G2/M arrest, and mitotic catastrophe in renal, ovarian, and lung carcinoma cells.Rivera A et al
164499962006Promoter methylation of P16, RARbeta, E-cadherin, cyclin A1 and cytoglobin in oral cancer: quantitative evaluation using pyrosequencing.Shaw RJ et al
225053172012Subset of Suz12/PRC2 target genes is activated during hepatitis B virus replication and liver carcinogenesis associated with HBV X protein.Studach LL et al
224389732012Comparison of promoter hypermethylation pattern in salivary rinses collected with and without an exfoliating brush from patients with HNSCC.Sun W et al
216463512011MicroRNA-372 is down-regulated and targets cyclin-dependent kinase 2 (CDK2) and cyclin A1 in human cervical cancer, which may contribute to tumorigenesis.Tian RQ et al
153423772004Inverse correlation between cyclin A1 hypermethylation and p53 mutation in head and neck cancer identified by reversal of epigenetic silencing.Tokumaru Y et al
174256822007Overexpressed active Notch1 induces cell growth arrest of HeLa cervical carcinoma cells.Wang L et al
186121292008Multiple cellular mechanisms related to cyclin A1 in prostate cancer invasion and metastasis.Wegiel B et al
215632162011Promoter methylation of cyclin A1 is associated with human papillomavirus 16 induced head and neck squamous cell carcinoma independently of p53 mutation.Weiss D et al
155263632004Methylation profile of the promoter CpG islands of 31 genes that may contribute to colorectal carcinogenesis.Xu XL et al
214121592011Human papillomavirus's physical state and cyclin A1 promoter methylation in cervical cancer.Yanatatsaneejit P et al
206827972010The histone demethylase JMJD2B is regulated by estrogen receptor alpha and hypoxia, and is a key mediator of estrogen induced growth.Yang J et al
202081412010Gene promoter methylation patterns throughout the process of cervical carcinogenesis.Yang N et al
90411941997Characterization of a second human cyclin A that is highly expressed in testis and in several leukemic cell lines.Yang R et al
100229261999Functions of cyclin A1 in the cell cycle and its interactions with transcription factor E2F-1 and the Rb family of proteins.Yang R et al
146725552003Methylation profiling of twenty four genes and the concordant methylation behaviours of nineteen genes that may contribute to hepatocellular carcinogenesis.Yu J et al
180944102007A novel set of DNA methylation markers in urine sediments for sensitive/specific detection of bladder cancer.Yu J et al

Other Information

Locus ID:

NCBI: 8900
MIM: 604036
HGNC: 1577
Ensembl: ENSG00000133101


dbSNP: 8900
ClinVar: 8900
TCGA: ENSG00000133101


Gene IDTranscript IDUniprot

Expression (GTEx)



PathwaySourceExternal ID
Cell cycleKEGGko04110
Progesterone-mediated oocyte maturationKEGGko04914
Acute myeloid leukemiaKEGGko05221
Cell cycleKEGGhsa04110
Pathways in cancerKEGGhsa05200
Acute myeloid leukemiaKEGGhsa05221
Progesterone-mediated oocyte maturationKEGGhsa04914
Transcriptional misregulation in cancerKEGGko05202
Transcriptional misregulation in cancerKEGGhsa05202
Epstein-Barr virus infectionKEGGhsa05169
Epstein-Barr virus infectionKEGGko05169
Viral carcinogenesisKEGGhsa05203
Viral carcinogenesisKEGGko05203
Hepatitis BKEGGhsa05161
AMPK signaling pathwayKEGGhsa04152
AMPK signaling pathwayKEGGko04152
Cell cycle - G2/M transitionKEGGhsa_M00693
Cell cycle - G2/M transitionKEGGM00693
Metabolism of proteinsREACTOMER-HSA-392499
Post-translational protein modificationREACTOMER-HSA-597592
Gene ExpressionREACTOMER-HSA-74160
Generic Transcription PathwayREACTOMER-HSA-212436
Transcriptional Regulation by TP53REACTOMER-HSA-3700989
Cell CycleREACTOMER-HSA-1640170
Cell Cycle CheckpointsREACTOMER-HSA-69620
G1/S DNA Damage CheckpointsREACTOMER-HSA-69615
p53-Dependent G1/S DNA damage checkpointREACTOMER-HSA-69580
p53-Dependent G1 DNA Damage ResponseREACTOMER-HSA-69563
Cell Cycle, MitoticREACTOMER-HSA-69278
Mitotic G1-G1/S phasesREACTOMER-HSA-453279
G0 and Early G1REACTOMER-HSA-1538133
G1/S TransitionREACTOMER-HSA-69206
Cyclin E associated events during G1/S transitionREACTOMER-HSA-69202
SCF(Skp2)-mediated degradation of p27/p21REACTOMER-HSA-187577
G1/S-Specific TranscriptionREACTOMER-HSA-69205
E2F mediated regulation of DNA replicationREACTOMER-HSA-113510
Cyclin A:Cdk2-associated events at S phase entryREACTOMER-HSA-69656
Synthesis of DNAREACTOMER-HSA-69239
Switching of origins to a post-replicative stateREACTOMER-HSA-69052
Orc1 removal from chromatinREACTOMER-HSA-68949
Regulation of DNA replicationREACTOMER-HSA-69304
Removal of licensing factors from originsREACTOMER-HSA-69300
Mitotic G2-G2/M phasesREACTOMER-HSA-453274
G2/M TransitionREACTOMER-HSA-69275
Cyclin A/B1 associated events during G2/M transitionREACTOMER-HSA-69273
Phosphorylation of proteins involved in the G2/M transition by Cyclin A:Cdc2 complexesREACTOMER-HSA-170145
Regulation of mitotic cell cycleREACTOMER-HSA-453276
APC/C-mediated degradation of cell cycle proteinsREACTOMER-HSA-174143
Regulation of APC/C activators between G1/S and early anaphaseREACTOMER-HSA-176408
Activation of APC/C and APC/C:Cdc20 mediated degradation of mitotic proteinsREACTOMER-HSA-176814
APC/C:Cdc20 mediated degradation of mitotic proteinsREACTOMER-HSA-176409
APC:Cdc20 mediated degradation of cell cycle proteins prior to satisfation of the cell cycle checkpointREACTOMER-HSA-179419
Cdc20:Phospho-APC/C mediated degradation of Cyclin AREACTOMER-HSA-174184
DNA ReplicationREACTOMER-HSA-69306
Cellular responses to stressREACTOMER-HSA-2262752
Cellular SenescenceREACTOMER-HSA-2559583
DNA Damage/Telomere Stress Induced SenescenceREACTOMER-HSA-2559586
Senescence-Associated Secretory Phenotype (SASP)REACTOMER-HSA-2559582
DNA Double-Strand Break RepairREACTOMER-HSA-5693532
Homology Directed RepairREACTOMER-HSA-5693538
HDR through Homologous Recombination (HR) or Single Strand Annealing (SSA)REACTOMER-HSA-5693567
Processing of DNA double-strand break endsREACTOMER-HSA-5693607
TP53 Regulates Transcription of Cell Cycle GenesREACTOMER-HSA-6791312
TP53 Regulates Transcription of Genes Involved in G1 Cell Cycle ArrestREACTOMER-HSA-6804116
Regulation of TP53 ActivityREACTOMER-HSA-5633007
Regulation of TP53 Expression and DegradationREACTOMER-HSA-6806003
Regulation of TP53 DegradationREACTOMER-HSA-6804757
Regulation of TP53 Activity through PhosphorylationREACTOMER-HSA-6804756
Ub-specific processing proteasesREACTOMER-HSA-5689880

Protein levels (Protein atlas)

Not detected


Pubmed IDYearTitleCitations
164499962006Promoter methylation of P16, RARbeta, E-cadherin, cyclin A1 and cytoglobin in oral cancer: quantitative evaluation using pyrosequencing.66
204578932010KDM8, a H3K36me2 histone demethylase that acts in the cyclin A1 coding region to regulate cancer cell proliferation.58
153423772004Inverse correlation between cyclin A1 hypermethylation and p53 mutation in head and neck cancer identified by reversal of epigenetic silencing.53
183729192008Cyclin A/cdk2 coordinates centrosomal and nuclear mitotic events.52
154568662004The cyclin A1-CDK2 complex regulates DNA double-strand break repair.43
216463512011MicroRNA-372 is down-regulated and targets cyclin-dependent kinase 2 (CDK2) and cyclin A1 in human cervical cancer, which may contribute to tumorigenesis.38
186121292008Multiple cellular mechanisms related to cyclin A1 in prostate cancer invasion and metastasis.34
198436772009Methylation markers for CCNA1 and C13ORF18 are strongly associated with high-grade cervical intraepithelial neoplasia and cervical cancer in cervical scrapings.31
158299812005Cyclin A1, the alternative A-type cyclin, contributes to G1/S cell cycle progression in somatic cells.26
202199232010Role of human immunodeficiency virus type 1 integrase in uncoating of the viral core.26


Immacolata Vocca ; Gianmarco Muzi ; Francesca Pentimalli ; Antonio Giordano

CCNA1 (cyclin A1)

Atlas Genet Cytogenet Oncol Haematol. 2012-05-01

Online version: