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evidence that cyclin A1-associated activity is a mediator of apoptosis and that cyclin A1/Cdk2 is sufficient to induce apoptosis
results suggest that cellular homeostasis of the CYCA1;2/TAM protein is linked to the control of nuclear sizes in trichomes and guard cells
We thus propose that a functional network composed of OSD1, CYCA1;2/TAM, and TDM controls three key steps of meiotic progression, in which OSD1 is a meiotic APC/C inhibitor.
Results propose a model that meiotic progression in Arabidopsis pollen mother cells is driven by a yet to be identified cyclin-CDK activity that is modulated by regulatory interactions between TDM1, SMG7, and TAM (CYCA1;2)
series of CYCA1;2 mutants failed to enter meiosis II and thus produced diploid spores and functional diploid gametes.
Thus, Cyclin A/Cdk1 phosphorylation primes MYPT1 for Plk1 binding. These data demonstrate cross-regulation between Cyclin A/Cdk1-dependent and Plk1-dependent phosphorylation of substrates during mitosis to ensure efficient correction of kinetochore microtubule attachment errors necessary for high mitotic fidelity.
Cyclin A1 functions as an oncogene that controls proliferative and survival activities in tumourigenesis and chemoresistance of ovarian cancer.
In the bone marrow, cyclin A1 and aromatase enhanced local bone marrow-releasing factors, including androgen receptor, estrogen and matrix metalloproteinase MMP9 and promoted the metastatic growth of prostate cancer cells
The data showed that E7 induced CCNA1 methylation by forming a complex with Dnmt1 at the CCNA1 promoter, resulting in the subsequent reduction of expression in cancers.
DNA methylation status of key cell-cycle regulators such as CDKNA2/p16 and CCNA1 correlates with treatment response to doxorubicin and 5-fluorouracil in locally advanced breast tumors.
These data from results indicated a significant connection of CCNA1 methylation with poor progression in human malignant tumors among both Caucasian and Asian populations.
Cyclin A1 immunoexpression is of potential utility in predicting disease progression in patients with pT1 urothelial carcinomas of the bladder
HS3ST2 and CCNA1 genes may play important roles in HPV-induced cervical cancer and patients with specific hypermethylated genes may have a greater risk of progressing to invasive cervical cancer.
CCNA1 promoter methylation is associated with cervical squamous intraepithelial lesions.
High CCNA1 expression is associated with nasopharyngeal carcinoma.
Mutations in genes such as AKT2, CCNA1, MAP3K4, and TGFBR1, were associated significantly with Epstein-Barr-positive gastric tumors, compared with EBV-negative tumors.
Promoter reporter assays with a series of deletion constructs determined that the DNA element from -102 to -96 bp of the cyclin A1 promoter is responsible for PITX2-induced gene expression.
presents CCNA1 and TIMP3 hypermethylation as a helpful tool to identify HNSCC subjects at risk of developing second primary carcinomas
Overexpression of cyclin A1 in FSHD indicates cell cycle dysregulation in FSHD and might contribute to clinical symptoms of this disease
Data indicate that induction of cyclin A1 overexpression in breast cancer cell line MCF-7 results in an enhanced invasiveness and a concomitant increase in vascular endothelial growth factor (VEGF) expression.
Nuclear FoxO3a promotes cell cycle progression by transcriptional upregulation of cyclin A1, promoting proliferation of human anaplastic thyroid carcinoma cells.
These findings indicate the possible involvement of cyclins A and E in the pathogenesis of malignant melanoma.
The organization of actin and cytokeratin cytoskeleton and the expression of TCTP, p53,cyclin A, RhoA and actin in HIO180 non-transformed ovarian epithelial cells, and OVCAR3 and SKOV3 ovarian epithelial cancer cells, was studied.
Cyclin A1 as overexpressed in induced lpuripotent stem cells cells compared to embryonic stem cells, suggesting that during reprogramming, cyclin A1 protein expression levels are not set correctly.
Cyclin A1 is an important cell cycle regulator with age-related increased expression in tonsils of children. HPV16 induces overexpression of Cyclin A1 in HNSCC despite promoter methylation.
wild type control, 14-3-3 is detected in both cytosolic and nuclear fractions whereas it is restricted to the cytoplasm in mutant testes. This differential distribution of 14-3-3 may contribute to the induction of apoptosis in Ccna1-deficient spermatocytes
cyclin A1 in association with vascular endothelial growth factor receptor 1 (VEGFR1), is required for HSPC and their niches to maintain their function and proper interaction
Neither overexpression nor loss of cyclin A1 significantly altered leukemogenesis in PML-RARalpha-knockin mice.
With the recent data on the functions of cyclins in somatic and stem cells, we also discussed the possibilities of further studies of cyclin A1 in mouse oocytes and perhaps in the oogonial stem cells
Sp1 and possibly GATA1 bind concomitantly to the Ccna1 promoter and suppress its activity in vivo.
CIZ1 interacts with germ-cell-specific cyclin A1.
Analysis of Ccna1 transgene expression indicated that sequences within -1.3 kilobases (kb) of the cyclin A1 putative transcriptional start site were sufficient to direct transgene expression uniquely to late spermatocytes.
decreased expression of Ccna1 mRNA and the accumulation of SCP3-positive spermatocytes showed the arrest of spermatogenesis at the pachytene stage in the Dmrt7-knockout mice.
Mip/LIN-9 is required for the expression of B-Myb, and both proteins collaborate in the control of the cell cycle progression via the regulation of S phase and cyclin A, cyclin B, and CDK1
cyclin A1 has a critical role in the pericentromeric region in late diplotene of meiosis, perhaps in assembly or function of the passenger protein complex
Ccna1-deficiency in spermatogenesis is associated with defects in DNA double-strand break repair, which is enhanced by loss of p53.
REVIEW. Some cyclins exhibit unique patterns of expression in germ cells that suggest possible concomitant distinct functions; meiosis-specific function has been shown for cyclin A1.
The results showed that cyclin A overexpression suppressed porcine circovirus type 2 replication.
The protein encoded by this gene belongs to the highly conserved cyclin family, whose members are characterized by a dramatic periodicity in protein abundance through the cell cycle. Cyclins function as regulators of CDK kinases. Different cyclins exhibit distinct expression and degradation patterns which contribute to the temporal coordination of each mitotic event. The cyclin encoded by this gene was shown to be expressed in testis and brain, as well as in several leukemic cell lines, and is thought to primarily function in the control of the germline meiotic cell cycle. This cyclin binds both CDK2 and CDC2 kinases, which give two distinct kinase activities, one appearing in S phase, the other in G2, and thus regulate separate functions in cell cycle. This cyclin was found to bind to important cell cycle regulators, such as Rb family proteins, transcription factor E2F-1, and the p21 family proteins. Multiple transcript variants encoding different isoforms have been found for this gene.
, cyclin A1