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miR-874 inhibits CCNE1 expression during growth factor deprivation and that miR-874 down-regulation in osteosarcomas leads to CCNE1 up-regulation and more aggressive growth phenotypes.
Amplified/cyclin E1(hi) and non-amplified/cyclin E1(hi) tumors have different pathological and biological characteristics and clinical outcomes indicating that they are separate subsets of cyclin E1(hi) HGSOC.
Breast cancer recurrence-free interval was significantly worse in patients with cyclin E (LMW-E)-positive tumors who received aromatase inhibitor (AI) neoadjuvant therapy, compared with those with LMW-E negative tumors.
in a series of human biopsies, non-metastatic SCCs displayed a higher degree of chromosomal alterations and higher expression of the S phase regulator Cyclin E and the DNA damage signal gammaH2AX than the less aggressive, non-squamous, basal cell carcinomas. However, metastatic Squamous cell carcinoma lost the gammaH2AX signal and Cyclin E, or accumulated cytoplasmic Cyclin E.
Cytoplasmic cyclin E identifies patients with the highest likelihood of recurrence consistently across different patient cohorts and subtypes. These patients may benefit from alternative therapies targeting the oncogenic isoforms of cyclin E.
our results validate the assumption that CBX7 is a tumor suppressor of gliomas. Moreover, CBX7 is a potential and novel prognostic biomarker in glioma patients. We also clarified that CBX7 silences CCNE1 via the combination of CCNE1 promoter and the recruitment of HDAC2.
Our findings suggest that gene copy-number gain and upregulation of CCNE1 occur in ovarian clear cell carcinoma and are associated with a worse clinical outcome, dictating the survival of early-stage patients.
YAP/ TAZ pathways contribute to the proliferation/quiescence switch during colon cancer 5FU treatment according to the concerted regulation of Cyclin E1 and CREB
Silencing of CDCA5 suppresses proliferation of gastric cancer cells by inducing G1-phase arrest via downregulating CCNE1.
Analysis of genomic data from TCGA demonstrated coamplification of CCNE1 and AKT2 Overexpression of Cyclin E1 and AKT isoforms, in addition to mutant TP53, imparted malignant characteristics in untransformed fallopian tube secretory cells, the dominant site of origin of high-grade serous ovarian cancer
Finding suggest that amplification of CCNE1 serves as one mechanism for the development of some serous tubal intraepithelial carcinomas.
Prognostic gene sets based on the 13 genes were developed, and their prognostic values were verified in three independent patient cohorts (n=501). Among them, a signature of CCNE1 and its coexpressed genes was significantly associated with disease progression and validated in the independent cohorts.
Cyclin E1 mRNA and protein expressions were suppressed.
The opposing effects of ORC1 (represor) and CDC6 (gene activator) in controlling the level of Cyclin E ensures genome stability and a mechanism for linking directly DNA replication and cell division commitment.
High cyclin E expression is associated with breast cancer.
High CCNC1 expression is associated with inflammatory breast cancer.
Inhibition of cell division cycle associated 2 (CDCA2) suppressed the proliferation of lung adenocarcinoma (LAC) cells via G1 phase arrest by downregulating cyclin E1(CCNE1), while overexpression of CDCA2 promoted LAC cells proliferation by upregulating CCNE1.
a PI3K/PKCiota/cyclin E signaling pathway as a therapeutic target during ovarian tumorigenesis
Amplification of the G1-S regulatory genes, CCNE1, CCND1 and CdK6, represent an early event, which precedes ERBB2, EGFR, or KRAS amplification in gastric adenocarcinoma.
Amplification of 19q12 CCNE1/URI was found in 10.4% (28/270) and was significantly associated with type II endometrial cancer (EC) high grade, advanced FIGO stage, and aberrant tumor supressor p53 expression.
study suggests that hepatocellular carcinoma initiation specifically depends on CcnE1 and Cdk2, while HCC progression requires expression of any E-cyclin, but no Cdk2.
ChIP-sequence/ChIP studies indicated that Ad4BP/SF-1 binds to the upstream region of Ccne1 (cyclin E1) gene during G1/S phase.
These results demonstrate a repressor role for NFAT1 in cell cycle progression and Cyclin E expression in B lymphocytes, and suggest a potential function for NFAT1 protein in B cell malignancies.
This approach allowed us to determine the identity of cyclin E protein partners, as well as phosphorylation substrates of cyclins E (cyclin E1and cyclin E2)and its associated kinase, Cdk2, in different mouse organs.
inhibition of PDK4 activity in Hepatocellular carcinoma cells increased cyclin E1, cyclin A2, and E2F1 proteins.
Spermatocytes lacking cyclin E2 and one E1 allele (E1+/-E2-/-) displayed a high rate of telomere abnormalities but can progress to pachytene and diplotene stages.
NF-kappaB-miR-195/497-Igf1r/Insr-Ccnd2/Ccne1 plays important roles in myogenesis.
Myb regulates Cyclin E1 expression in normal gastrointestinal tract epithelial cells and is required during intestinal tumorigenesis
These results highlight a new role for E-type cyclins (Ccne1 and Ccne2) as important regulators of male meiosis.
Concurrent deletion of cyclin E1 and cyclin-dependent kinase 2 in hepatocytes inhibits DNA replication and liver regeneration in mice.
Superoxide dismutase induces G1-phase cell cycle arrest by down-regulated expression of Cdk-2 and cyclin-E in sarcoma tumor cells.
Ablation of cyclin E led to a decreased number of synapses, reduced number and volume of dendritic spines, and resulted in impaired synaptic plasticity and memory formation.
Data show that gastric cancer markers MUC2, and oncogenes c-myc, cyclin E1 were expressed in the gastric carcinoma cell line 3I (MGCC3I).
our fi ndings reveal a direct link between cyclin E and HIF-1 activities in mammary epithelial cells and implicate HIF-1 as a mediator of proliferation-independent phenotypes associated with high cyclin E expression in some human breast cancers.
Report presents the first detailed analysis of cyclin E expression in postmitotic neurons during development and in the adult mouse brain
Results show that deregulation of cyclin E expression contribute to infertility, due to inability of the spermatogonial cells to start the mitotic cycles prior to entering meiosis.
Depletion of cyclin E promoted apoptosis of breast cancer cells and blocked proliferation and transformation.
These results suggest that cyclin E up-regulation and p27(Kip1) loss-of-function act cooperatively on pituitary adenoma development.
Data show that liver-specific ablation of the cyclin E regulator Cullin 3 in mice results in the persistence and massive expansion of hepatic progenitor cells.
cyclin E has a role in megakaryocytic polyploidization
miR-15/16 and CPEB co-regulate cyclin E1 mRNA.
cyclin E is dynamically and highly conjugated to SUMO2/3 on chromatin, independently of Cdk2 activity and origin activation.
These results show that cyclin E destruction at the midblastula transition requires both phosphorylation and nuclear import, as well as proteasomal activity.
intestinal clock controls the expression of key cell cycle regulators, such as cdc2, wee1, p21, PCNA and cdk2, but only weakly influences cyclin B1, cyclin B2 and cyclin E1 expression.
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. This cyclin forms a complex with and functions as a regulatory subunit of CDK2, whose activity is required for cell cycle G1/S transition. This protein accumulates at the G1-S phase boundary and is degraded as cells progress through S phase. Overexpression of this gene has been observed in many tumors, which results in chromosome instability, and thus may contribute to tumorigenesis. This protein was found to associate with, and be involved in, the phosphorylation of NPAT protein (nuclear protein mapped to the ATM locus), which participates in cell-cycle regulated histone gene expression and plays a critical role in promoting cell-cycle progression in the absence of pRB. Two alternatively spliced transcript variants of this gene, which encode distinct isoforms, have been described. Two additional splice variants were reported but detailed nucleotide sequence information is not yet available.
, G1/S-specific cyclin-E1
, G1/S-specific cyclin-E1-like
, g1/S-specific cyclin-E1-like
, cyclin Es
, cyclin Et
, cyclin E
, G1/S-specific cyclin-E2
, G1/S-specific cyclin-E3
, cyclin E3