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Silencing of CDCA5 (zeige CDCA5 Proteine) 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 (zeige AKT2 Proteine) Overexpression of Cyclin E1 and AKT (zeige AKT1 Proteine) isoforms, in addition to mutant TP53 (zeige TP53 Proteine), 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 (zeige ORC1L Proteine) (represor) and CDC6 (zeige CDC6 Proteine) (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 (zeige CNGA3 Proteine) expression is associated with inflammatory breast cancer.
Inhibition of cell division cycle associated 2 (CDCA2) suppressed the proliferation of lung adenocarcinoma (LAC (zeige LCT Proteine)) cells via G1 phase arrest by downregulating cyclin E1(CCNE1), while overexpression of CDCA2 promoted LAC (zeige LCT Proteine) cells proliferation by upregulating CCNE1.
a PI3K (zeige PIK3CA Proteine)/PKCiota/cyclin E signaling pathway as a therapeutic target during ovarian tumorigenesis
These results demonstrate a repressor role for NFAT1 (zeige NFAT1 Proteine) in cell cycle progression and Cyclin E expression in B lymphocytes, and suggest a potential function for NFAT1 (zeige NFAT1 Proteine) 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 (zeige PCNA Proteine) E1and cyclin E2 (zeige CCNE2 Proteine))and its associated kinase, Cdk2 (zeige CDK2 Proteine), in different mouse organs.
inhibition of PDK4 (zeige PDK4 Proteine) activity in Hepatocellular carcinoma cells increased cyclin E1, cyclin A2 (zeige CCNA2 Proteine), and E2F1 (zeige E2F1 Proteine) proteins.
Spermatocytes lacking cyclin E2 (zeige CCNE2 Proteine) and one E1 allele (E1+/-E2-/-) displayed a high rate of telomere abnormalities but can progress to pachytene and diplotene stages.
NF-kappaB (zeige NFKB1 Proteine)-miR (zeige MLXIP Proteine)-195/497-Igf1r (zeige IGF1R Proteine)/Insr (zeige INSR Proteine)-Ccnd2 (zeige CCND2 Proteine)/Ccne1 plays important roles in myogenesis.
Myb (zeige MYB Proteine) 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 (zeige CCNE2 Proteine)) as important regulators of male meiosis.
Concurrent deletion of cyclin E1 and cyclin-dependent kinase 2 (zeige CDK2 Proteine) in hepatocytes inhibits DNA replication and liver regeneration in mice.
Superoxide dismutase (zeige SOD1 Proteine) induces G1-phase cell cycle arrest by down-regulated expression of Cdk-2 (zeige CDK2 Proteine) 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.
miR (zeige MYLIP Proteine)-15/16 and CPEB co-regulate cyclin E1 mRNA.
cyclin E is dynamically and highly conjugated to SUMO2 (zeige SUMO2 Proteine)/3 on chromatin, independently of Cdk2 (zeige CDK2 Proteine) 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 (zeige CDK1 Proteine), wee1 (zeige WEE1 Proteine), p21 (zeige CDKN1A Proteine), PCNA (zeige PCNA Proteine) and cdk2 (zeige CDK2 Proteine), but only weakly influences cyclin B1 (zeige CCNB1 Proteine), cyclin B2 (zeige CCNB2 Proteine) 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