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