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miR (show MYLIP Antibodies)-15/16 and CPEB co-regulate cyclin E1 (show CCNE1 Antibodies) mRNA.
cyclin E (show CCNE1 Antibodies) is dynamically and highly conjugated to SUMO2 (show SUMO2 Antibodies)/3 on chromatin, independently of Cdk2 (show CDK2 Antibodies) activity and origin activation.
These results show that cyclin E (show CCNE1 Antibodies) destruction at the midblastula transition requires both phosphorylation and nuclear import, as well as proteasomal activity.
These observations indicate an absolute requirement of cyclin E2 for Xenopus embryogenesis.
Combinatorial PX-866 and Raloxifene Decrease Rb Phosphorylation, Cyclin E2 Transcription, and Proliferation of MCF-7 Breast Cancer Cells
The results suggest that miR30a may function as a novel tumor suppressor in CRPC. Its antioncogenic activity may occur by the reduced expression of a distinct cell cycle protein, CCNE2.
Overexpression of cyclin E2 is an early event in gastric carcinogenesis.
Survivin (show BIRC5 Antibodies) and cyclin E2 genes expression may have clinical relevance and can be considered as molecular risk factors for AL. Also they may be useful as predictive markers for treatment outcome in leukemic patients.
miR (show MLXIP Antibodies)-26a regulated mouse hepatocyte proliferation by directly targeting the 3' untranslated regions of cyclin D2 (show CCND2 Antibodies)/cyclin E2.
In breast cancer patients, high levels of HMGA1 (show HMGA1 Antibodies) and CCNE2 expression are associated with the YAP (show YAP1 Antibodies)/TAZ (show TAZ Antibodies) signature.
data suggests the potential role of monomorphic morphology, high cyclin E2 and Ki67 (show MKI67 Antibodies) expression as adverse prognostic factors for TNKLPD
miR (show MLXIP Antibodies)-144-5p functions as tumour suppressor in BC cells. CCNE1 (show CCNE1 Antibodies) and CCNE2 were directly regulated by miR (show MLXIP Antibodies)-144-5p and might be good prognostic markers for survival of bladder cancer patients
Our study shows miR (show MLXIP Antibodies)-25 is overexpressed in small cell lung cancer and acting as oncogenic regulator by regulating cyclin E2.
Results suggest that the miR (show MLXIP Antibodies)-30d-5p/CCNE2 axis may contribute to NSCLC cell proliferation and motility.
This approach allowed us to determine the identity of cyclin E (show CCNE1 Antibodies) protein partners, as well as phosphorylation substrates of cyclins E (cyclin (show PCNA Antibodies) E1and cyclin E2)and its associated kinase, Cdk2 (show CDK2 Antibodies), in different mouse organs.
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.
These results highlight a new role for E-type cyclins (Ccne1 (show CCNE1 Antibodies) and Ccne2) as important regulators of male meiosis.
These findings define a molecular function for E type cyclins (cyclins E1 and E2) in cell cycle reentry and reveal a differential requirement for cyclin E (show CCNE1 Antibodies) in normal versus oncogenic proliferation.
During embryonic development, the needs for this cyclin (show PCNA Antibodies) can be overcome in mitotic cycles but not in endoreplicating cells.
We propose that such increased E2F (show E2F1 Antibodies) activity stabilizes cyclin E (show CCNE1 Antibodies) and contributes to establish the high and persistent levels of the protein commonly found in human neoplasias.
CaM-dependent cyclin E (show CCNE1 Antibodies)/CDK2 (show CDK2 Antibodies) activity is mediator of known Ca2 (show CA2 Antibodies)+ sensitivity of G1/S transition of vascular smooth muscle cells.
This work indicates that-in addition to their function as CDK (show CDK4 Antibodies) activators-E cyclins play kinase-independent functions in cell-cycle progression.
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. This cyclin has been shown to specifically interact with CIP/KIP family of CDK inhibitors, and plays a role in cell cycle G1/S transition. The expression of this gene peaks at the G1-S phase and exhibits a pattern of tissue specificity distinct from that of cyclin E1. A significantly increased expression level of this gene was observed in tumor-derived cells.
, G1/S-specific cyclin-E2
, g1/S-specific cyclin-E2-like
, G1/S-specific cyclin-E1