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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.
These observations indicate an absolute requirement of cyclin E2 for Xenopus embryogenesis.
Up-regulation of cyclin E2 was observed in gastric cancer tissues.Cyclin E2 was a target of miR-383 in gastric cancer cells.
cyclin E2 participates in regulating viral replication through the CDK2/SAMHD1 phosphorylation pathway in an HBV infection system.
Cyclin A2 or E1 alterations define a homogenous entity of aggressive hepatocellular carcinoma (HCC) subgroup.
the molecular mechanism of trastuzumab action in BT474 cell line may be regulated by miR-26a and miR-30b and CCNE2 overexpression might play an important role in acquired trastuzumab resistance in HER2+ breast cancer.
Knockdown of CCNE2 promoted MCF7 cell apoptosis and G2-stage cell cycle arrest.
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 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-26a regulated mouse hepatocyte proliferation by directly targeting the 3' untranslated regions of cyclin D2/cyclin E2.
In breast cancer patients, high levels of HMGA1 and CCNE2 expression are associated with the YAP/TAZ signature.
data suggests the potential role of monomorphic morphology, high cyclin E2 and Ki67 expression as adverse prognostic factors for TNKLPD
miR-144-5p functions as tumour suppressor in BC cells. CCNE1 and CCNE2 were directly regulated by miR-144-5p and might be good prognostic markers for survival of bladder cancer patients
Our study shows miR-25 is overexpressed in small cell lung cancer and acting as oncogenic regulator by regulating cyclin E2.
Results suggest that the miR-30d-5p/CCNE2 axis may contribute to NSCLC cell proliferation and motility.
Data indicate that miR-26a overexpression inhibited pancreatic cancer cell growth by the downregulation of cyclin E2 expression.
In cancer cells Fbw7, fails to effectively target cyclin E2 for proteosomal degradation.
Cyclin E2 induction of genomic instability by a mechanism distinct from cyclin E1 indicates that these two proteins have unique functions in a cancer setting.
protein and mRNA expressions of Cyclin E2 in nasopharyngeal carcinoma
Tamoxifen resistant tumors displayed enriched expression of genes related to cell cycle and proliferation, as well as elevated activity of E2F transcription factors.
High CCNE2 expression is associated with hepatitis and hepatocarcinogenesis.
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.
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 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 in normal versus oncogenic proliferation.
During embryonic development, the needs for this cyclin can be overcome in mitotic cycles but not in endoreplicating cells.
We propose that such increased E2F activity stabilizes cyclin E and contributes to establish the high and persistent levels of the protein commonly found in human neoplasias.
CaM-dependent cyclin E/CDK2 activity is mediator of known Ca2+ sensitivity of G1/S transition of vascular smooth muscle cells.
This work indicates that-in addition to their function as CDK 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