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E2F directly regulates the expression of late myogenic genes, with E2f1 (zeige E2F1 ELISA Kits) providing the major contribution compared with E2f2.
The dE2F2 protein repress the expression of buffy, the anti-apoptotic member of the Bcl-2 (zeige BCL2 ELISA Kits) family and activate the expression of an RNA-binding protein that destabilizes diap1 (zeige DIAPH1 ELISA Kits) in Drosophila.
Heterozygous mutation of mip120 (zeige LIN54 ELISA Kits) or E2f2 suppressed the binucleate cell phenotype in the peripodial epithelium of Myb (zeige MYB ELISA Kits)-null wing discs.
dE2F2, as well as the net E2F activity, which can be depleted by mutating the common cofactor, dDp (zeige TIMM8A ELISA Kits), is inhibitory for p53 (zeige TUBB ELISA Kits)-independent apoptosis.
RBF1 and RBF2 interact with different subsets of E2F proteins; this enables the RBF (zeige ATP5I ELISA Kits) proteins to regulate E2F-dependent transcription in distinct ways
cells containing dE2F2 require dE2F1 (zeige E2F1 ELISA Kits) to either prevent, or reverse, dE2F (zeige E2F1 ELISA Kits)-mediated repression
Data show that removal of p55 deregulated the expression of E2F targets that are normally repressed by dE2F2/RBF-1 and -2 complexes in a cell cycle-independent manner but had no effect on the expression of targets normally coupled with cell proliferation.
examination of linking together the Myb (zeige MYB ELISA Kits) and E2F2 complexes in higher-order assembly to specific chromosomal sites for the regulation of transcription
RBF2 has a unique function in repressing E2F-regulated differentiation markers and dE2F2 and RBF2 are required to regulate different sets of target genes in different tissues
Thease results demonstrate epigenetic regulation of gene expression by Myb (zeige MYB ELISA Kits), and E2F2-RBF (zeige ATP5I ELISA Kits) in vivo, and also provide an explanation for the ability of Mip130-null mutants to rescue the lethality of Myb (zeige MYB ELISA Kits)-null mutants in vivo.
Accordingly, our results demonstrated that NAMPT (zeige NAMPT ELISA Kits) is a prognostic marker in melanoma, and the identificationofNAMPT-E2F2-SIRT1 (zeige SIRT1 ELISA Kits) pathway establishes another link between NAMPT (zeige NAMPT ELISA Kits) and apoptosis events in melanoma, with therapeutic implications for this deadly cancer.
Compared with patients with variant genotypes of E2F2-rs2742976 and E2F2-rs3218123, patients with common homozygous genotypes had better disease-free survival (both log-rank, P < 0.001) and lower squamous cell carcinoma of the oropharynx recurrence risk (HR, 0.4, 95% CI, 0.3-0.6 and HR, 0.3, 95% CI, 0.2-0.5, respectively) after multivariable adjustment.
Let-7b inhibits the malignant behavior of glioma cells and glioma stem-like cells via downregulation of E2F2.
In NSCLC patients, E2F2 expression was found to be significantly correlated with sex and tumor size. E2F1 (zeige E2F1 ELISA Kits) and E2F2 overexpression showed a significant association with poor prognosis.
Data indicate that microRNA miR (zeige MLXIP ELISA Kits)-214 has tumor-suppressive activity in hepatocellular carcinoma (HCC (zeige FAM126A ELISA Kits)) through inhibition of E2F2 transcription factor (E2F2), cyclin (zeige PCNA ELISA Kits)-dependent kinases CDK3 (zeige CDK3 ELISA Kits) and CDK6 (zeige CDK6 ELISA Kits).
we validated for the first time that E2F2 acts as a tumor activator in non-small cell lung carcinoma.
E2F2 loss results in increased lung metastasis in breast cancer, potentially functioning through a PTPRD (zeige PTPRD ELISA Kits) dependent mechanism.
Elevated E2F2 expression in glioblastoma cells weakens the effect of elevated levels of miR (zeige MLXIP ELISA Kits)-218.
cell cycle-dependent transcription of the TRAIP (zeige TRAIP ELISA Kits) gene by E2F1 (zeige E2F1 ELISA Kits), E2F2, and E2F4 (zeige E2F4 ELISA Kits) and rapid protein degradation leads to cell cycle-dependent expression with a maximum in G2/M
miR218 and miR520a are crucial in the development of hepatocellular carcinoma via the inhibition of cell proliferation and cycle progression by downregulating E2F2.
Genomic structure, expression pattern, and functional characterization of transcription factor E2F-2 from black tiger
Findings implicate E2F-2 in regulating the expression of mitotic kinases that are adapted to perform specialized functions in nuclear condensation and enucleation of maturing erythroblasts.
Spinal cord injury-induced activation of E2F1 (zeige E2F1 ELISA Kits)-2 mediates cell cycle activation, contributing to gliopathy and neuronal/tissue loss associated with motor impairments and post-traumatic hyperesthesia.
A role for E2F1 (zeige E2F1 ELISA Kits) and E2F2 as suppressors of replicative stress in differentiating cells, and the existence of a robust E2F (zeige E2F1 ELISA Kits)-p53 (zeige TP53 ELISA Kits) regulatory axis in tissue homeostasis enabling and tumorigenesis preventing is shown.
E2F2 accumulates at sites of oxidative and UV-induced DNA damage, and interact with gammaH2AX (zeige H2AFX ELISA Kits) DNA repair factor.
E2F2 activity sustains the hepatic homeostasis of major membrane glycerolipid components while it is dispensable for storage glycerolipid balance.
Rb-deficient cells hijack and redeploy Myc (zeige MYC ELISA Kits) and E2f3 from an S-G2 (zeige STRN3 ELISA Kits) program essential for normal cell cycles to a G1-S program that re-engages ectopic cell cycles, exposing an unanticipated addiction of Rb-null cells on Myc (zeige MYC ELISA Kits).
showed that the D326V missense pRb (zeige PGR ELISA Kits) bound to E2F1 (zeige E2F1 ELISA Kits) but failed to interact with E2F2/3
E2F3 promotes while E2F2 suppresses ischemic cardiac repair through corresponding changes in endothelial cell proliferation.
The protein encoded by this gene is a member of the E2F family of transcription factors. The E2F family plays a crucial role in the control of cell cycle and action of tumor suppressor proteins and is also a target of the transforming proteins of small DNA tumor viruses. The E2F proteins contain several evolutionally conserved domains found in most members of the family. These domains include a DNA binding domain, a dimerization domain which determines interaction with the differentiation regulated transcription factor proteins (DP), a transactivation domain enriched in acidic amino acids, and a tumor suppressor protein association domain which is embedded within the transactivation domain. This protein and another 2 members, E2F1 and E2F3, have an additional cyclin binding domain. This protein binds specifically to retinoblastoma protein pRB in a cell-cycle dependent manner, and it exhibits overall 46% amino acid identity to E2F1.
, transcription factor E2F2
, E2F transcription factor 2
, hepatocyte growth factor-like protein