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anti-Human E2F2 Antibodies:
anti-Mouse (Murine) E2F2 Antibodies:
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Human Polyclonal E2F2 Primary Antibody for WB - ABIN3043044
Liu, Zhang, Lan, Wang, Mou, Shao, Liu, Yang, Lin, Lin, Ji: GCN5 Potentiates Glioma Proliferation and Invasion via STAT3 and AKT Signaling Pathways. in International journal of molecular sciences 2016
Human Polyclonal E2F2 Primary Antibody for IHC - ABIN6712469
Vui-Kee, Mohd Dali, Mohamed Rose, Ghazali, Jamal, Mokhtar: Molecular markers associated with nonepithelial ovarian cancer in formalin-fixed, paraffin-embedded specimens by genome wide expression profiling. in The Kaohsiung journal of medical sciences 2012
Cow (Bovine) Polyclonal E2F2 Primary Antibody for WB - ABIN2777378
Iwata, Maruyama, Akagi, Hashikawa, Kanazawa, Tsuji, Nukina: Alpha-synuclein degradation by serine protease neurosin: implication for pathogenesis of synucleinopathies. in Human molecular genetics 2003
Show all 2 Pubmed References
these findings indicate that E2F2 may play an important role in pathogenesis of rheumatoid arthritis.
A pathological role for E2F2 was identified in rheumatoid arthritis synovial fibroblasts.
p16INK4a promoted cartilage injury by increasing the expression of E2F2 in chondrocytes.
miR-214 overexpression inhibits glioma cell growth in vitro and in vivo by inducing cell cycle arrest in G0/G1. Collectively, these data uncover a novel role for a PPARalpha-miR-214-E2F2 pathway in controlling glioma cell proliferation.
miR-99a reveals two novel targets E2F2 and EMR2 that play a key role in lung tumourigenesis. By inhibiting E2F2 and EMR2, miR-99a represses in vivo the transition of epithelial cells through an EMT process concomitantly with the inhibition of stemness features and consequently decreasing the CSC population.
Low E2F2 expression is associated with invasion in clear cell renal cell carcinoma.
Data indicate E2F transcription factor 2 protein (E2F2) as the direct target of miR-31 in gastric cancer cells.
Using iterative experimental and computational analyses, the authors show physical and functional interactions between NF-kappaB and the E2 Factor 1 (E2F-1) and E2 Factor 4 (E2F-4) cell cycle regulators.
These results suggest that miR-125a acts as a tumor suppressor via regulation of E2F2 expression in osteosarcoma progression, and miR-125a may represent a novel therapeutic target for the treatment of osteosarcoma.
Accordingly, our results demonstrated that NAMPT is a prognostic marker in melanoma, and the identificationofNAMPT-E2F2-SIRT1 pathway establishes another link between NAMPT 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 and E2F2 overexpression showed a significant association with poor prognosis.
Data indicate that microRNA miR-214 has tumor-suppressive activity in hepatocellular carcinoma (HCC) through inhibition of E2F2 transcription factor (E2F2), cyclin-dependent kinases CDK3 and CDK6.
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 dependent mechanism.
Elevated E2F2 expression in glioblastoma cells weakens the effect of elevated levels of miR-218.
cell cycle-dependent transcription of the TRAIP gene by E2F1, E2F2, and E2F4 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.
miR-31 regulated the proliferation of colon cancer cells by targeting E2F2.
E2F directly regulates the expression of late myogenic genes, with E2f1 providing the major contribution compared with E2f2.
The dE2F2 protein repress the expression of buffy, the anti-apoptotic member of the Bcl-2 family and activate the expression of an RNA-binding protein that destabilizes diap1 in Drosophila.
Heterozygous mutation of mip120 or E2f2 suppressed the binucleate cell phenotype in the peripodial epithelium of Myb-null wing discs.
dE2F2, as well as the net E2F activity, which can be depleted by mutating the common cofactor, dDp, is inhibitory for p53-independent apoptosis.
RBF1 and RBF2 interact with different subsets of E2F proteins; this enables the RBF proteins to regulate E2F-dependent transcription in distinct ways
cells containing dE2F2 require dE2F1 to either prevent, or reverse, dE2F-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 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, and E2F2-RBF in vivo, and also provide an explanation for the ability of Mip130-null mutants to rescue the lethality of Myb-null mutants in vivo.
Combined inactivation of dE2F1 and dE2F2 had no significant effect on cell division of Hippo pathway mutant cells.
histone H4 and E2F2 bind to the -216/-28 region and play important roles in SIX1 methylation regulation during development.
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 E2F1-2 mediates cell cycle activation, contributing to gliopathy and neuronal/tissue loss associated with motor impairments and post-traumatic hyperesthesia.
A role for E2F1 and E2F2 as suppressors of replicative stress in differentiating cells, and the existence of a robust E2F-p53 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 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 and E2f3 from an S-G2 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.
showed that the D326V missense pRb bound to E2F1 but failed to interact with E2F2/3
E2F3 promotes while E2F2 suppresses ischemic cardiac repair through corresponding changes in endothelial cell proliferation.
E2F2 impairs, and endothelial E2F3 promotes, the angiogenic response to peripheral ischemic injury through corresponding changes in EC cell-cycle progression.
E2f2 induces cone photoreceptor apoptosis independent of E2f1 and E2f3 in mice.
these results indicate that the transcriptional activity of E2F2 contributes to promote adult hepatocyte proliferation and liver regeneration.
E2F1-3 in mediating transcriptional repression by retinoblastoma tumor suppressor during cell cycle exit and point to a critical role for their repressive functions in cell survival.
functions for E2f1-3 at distinct stages of myeloid development in vivo, first as repressors in cell survival and then as activators in cell proliferation.
loss of E2F2 results in a deregulated Aryl-hydrocarbon-receptor pathway
Findings show that rapid proliferation of E2F1/E2F2 compound mutant cultures is temporally followed by induction of a DNA damage response and the implementation of a p21(CIP1)-dependent senescence.
Control of miRNAs by E2F is likely to play multiple roles in cell proliferation and in proliferative diseases such as cancer.
we have examined the effect that a simultaneous inactivation of the E2F2 gene and over-expression of the Bcl-2 gene in B cells has on lymphoid homeostasis and autoimmunity
findings demonstrate that E2F2 can function as a tumor suppressor in epithelial tissues, perhaps by limiting proliferation in response to Myc
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
, LOW QUALITY PROTEIN: transcription factor E2F2
, E2F transcription factor 2