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Human E2F1 Protein expressed in HEK-293 Cells - ABIN2719894
Tarangelo, Lo, Teng, Kim, Le, Watson, Furth, Raman, Ehmer, Viatour: Recruitment of Pontin/Reptin by E2f1 amplifies E2f transcriptional response during cancer progression. in Nature communications 2015
dE2F1b is a novel member of the E2F family, revealing a previously unappreciated complexity in the Drosophila RB/E2F network.
specific alternate transcripts of activator E2F, dE2F1, may have a dual function on cell cycle progression and cannot simply be viewed as a pro-proliferative transcription factor
These findings identify a key function of E2F in skeletal muscle required for animal viability, and illustrate how the cell cycle regulator is repurposed in post-mitotic cells.
Mechanistically, miR-998 operates by repressing dCbl, a negative regulator of EGFR signaling. Significantly, dCbl is a critical target of miR-998 since dCbl phenocopies the effects of miR-998 on dE2f1-dependent apoptosis in rbf mutants
also demonstrated that an optimum level of dLin52 is needed for dE2F1/2 activity on the hid promoter
Results show that regulation of e2f1 and PCNA by DREF in vivo is complex and the regulation mechanism may differ with the tissue and/or positions in the tissue.
Loss of dE2F compromises mitochondrial function.
Data propose that the interaction between ORC5 and dE2F1 may reflect a feedback mechanism between replication initiation proteins and dE2F1 that ensures that proliferating cells maintain a robust level of replication proteins for the next cell cycle.
results suggest that E2F/DP complexes are essential for all genomic targeting of RBF1
Inappropriate accumulation of E2f1 protein during S phase triggers the elimination of potentially hyperplastic cells via apoptosis in order to ensure normal development of rapidly proliferating tissues.
endocycles of Drosophila are driven by a molecular oscillator in which the E2F1 transcription factor promotes CycE expression and S-phase initiation, S-phase then activates the CRL4(CDT2) ubiquitin ligase, and this in turn mediates the destruction of E2F1
coexpression of miR-11 limits the proapoptotic function of its host gene, dE2f1, upon DNA damage by directly modulating a dE2F1-dependent apoptotic transcriptional program
dE2F1 is needed for Yki/Sd-dependent full activation of these target genes, and a de2f1 mutation strongly blocks yki-induced proliferation in vivo.
Dampened transcriptional activation by E2F1-DP and Myb-MuvB is important to repress mitosis and coordinate the endocycle transcription
TSC1 regulates E2F1 expression during development and cooperates with RBF1 to control proliferation and survival.
report here that dE2F1 promotes ionizing radiation-induced p53-independent apoptosis in larval imaginal discs
Screening strategy for studying regulation of the dE2F/RBF pathway in vivo.
RBF1 and RBF2 interact with different subsets of E2F proteins; this enables the RBF proteins to regulate E2F-dependent transcription in distinct ways
dE2F1 has a role in nurse cell apoptosis
The caudal homeodomain protein activates Drosophila E2F gene expression.
TopBP1 transcriptional activity is regulated by AKT, and treatment with AKT inhibitors suppresses expression of E2F1 and p73 without interfering with ATR signaling.
inhibition of hsa-mir183 reduced proliferation and impaired colony formation of CML SPCs. Downstream of this, inhibition of E2F1 also reduced proliferation of CML SPCs, leading to p53-mediated apoptosis. In addition, we demonstrate that E2F1 plays a pivotal role in regulating CML SPC proliferation status.
ANP32E is an efficient prognostic marker, and it promotes the G1/S transition and induces tumorigenesis of Triple-negative breast cancer cells by transcriptionally inducing E2F1.
identification of protumorigenic transcriptional networks specific to RB loss that were validated in clinical samples demonstrated the ability of RB loss to differentially reprogram E2F1 in human cancers.
E2F1 enhances the invasion and metastasis of prostate cancer through a variety of mechanisms, and its expression level has an important relationship with the adverse prognosis of patients with prostate cancer
E2F1 requires cIAP1 for chromatin binding.
The authors predict that the induction of expression of RNASEH2A via human papillomavirus 16 E7 and E2F1 may promote DNA replication and cancer cell proliferation.
KPNA2 mediated nuclear localization of E2F1 and E2F7, where they in turn controlled KPNA2 expression. Taken together, our data provided mechanistic insights into divergently transcriptional regulation of KPNA2, thus pointing to KPNA2 as a potential target for cancer therapy.
Study demonstrated that CDCA3 may target p21 to promote colorectal cancer (CRC) cell proliferation and tumorigenesis, at least partially in an E2F1-mediated manner, and that CDCA3 may serve as a potential prognostic and therapeutic target of CRC.
The network model simulations and experimental data indicate the ability of enhanced expression of both miR-205-5p and miR-342-3p to decrease tumor chemoresistance by cooperatively repressing E2F1.
E2F1 interacts with BCL-xL independently from its BH3 binding interface and induces a stabilization of BCL-xL at mitochondrial membranes. This prevents efficient control of BCL-xL over its binding partners, in particular over BAK resulting in the induction of cell death.
ANKRD22 exhibits oncogene activity that promotes tumor progression in NSCLC through the transcriptional regulation of E2F1.
finding supports that DLX6-AS1 accelerates the glioma carcinogenesis by competing endogenous sponging miR-197-5p to relieve E2F1, acting as a novel therapeutic target for glioma.
XPC is an RNA polymerase II cofactor recruiting ATAC coactivator complex to promoters by interacting with E2F1.
Our findings reveal that the rs3213173 (C/T) and rs3213176 (G/A) polymorphisms of the E2F1 gene are genetic risk factors for susceptibility to lung cancer and Head and Neck cancer in the North Indian Population.
CacyBP expression is regulated by E2F1, EGR1, and CREB transcription factors in colorectal cancer HCT116 cells.
High E2F1 expression is associated with hepatocellular carcinoma progression.
the expression of miR175p inhibited high glucoseinduced endothelial cell injury by targeting E2F1.
The nuclear transcription factor Y subunit beta (NFYB)-E2F transcription factor 1 (E2F1) pathway displays a crucial role in the chemoresistance ofoxaliplatin-resistant colorectal cancer (OR-CRC) by inducing the expression and activation of checkpoint kinase 1 (CHK1), suggesting a possible therapeutic target for oxaliplatin resistance in CRC.
If, as expected, the consequences of the deregulation of the CDKN1C-E2F1-TP53 axis were the same as those experimentally demonstrated in mouse models, the disruption of this axis might be useful to predict tumor aggressiveness, and to provide the basis towards the development of potential therapeutic strategies in human Precursor T-cell lymphoblastic lymphomas
Lack of E2F1 impaired gluconeogenesis in primary hepatocytes. E2F1 overexpression increased glucose production in hepatocytes and in mice.
Methylation-dependent E2F1 degradation is also controlled by L3MBTL3-CRL4(DCAF5).
E2f1 mediates high glucose-induced neuronal death in cultured mouse retinal explants.
p63alpha protein up-regulates heat shock protein 70 expression via E2F1 transcription factor 1, promoting Wasf3/Wave3/MMP9 signaling and bladder cancer invasion
The evidence has been presented that the retinoblastoma protein utilizes a cell-cycle-independent interaction with E2F1 to recruit EZH2 to diverse repeat sequences.
germ-line loss of E2f1 or E2f3b, but not E2f3a, protected mice against hepatocellular carcinoma
E2F1 hinders skin wound healing by suppressing VEGF expression, neovascularization, and macrophage recruitment. Strategies that target E2F1 may enhance wound healing.
systems-level control of cell cycle arrest by pRB-E2F and p27-CDK regulation, is reported.
TERT has a role in neointima formation through epigenetic regulation of proliferative E2F1 target gene expression in smooth muscle cells.
inhibition of PDK4 activity in Hepatocellular carcinoma cells increased cyclin E1, cyclin A2, and E2F1 proteins.
Data indicate that adenosine and CGS21680 upregulate CD39 and CD73 via E2F-1 and CREB.
Expression of Kv10.1 driven by phosphorylated Rb/E2F1 contributes to G2/M progression of cancer and non-transformed cells.
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.
In the initial stage of myocyte differentiation, transcription of the YB-1 gene was regulated by E2F1 and Sp1, and was then gradually replaced under the control of both MyoD and myogenin.
Protease Omi facilitates neurite outgrowth by cleaving the transcription factor E2F1 in differentiated neuroblastoma cells; E2F1 is a substrate of Omi.
accumulating E2f1 progressively recruits a Pontin/Reptin complex to open the chromatin conformation at E2f target genes and amplifies the E2f transcriptional response.
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.
E2F1 promotes apoptosis of spermatogonia during the first wave of spermatogenesis, is involved in the maintenance of the spermatogonial stem cell pool in the adult and inhibits apoptosis of the meiotic germ cells.
Data (including data from studies in knockout/transgenic mice) suggest CDKN1B-RB1-E2F1 (cyclin-dependent kinase inhibitor 1B-retinoblastoma 1-E2F1) pathway is essential for SSC (spermatogonial stem cell) self-renewal/protection against genomic damage.
Conditional knockout of Poh1 alleles results in reduced E2F1 expression in primary mouse liver cells.
Xphb1 represses E2F1 activity.
SIM and SMR1 are involved in hyperphosphorylation of the cell-cycle regulator RBR1 and overexpression of E2F target genes.
S6K1 interacts with retinoblastoma protein RBR via its N-terminal RBR binding motif, promotes its nuclear localization and consequent RBR-dependent repression of cell cycle genes through transcription factor E2FB.
The Arabidopsis (Arabidopsis thaliana) DEL1 gene was identified as a transcriptional target of the classical E2Fb and E2Fc transcription factors.
The authors found that S6K1 associates with the Retinoblastoma-related 1 (RBR1)-E2FB complex and this is partly mediated by its N-terminal LVxCxE motif.
Results suggest that E2FB is one of the key targets for auxin to determine whether cells proliferate or whether they exit the cell cycle, enlarge, and endoreduplicate their DNA.
AtE2Fa and AtE2Fb have specific expression patterns and may play similar but distinct roles during cell cycle progression.
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, E2F2 and E2F3, have an additional cyclin binding domain. This protein binds preferentially to retinoblastoma protein pRB in a cell-cycle dependent manner. It can mediate both cell proliferation and p53-dependent/independent apoptosis.
, E2-promoter binding factor
, PRB-binding protein E2F-1
, retinoblastoma-associated protein 1
, retinoblastoma-binding protein 3
, transcription factor E2F1
, E2F-1 transcription factor