|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for E2F1(NM_005225.2) Search again
Product ID:
HQP004524
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
E2F-1, RBAP1, RBBP3, RBP3
Gene Description:
E2F transcription factor 1
Target Gene Accession:
NM_005225.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
|
|
| A | B |
|
Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
|
Summary
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. [provided by RefSeq].
Gene References into function
- transcriptional inhibition of the plasminogen activator inhibitor type 1 gene
- expression reduced in primary and metastatic breast carcinoma
- selection and characterization of active hammerhead ribozymes targeted against E2F1 full-length mRNA
- Regulation of E2F1-dependent gene transcription and apoptosis by the ETS-related transcription factor GABPgamma1
- increased ppRb and E2FI immunoreactivity in Alzheimer disease brain, with ppRb predominately located in the nucleus and E2F1 in the cytoplasm.
- Human telomerase accelerates growth of lens epithelial cells through regulation of the genes mediating RB/E2F pathway.
- Overexpression of E2F-1 induces apoptosis and increases chemosensitivity in human pancreatic carcinoma cells. Cell cycle, PARP cleavage and morphology supported apoptosis as the cell death mechanism in reponse to E2F1.
- conclude that E2F proteins and Sp1 play an important role in the control of p18 expression
- p14(ARF) regulates E2F activity in different cell types and down-regulates E2F-dependent transcription, and in cells undergoing E2F-dependent apoptosis prompts cell cycle arrest. p14(ARF) possesses multiple binding domains for E2F-1.
- p73beta is transcriptionally induced by E2F-1 and functions as a positive regulator of apoptosis.
- Most of the TGF-beta1-induced preapoptotic cells were arrested in G(1) phase of the cell cycle. This was associated with a significant increase in both E2F-DNA-binding activity and transcription of E2F-responsive reporter constructs.
- E2F-1 regulates the expression of APAF-1 in human cells
- E2F-1 has a role in regulation of caspase proenzymes through a direct transcriptional mechanism
- Che-1 contacts the pocket region of Rb and removes HDAC1 from the Rb/E2F1 complex, affecting the activation of E2F-dependent promoters and cell division.
- During thyroid hormone-induced differentiation of embryonic carcinoma cells and of oligodendrocyte precursor cells, levels of E2F-1 mRNA and E2F-1 protein decrease, caused by thyroid hormone receptor regulating the transcription of the E2F-1 gene.
- IFN-gamma is an effective inhibitor of ASM cell proliferation by blocking transition from G1-to-S phase by acting at two different levels: modulation of cdk2/cyclin E activation and inhibition of E2F-1 gene expression.
- expression of the transcription factor DP-1 and its heterodimeric partner E2F-1 in non-Hodgkin lymphoma
- We found that E2F1 was present at most of the CpG islands bound by pRb, independent of the phase of the cell cycle, our data suggest that the majority of DNA-bound pRb is recruited to E2F target promoters during both G(0)/G(1) and S phases.
- P202 inhibits E2F1-mediated apoptosis in prostate cancer cells
- E2F1 is involved in heat shock-induced cell cycle arrests at the G1/S and G2/M checkpoints, which also may be relevant for hyperthermic cancer therapy
- esf-1 induces apoptosis and inhibits proliferation of human colon cancer cell lines; a caspase-independent pathway is suggested
- Chk2 phosphorylates and activates E2F-1 in response to DNA damage, resulting in apoptosis. This suggests a role for E2F-1 in checkpoint control and tumour suppression.
- In response to DNA damage, E2F1 is directed from cell cycle progression to apoptotic E2F target genes.
- Analysis of gene expression level profiles showed that parental cell line undergoes apoptosis through an E2F1/p73-dependent pathway while its drug resistant variant evades it.
- Both senescence-associated heterochromatin foci formation and the silencing of E2F target genes depend on the integrity of the Rb pathway and do not occur in reversibly arrested cells
- C/EBPepsilon interacts with Rb and E2F1 during granulocytic differentiation
- E2F1 is upregulated by TR3 orphan nuclear receptor in human prostate cancer cells
- the Cyclin D1/E2F1 pathway may be involved in apoptotic death of bone marrow cells in myelodysplastic syndromes
- E2F1 activity is repressed by BRG1, but this repression is blocked when BRG1 interacts with EVI1
- two E2F-binding sites play distinct roles in the regulation of E2F1 transcription by interacting with different sets of E2F members and cooperating with the contiguous repressor element
- Here we show that the E2F1 binding domain of prohibitin has the potential to fold into a coiled-coil structure.
- E2F and Sp1/Sp3 synergize but are not sufficient to activate the MYCN gene in neuroblastoma
- results establish that tumor necrosis factor alpha targets insulin-like growth factor-I induced E2F-transcription facor 1 synthesis, leading to inhibition of accumulation in cyclin A and hyperphosphorylation of RB protein
- E2F1 transactivation is repressed by MdmX
- Our results suggest that overexpression of E2F1, induced both by LOH at the RB locus and anomalous phosphorylation of the RB protein, is involved in the development of non-small cell lung carcinoma.
- Results suggest that E2F1 plays a central role in signaling disturbances in the retinoblastoma growth control pathway and, by upregulation of Chk2 by Atm and Nbs1, may sensitize cells to undergo apoptosis.
- The data suggest that E2F-1 overexpression plays a role in suppression of tumor, at least in part trough transcriptional regulation of FHIT and relevant activation of WWOX.
- ErbB3-binding protein Ebp1 binding to E2F promoter elements and E2F-mediated transcription are regulated by heregulin
- increased expression of the E2F1 gene might play a significant role in human thyroid carcinogenesis through derangement of the Rb-E2F signaling pathway
- E2F1-dependent recruitment of Tip60 to chromatin occurred in late G(1)
- E2F1 stabilization in response to DNA damage requires p300/CREB-binding protein-associated factor
- new roles for several DNA damage response factors by demonstrating that they also participate in the oncogenic stress signaling pathway between E2F1 and p53
- results reveal an essential role of ACTR in control of breast cancer cell proliferation and implicate the ACTR-E2F1 pathway as a novel mechanism in antiestrogen resistance
- IL-1beta reduces the ability of IGF-I to activate Cdk2 and to induce E2F-1, cyclin A, and cyclin A-dependent phosphorylation of a retinoblastoma tumor suppressor
- E2F-1 may play a role in the detection and subsequent repair of damaged DNA [review]
- mitotic checkpoint protein Mad2 is a direct E2F target and, as a consequence, is aberrantly expressed in cells with Rb pathway defects
- Thus, expression of dbpA was positively regulated by E2F1, suggesting that one of the effects of E2F1 on cell proliferation might be mediated by dbpA at the carcinogenesis step.
- Expression of ICBP90 was upregulated by E2F-1, and the upregulation was caused by binding of E2F-1 to the intron1 of ICBP90.
- repression of hTERT by endogenous p53 is mediated by p21 and E2F
- RB/E2F signaling pathway activation is required for the modulation of hepatitis C virus core protein-induced cell growth in liver and non-liver cells
- upregulation of E2F-1 expression by heregulin beta 1 was directly inhibited by HES-1 through the same CACGAG-site as seen with estrogen-stimulated induction
- Increased expression in myelodysplastic bone marrow cells.
- the central acidic domain of MDM2 is critical in inhibition of retinoblastoma-mediated suppression of E2F and cell growth
- The N-terminal 72 amino acids of Pura were involved in E2F-1 binding, inhibition of promoter activation by E2F-1 and reversal of E2F-mediated growth inhibition.
- E2F-1 expression is inversely correlated with tumor growth in colon adenocarcinoma.
- there is a negative feedback loop in apoptosis involving E2F and AKT
- BMP-2 inhibits DHT-induced growth of LNCaP cells through a decrease in E2F protein expression and suppression of E2F activity by hypophosphorylation of Rb
- induction of p27 acts as a negative feedback mechanism for E2F1 and may also contribute to other functions of E2F1
- Induction of the metallothionein 1G promoter by VEGF and heavy metals occurs through the utilization of different transcription factors, notably E2F1.
- We report a novel, noncompetitive mechanism linking acetylation and ubiquitination, in which the association of transcription factor E2F-1 with the cellular coactivator and acetyltransferase p300 determines its acetylation and subsequent ubiquitination.
- expression of E2F1 is negatively regulated by two miRNAs in the cluster, miR-17-5p and miR-20a
- E2F1/p53 interaction regulates the transcriptional activity of p53 throughout the cell cycle.
- data identify E2F1 as a critical determinant of the cellular response to death-receptor-mediated apoptosis, and suggest that its downregulation contributes to the immune escape of lung adenocarcinoma tumor cells
- the expression of the E2F6 repressor is influenced at the transcriptional level by E2F family members and suggest that interplay among these transcriptional regulators, especially E2F1, may be critical for cell cycle regulation
- A subset of E2F1 targets are instrumental in altering proliferative, differentiation, and apoptotic properties. Deregulation of the E2F/RB pathway may promote the development of hormone-refractory prostate tumors.
- MDM2 stabilizies E2F1 protein through the E2F1 ubiquitination pathway.
- E2F1 contributes to the genetic instability associated with transformation and tumorigenesis
- data show that E2F1 has potential binding activity to the retinoblastoma control element and a different transcriptional regulation pathway which cooperates with the retinoblastoma tumor suppressor protein
- regulation of p14(ARF) gene by E2F is distinct from that of classical E2F targets. It is directly mediated by E2F through a novel E2F-responsive element that varies from the typical E2F site.
- E2F1 may participate in telomerase activity regulation in malignant glioma cells. Its expression appears to be strongly associated with the survival of patients with malignant brain tumors.
- E2F1, in addition to EGFR, target sites induce B-Myb promoter
- MDM2 has critical roles in the regulation of p21 and E2F1 expression, stability and function [review]
- Regulation of E2F1 by IKK alpha influences estrogen-mediated cell cycle progression
- E2F1-induced Mre11-Rad50-Nbs1 (MRN) foci generate a cell cycle checkpoint that with sustained E2F1 activity eventually yields to apoptosis.
- concomitant induction of E2F1 targets ASK1 and Bim by HDACIs warrants an effective activation of E2F1-dependent apoptosis in response to suberoylanilide hydroxamic acid
- the release of E2F activity by elevated E2F1 gene copy numbers may play a functional role in melanoma growth
- Can bind the rRNA promoter and modulate its activity through the interaction with two identifiable E2F1-binding sequences.
- Up-regulation of ASK-1 may also favour the p53-independent E2F1 apoptotic activity.
- JPO1/CDCA7 is a unique transcription regulator whose expression is activated by E2F1 as well as c-Myc.
- Myc and E2F1 engage the ATM signaling pathway to activate p53 and induce apoptosis [review]
- Results provide insights into the possibility of using E2F1 as a therapeutic target in the treatment of cancer.
- Deregulation of E2F1 underlies much of the chromosomal instability in breast tumors.
- only 75 amino acids from within the DNA-binding domain of E2F-1 are sufficient for cell death and that this activity is also present in the DNA-binding domains of E2F-2 and E2F-3
- histone deacetylase inhibitor sodium butyrate induces G1/S phase arrest in E1A + Ras-transformed cells through down-regulation of E2F1 activity and stabilization of beta-catenin
- E2F1 may cooperate with alterations in the MAPK or Rb pathways in the promotion of proliferation in many or most types of melanoma and may become a target for therapeutic intervention.
- There is a mutual regulation between E2F1 and SirT1 that affects cellular sensitivity to DNA damage.
- E2F and Wip1 are modulators of E2F1-induced apoptosis involving p38 MAP kinase
- There is a positive feedback regulatory loop consisting of E2F1 and SRC-3 to maintain high levels of SRC-3 and E2F1 activity, which may partially interpret the oncogenic role of SRC-3 overexpression.
- Depletion of E2F1 prevented prohibitin from repressing the YY1 promoter.
- Data demonstrate a novel physiological aspect of E2F1 in human cancer cells, where activated mitochondrial biogenesis occurs as a consequence of the acute loss of E2F1.
- CDCA4 participates in the regulation of cell proliferation, mainly through the E2F/retinoblastoma protein pathway
- Levels of E2F1 protein were greater in the nucleus of neurons in brains of HIV-infected patients exhibiting dementia when compared to HIV-negative subjects or HIV-positive neurologically normal patients
- p53 family proteins are potent therapeutic agents for human papilomavirus-associated uterine cervical cancers carrying the E2F1 promoter.
- offer a new mechanism of regulation of E2F1 by direct binding of glycogen synthase kinase 3 beta to its transactivation domain
- TFDP3, a novel DP protein, inhibits DNA binding and transactivation by E2F
- expression of mammalian GINS is regulated by 17beta-Estradiol-stimulated estrogen receptor alpha, and PSF3 acts as a gene responsive to transcription factor E2F1
- E2F1, E2F2, and E2F3 directly bind the promoter of the mir-17-92 cluster, activating its transcription. miR-20a from the mir-17-92 cluster in turn modulates the translation of E2F2 and E2F3, suggesting an autoregulatory feedback loop.
- Elevated E2F1, through its ability to repress androgen receptor transcription, may contribute to the progression of hormone-independent prostate cancer.
- the expression of human ASF1A and ASF1B are upregulated followed by cell proliferation signal, but that of ASF1B is uniquely regulated by transcription factors E2F during cell cycle progression
- Proliferation-promoting E2F transcription factor E2F-1 plays a pivotal role in the tumor biology of ovarian cancer.
- The pRb/E2F cell-cycle pathway mediates cell death in Parkinson's disease.
- E2F-1 is a transcriptional activator of MKP-2 and MKP-2 is an essential cell death mediator in the E2F-1 pathway
- Overexpression of E2F-1 is associated with neuroendocrine lung tumors
- Our study demonstrates that E2F-1 mediates apoptosis through transcriptional regulation of PAC1 and subsequent suppression of the ERK signaling
- Assessment of E2F1 at the mRNA level in primary breast cancer is a strong determinant of breast cancer patient outcome.
- Critical for hormone regulation of the proliferative program of breast cancer cells.
- LA's ability to inhibit apoptosis and proliferation of ECs could beneficially affect endothelial dysfunction, which precedes manifestation of late diabetic vascular complications.
- Alien inhibits E2F1 gene expression and cell proliferation.
- Epstein-Barr virus-encoded latent membrane protein 1inhibited p16(INK4A) expression, promoted phosphorylation of p105 Rb and upregulated E2F1 expression and overexpression of E2F1 alone was sufficient to upregulate telomerase activity.
- Results show that p14ARF regulates E2F-1 ubiquitination and degradation via a p53-dependent mechanism.
- Chk1 is E2F regulated and highly expressed in triple-negative estrogen receptor /progesterone receptor /HER-2 breast carcinomas
- E2F-1 is a transcriptional activator of DUSP1 and DUSP1 is a link between E2F-1 and MAP kinases
- The mutation and expression of E2F-1 in human gastric cancer tissues and the effect of E2F-1 overexpression on the proliferation of gastric carcinoma cells, was investigated.
- ectopically BRCA2-expressing cells have different intracellular levels of Aurora A, Aurora B, p21, E2F-1, and pRb, suggesting a BRCA2-mediated suppression of polyploidy via stabilization of the checkpoint proteins levels
- by disrupting the DNA binding activity of E2F1, BTG3 participates in the regulation of E2F1 target gene expression. Therefore, our studies have revealed a previously unidentified pathway through which the activity of E2F1 may be guarded by activated p53.
- E2F-1 protein overexpression can be useful as a prognostic indicator in epithelial ovarian neoplasms.
- KAP1 contributes to the negative regulation of E2F1 and may serve as a partial backup to prevent E2F1-mediated apoptosis in the absence of pRb
- NF-kappaB recruits E2F1 to fully activate the transcription of NF-kappaB target genes.
- A hitherto unrecognized mechanism to control E2F1 function through modulation of its subcellular localization, is identified.
- the E2F1 transcription factor, which is implicated in carcinoma invasiveness, upregulates the expression of PACE4
- Transcriptional regulation of a new variant of PDGFRA by E2F1.
- E2F1binding sites are located within 2 kb of a transcription start site, in both normal and tumor cells
- Clear cell renal cell carcinoma is characterized by the overexpression of E2F1, which is likely a result of a deregulated control of T3-dependent molecular processes.
- Human herpesvirus 6A (HHV-6A) and HHV-6B infection was associated with significant reduction of E2F1/Rb complexing, altered E2F1 localization and cell cycle arrest in T cells.
- RhoBTB2 up-regulated during drug-induced apoptosis, with this being primarily dependent on E2F1.
- E2F1 gene expression correlates with thymidylate synthase and survivin gene expressions and tumor proliferation. During the progression of NSCLC, E2F1 overexpression could produce more aggressive tumors with a high proliferation rate and chemoresistance.
- A subset of E2F1 target genes that are specifically repressed by PI3K/Akt signaling, thus distinguishing the E2F1 proliferative or apoptotic function, is identified.
- E2F-1 is a potentially novel independent prognostic factor that may identify gastric cancer patients who will likely benefit from adjuvant chemoradiation therapy following curative resection.
- CARM1 is a critical factor in the pathway of estrogen-stimulated breast cancer growth downstream of ERA and AIB1and upstream of the cell cycle regulatory transcription factor E2F1.
- E2F1 stimulates ataxia telangiectasia mutated (ATM) kinase-dependent p53 phosphorylation and apoptosis through a mechanism that does not involve DNA damage.
- These studies identify E2F1 as a positive transcriptional regulator for delta-catenin.
- Suggest that the miR-106b-25 cluster is involved in E2F1 posttranscriptional regulation and may play a key role in the development of TGFbeta resistance in gastric cancer.
- Myc is required to allow the interaction of the E2F1 protein with the E2F gene promoters.
- Brip1 is a genuine target gene for the E2F/Rb pathway; elevated expression levels of Brip1 are detected in primary invasive breast carcinomas with unfavorable characteristics.
- Results suggest that Bin1 gene suppression caused by oncogenic E1A via Rb/E2F1 inactivation is an essential step in cell cycle progression promoted by c-Myc, and subsequently, E1A transformation.
- E2F1 contributes to the transcriptional activation of the KIR3DL1 gene.
- The regulatory effect of E2F1 suggests that DYRK1A may play a role in cell cycle regulation or apoptosis.
- These results suggest that E2F1 plays an important role in regulating RANKL transcription through binding to the E2F consensus binding site.
- EBNA-6 binds to a MRPS18-2 protein, and targets it to the nucleus, where MRPS18-2 competes with the binding of E2F1 to pRb, thereby raising the level of free E2F1, and lifting the block preventing S-phase entry.
- The current findings demonstrated that loss of Rb and p16/INKa expression and high E2F1 expression indicate impairment of the Rb suppressor pathway.
- ASK/Dbf4, a novel cell survival gene in melanoma is transcriptionally regulated by E2F1.
- DAPK2 as a novel Sp1-dependent target gene for E2F1 and KLF6 in cell death response.
- AHR binds to E2F1 and inhibits E2F1-induced apoptosis
- E2F6 has a role in control of hypoxia-induced apoptosis through regulation of E2F1
- PTPRO gene is co-regulated by both E2F1 and miR-17-92.
- E2F may regulate G2/M transition through the induction of SIL. Furthermore, as silencing of SIL cause apoptosis in cancer cells, these finding may have therapeutic relevance in tumors with constitutive activation of E2F
- E2F1, not Par-4, was found to be directly bound to the Smac promoter, suggesting that Par-4 exerted indirectly its transcriptional control on the Smac gene though interacting with E2F1.
- Data show that MCPH1 cooperates with E2F1 to regulate genes involved in DNA repair, checkpoint and apoptosis, and might participate in the maintenance of genomic integrity.
- activation of E1AF provides a means for E2F1 to induce cell apoptosis in response to DNA damage
- E2F-1 and COX-2 are overexpressed in oral cancer
- E2F1 may function as a critical antiapoptotic factor both in human and in rodent liver cancer through its ability to counteract c-Myc-driven apoptosis via activation of PIK3CA/Akt/mTOR and c-Myb/COX-2 pathways
- The levels of E2F1 mRNA were lower in malignant breast tissues. They declined further with increasing TNM stage. Results suggest E2F1 is a tumour suppressive gene in human breast cancer.
- E2F1 is a potent and specific inhibitor of beta-catenin/T-cell factor (TCF)-dependent transcription, and that this function contributes to E2F1-induced apoptosis
- E2F1 controls pre-mRNA processing events to induce apoptosis and identify the SC35 Ser-Rich Arg protein as a key direct E2F1-target in this setting.
- paclitaxel induces apoptosis in human retinoblastoma Y79 cells by up-regulating E2F1
- These data provide a mechanistic view of miRNA-based regulation of E2F1 in the context of the emerging model that miRNAs coordinate the timing of cell cycle progression.
- analysis of transcriptional repression of the prosurvival endoplasmic reticulum chaperone GRP78/BIP by E2F1
- study reports that mitotic complex genes Ect2, RacGAP, and MKLP1 are coordinately induced in S phase in proliferating T lymphocytes as well as in epithelial cells, depending upon activity of the CUX1 and E2F1 transcription factors
- deregulation of c-MYC in lymphoma cells does not overcome the tumor suppressor function of TGF-beta and that repression of E2F-1 transcription is sufficient for the efficient induction of cytostasis.
- expression of miRNAs is downregulated in senescent cells and in breast cancers harboring wild-type p53. These miRNAs are repressed by p53 in an E2F1-mediated manner
- under basal nonapoptotic conditions that NF-kappaB constitutively occupies and transcriptionally silences Bnip3 gene transcription by competing with E2F-1
- overlapping E2F1/Sp1 site, being present in multiple copies in the p14ARF promoter, may serve as the targets for both E2F1 and Sp1, thereby playing a crucial role in response to some oncogenic signals and stimulators