HCSGD entry for E2F1
1. General information
Official gene symbol | E2F1 |
---|---|
Entrez ID | 1869 |
Gene full name | E2F transcription factor 1 |
Other gene symbols | E2F-1 RBAP1 RBBP3 RBP3 |
Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network

3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
---|---|---|---|
GO:0000077 | DNA damage checkpoint | IMP | biological_process |
GO:0000080 | Mitotic G1 phase | TAS | biological_process |
GO:0000082 | G1/S transition of mitotic cell cycle | TAS | biological_process |
GO:0000085 | Mitotic G2 phase | TAS | biological_process |
GO:0000122 | Negative regulation of transcription from RNA polymerase II promoter | IMP | biological_process |
GO:0000278 | Mitotic cell cycle | TAS | biological_process |
GO:0001047 | Core promoter binding | IDA | molecular_function |
GO:0003677 | DNA binding | IDA IMP | molecular_function |
GO:0003700 | Sequence-specific DNA binding transcription factor activity | IDA TAS | molecular_function |
GO:0003714 | Transcription corepressor activity | TAS | molecular_function |
GO:0005515 | Protein binding | IPI | molecular_function |
GO:0005634 | Nucleus | IDA | cellular_component |
GO:0005654 | Nucleoplasm | TAS | cellular_component |
GO:0005737 | Cytoplasm | IEA | cellular_component |
GO:0006351 | Transcription, DNA-templated | IEA | biological_process |
GO:0006355 | Regulation of transcription, DNA-templated | IDA | biological_process |
GO:0007283 | Spermatogenesis | IEA | biological_process |
GO:0008134 | Transcription factor binding | IPI | molecular_function |
GO:0008283 | Cell proliferation | TAS | biological_process |
GO:0008630 | Intrinsic apoptotic signaling pathway in response to DNA damage | IMP | biological_process |
GO:0010628 | Positive regulation of gene expression | IDA | biological_process |
GO:0030900 | Forebrain development | IEA | biological_process |
GO:0035189 | Rb-E2F complex | IDA | cellular_component |
GO:0043276 | Anoikis | IEA | biological_process |
GO:0043565 | Sequence-specific DNA binding | IEA | molecular_function |
GO:0045892 | Negative regulation of transcription, DNA-templated | IMP | biological_process |
GO:0045893 | Positive regulation of transcription, DNA-templated | IMP | biological_process |
GO:0045944 | Positive regulation of transcription from RNA polymerase II promoter | IMP | biological_process |
GO:0048146 | Positive regulation of fibroblast proliferation | IMP | biological_process |
GO:0048255 | MRNA stabilization | IDA | biological_process |
GO:0071398 | Cellular response to fatty acid | IEA | biological_process |
GO:0071456 | Cellular response to hypoxia | IEA | biological_process |
GO:0071930 | Negative regulation of transcription involved in G1/S transition of mitotic cell cycle | IMP | biological_process |
GO:0072332 | Intrinsic apoptotic signaling pathway by p53 class mediator | IEA | biological_process |
GO:1990086 | Lens fiber cell apoptotic process | IEA | biological_process |
GO:2000045 | Regulation of G1/S transition of mitotic cell cycle | IMP | biological_process |
Entries Per Page
Displaying Page of
4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.9782378861 | 0.0177104821 | 0.9999902473 | 0.2607145414 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
Data source | Up or down | Log fold change |
---|---|---|
GSE11954 | Down | -0.1304928466 |
GSE13712_SHEAR | Down | -0.0108976141 |
GSE13712_STATIC | Up | 0.0177832581 |
GSE19018 | Up | 0.0219826298 |
GSE19899_A1 | Down | -0.1581753789 |
GSE19899_A2 | Down | -0.1159045215 |
PubMed_21979375_A1 | Down | -1.0422937916 |
PubMed_21979375_A2 | Down | -0.3788859203 |
GSE35957 | Down | -0.5055339736 |
GSE36640 | Down | -1.8893710366 |
GSE54402 | Down | -0.2882849509 |
GSE9593 | Down | -0.2797548628 |
GSE43922 | Up | 0.0425220538 |
GSE24585 | Down | -0.0434422071 |
GSE37065 | Down | -0.3865568917 |
GSE28863_A1 | Down | -0.2096005063 |
GSE28863_A2 | Up | 0.2359552749 |
GSE28863_A3 | Up | 0.3019484407 |
GSE28863_A4 | Down | -0.0675317413 |
GSE48662 | Down | -1.3905921393 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
---|---|---|---|---|---|
hsa-miR-20a-5p | MIMAT0000075 | MIRT000180 | Western blot | Functional MTI | 19110058 |
hsa-miR-20a-5p | MIMAT0000075 | MIRT000180 | Western blot | Functional MTI | 18025036 |
hsa-miR-20a-5p | MIMAT0000075 | MIRT000180 | Western blot | Functional MTI | 18836483 |
hsa-miR-20a-5p | MIMAT0000075 | MIRT000180 | Luciferase reporter assay//Northern blot//Western blot//Reporter assay | Functional MTI | 15944709 |
hsa-miR-20a-5p | MIMAT0000075 | MIRT000180 | Luciferase reporter assay | Functional MTI | 21283765 |
hsa-miR-106a-5p | MIMAT0000103 | MIRT000374 | Immunohistochemistry//Microarray//Western blot | Functional MTI | 20643754 |
hsa-miR-106a-5p | MIMAT0000103 | MIRT000374 | qRT-PCR | Functional MTI (Weak) | 18521848 |
hsa-miR-106a-5p | MIMAT0000103 | MIRT000374 | Luciferase reporter assay//Western blot | Functional MTI | 21656380 |
hsa-miR-223-3p | MIMAT0000280 | MIRT000632 | Luciferase reporter assay//Western blot | Functional MTI | 20029046 |
hsa-miR-330-3p | MIMAT0000751 | MIRT000718 | Luciferase reporter assay//Western blot | Functional MTI | 19597470 |
hsa-miR-98-5p | MIMAT0000096 | MIRT001124 | Luciferase reporter assay | Non-Functional MTI | 19528081 |
hsa-miR-21-5p | MIMAT0000076 | MIRT001191 | qRT-PCR//Western blot | Functional MTI | 19906824 |
hsa-miR-21-5p | MIMAT0000076 | MIRT001191 | Luciferase reporter assay | Non-Functional MTI | 19528081 |
hsa-miR-93-5p | MIMAT0000093 | MIRT002472 | Luciferase reporter assay//Western blot | Functional MTI | 19486339 |
hsa-miR-93-5p | MIMAT0000093 | MIRT002472 | Luciferase reporter assay//Microarray//Western blot | Functional MTI | 18328430 |
hsa-miR-93-5p | MIMAT0000093 | MIRT002472 | Sequencing | Functional MTI (Weak) | 20371350 |
hsa-miR-17-5p | MIMAT0000070 | MIRT002935 | qRT-PCR | Functional MTI (Weak) | 18521848 |
hsa-miR-17-5p | MIMAT0000070 | MIRT002935 | Western blot | Functional MTI | 18836483 |
hsa-miR-17-5p | MIMAT0000070 | MIRT002935 | Luciferase reporter assay//Northern blot//Western blot//Reporter assay | Functional MTI | 15944709 |
hsa-miR-17-5p | MIMAT0000070 | MIRT002935 | Northern blot//qRT-PCR//Western blot | Functional MTI | 16940181 |
hsa-miR-17-5p | MIMAT0000070 | MIRT002935 | Luciferase reporter assay | Functional MTI | 21283765 |
hsa-miR-106b-5p | MIMAT0000680 | MIRT003045 | Luciferase reporter assay//qRT-PCR | Functional MTI | 18676839 |
hsa-miR-106b-5p | MIMAT0000680 | MIRT003045 | Luciferase reporter assay//Western blot | Functional MTI | 19486339 |
hsa-miR-106b-5p | MIMAT0000680 | MIRT003045 | Luciferase reporter assay//Microarray//Western blot | Functional MTI | 18328430 |
hsa-miR-106b-5p | MIMAT0000680 | MIRT003045 | Luciferase reporter assay | Functional MTI | 21283765 |
hsa-miR-106b-5p | MIMAT0000680 | MIRT003045 | Reporter assay | Functional MTI | 18212054 |
hsa-miR-205-5p | MIMAT0000266 | MIRT003322 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 22578566 |
hsa-miR-205-5p | MIMAT0000266 | MIRT003322 | Reporter assay | Functional MTI | 21454583 |
hsa-miR-23b-3p | MIMAT0000418 | MIRT003424 | flow//Microarray | Functional MTI (Weak) | 20133741 |
hsa-let-7a-5p | MIMAT0000062 | MIRT003904 | Western blot | Non-Functional MTI | 19110058 |
hsa-miR-34a-5p | MIMAT0000255 | MIRT004821 | Immunoblot//Immunohistochemistry//qRT-PCR | Functional MTI (Weak) | 17875987 |
hsa-miR-34a-5p | MIMAT0000255 | MIRT004821 | Western blot | Non-Functional MTI | 21128241 |
hsa-miR-126-3p | MIMAT0000445 | MIRT005020 | qRT-PCR | Non-Functional MTI (Weak) | 18521848 |
hsa-miR-149-3p | MIMAT0004609 | MIRT005356 | Luciferase reporter assay//qRT-PCR//Western blot//Reporter assay;Western blot;qRT-PCR;Other | Functional MTI | 20623644 |
hsa-miR-331-3p | MIMAT0000760 | MIRT006506 | Luciferase reporter assay//Western blot | Functional MTI | 20510161 |
hsa-miR-362-3p | MIMAT0004683 | MIRT007349 | Western blot | Functional MTI | 23280316 |
hsa-miR-193b-3p | MIMAT0002819 | MIRT016529 | Microarray | Functional MTI (Weak) | 20304954 |
hsa-miR-130b-3p | MIMAT0000691 | MIRT020292 | Sequencing | Functional MTI (Weak) | 20371350 |
hsa-miR-24-3p | MIMAT0000080 | MIRT030626 | qRT-PCR | Functional MTI (Weak) | 19748357 |
hsa-miR-181b-5p | MIMAT0000257 | MIRT035553 | Luciferase reporter assay//Western blot | Functional MTI | 23083446 |
hsa-miR-181b-5p | MIMAT0000257 | MIRT035553 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-10a-5p | MIMAT0000253 | MIRT047521 | CLASH | Functional MTI (Weak) | 23622248 |
Entries Per Page
Displaying Page of
- mirRecord
MicroRNA name | mirBase ID | Target site number | MiRNA mature ID | Test method inter | MiRNA regulation site | Reporter target site | Pubmed ID |
---|---|---|---|---|---|---|---|
hsa-miR-21-5p | MIMAT0000076 | NA | hsa-miR-21 | {Western blot} | {overexpression by miRNA precursor transfection} | 19906824 | |
hsa-miR-330-3p | MIMAT0000751 | 1 | hsa-miR-330-3p | {Western blot} | {overexpression by miRNA precursor transfection} | 19597470 | |
hsa-miR-106b-5p | MIMAT0000680 | NA | hsa-miR-106b | {Western blot} | {overexpression by miRNA mimics tranfection} | 19486339 | |
hsa-miR-93-5p | MIMAT0000093 | NA | hsa-miR-93 | {Western blot} | {overexpression by miRNA mimics tranfection} | 19486339 |
Entries Per Page
Displaying Page of
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 39 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
---|---|
27362652 | Targets of miR-34 miRNAs, including E2F1, c-Myc, and cyclin E2, were lower in IPF type II AECs |
26873092 | We found that circ-Foxo3 was mainly distributed in the cytoplasm, where it interacted with the anti-senescent protein ID-1 and the transcription factor E2F1, as well as the anti-stress proteins FAK and HIF1alpha |
26873092 | CONCLUSION: We conclude that ID-1, E2F1, FAK, and HIF1alpha interact with circ-Foxo3 and are retained in the cytoplasm and could no longer exert their anti-senescent and anti-stress roles, resulting in increased cellular senescence |
26505814 | Depletion of NML reduced the levels of H3K9Me3 and H3K27Me3 heterochromatin markers on rDNA and E2F1 target promoters in senescent cells, increased rRNA transcription, and increased the frequency of cell cycle re-entry |
25344604 | E2F1 and FOXO3 are two transcription factors that have been shown to participate in cellular senescence |
25344604 | Here we use E2F1 knock-out murine Embryonic fibroblasts (MEFs), knockdown RNAi constructs, and ectopic expression of E2F1 to show that it functions by negatively regulating FOXO3 |
25344604 | Here we use E2F1 knock-out murine Embryonic fibroblasts (MEFs), knockdown RNAi constructs, and ectopic expression of E2F1 to show that it functions by negatively regulating FOXO3 |
25344604 | We mapped the interaction between E2F1 and FOXO3 to a region including the DNA binding domain of E2F1 and the C-terminal transcription-activation domain of FOXO3 |
25344604 | We mapped the interaction between E2F1 and FOXO3 to a region including the DNA binding domain of E2F1 and the C-terminal transcription-activation domain of FOXO3 |
25344604 | We propose that E2F1 inhibits FOXO3-dependent transcription by directly binding FOXO3 in the nucleus and preventing activation of its target genes |
25344604 | Moreover, knockdown of the Caenorhabditis elegans E2F1 ortholog efl-1 significantly extends lifespan in a manner that requires the activity of the C |
25344604 | We conclude that there is an evolutionarily conserved signaling connection between E2F1 and FOXO3, which regulates cellular senescence and aging by regulating the activity of FOXO3 |
25216853 | Using interphase FISH (iFISH) suggests that the androgen-induced cellular senescence is associated with localizing the genomic E2F1 locus to senescence associated heterochromatic foci |
24913980 | Reactive oxygen species ligand upregulation occurs at transcriptional levels and requires the transcriptional factor E2F1 |
24913980 | Drug-induced MICA and PVR gene expression are transcriptionally regulated and involve DDR-dependent E2F1 transcription factor activity |
24322375 | Analysis of expression levels of p53, p21(CIP1), p16(INK4a), p27(KIP1), pRb and E2F1 and genetic knockdown of p21(CIP1) demonstrated an important role of p21(CIP1) in RD-triggered cellular senescence |
24122992 | The cells treated with Doxorubicin (0-500 nm) or vehicle control were analyzed for apoptosis, senescence (SA-beta Galactosidase), and expression of CDKN1A (p21), CDKN1B(p27), CDKN2A (p16), E2F1, vimentin and E-cadherin by immuno-histochemistry and/or Western blot |
24122992 | CONCLUSION: The absence of functional p16, pRB and p53 in DU145 suggests that Id4 could alter additional molecular pathways such as those involving E2F1 to promote senescence and increased sensitivity to doxorubicin-induced apoptosis |
23868058 | E2F1 in renal cancer: Mr Hyde disguised as Dr Jekyll |
23868058 | The transcription factor E2F1 has both oncogenic and tumour suppressor properties, depending on the context |
23868058 | Clarifying the function of E2F1 in different types of cancer is relevant because in those situations in which it acts as an oncogene there may be a route for therapeutic interference |
23868058 | This malignancy represents a challenge for standard therapies due to drug- and radio-resistance, effects that fit well within the scope of functions of E2F1 |
23868058 | A new report by Mans et al postulates that up-regulation of E2F1 in VHL-defective renal cell carcinoma induces cell senescence and can thus be considered a good prognostic factor |
23868058 | Here we discuss these findings in a wider context and propose that E2F1 may actually not play a uniform role in renal cell carcinoma but rather an ambiguous one whose deeper understanding could have practical implications |
23744542 | Regulation of E2F1 by the von Hippel-Lindau tumour suppressor protein predicts survival in renal cell cancer patients |
23744542 | We report that the VHL gene product (pVHL) inhibits E2F1 expression at both mRNA and protein level in zebrafish and human RCC cells, while loss of VHL increases E2F1 expression in patient kidney tumour tissue and RCC cells, resulting in a delay of cell cycle progression |
23744542 | We report that the VHL gene product (pVHL) inhibits E2F1 expression at both mRNA and protein level in zebrafish and human RCC cells, while loss of VHL increases E2F1 expression in patient kidney tumour tissue and RCC cells, resulting in a delay of cell cycle progression |
23744542 | RCCs from von Hippel-Lindau patients with known germline VHL mutations express significantly more E2F1 compared to sporadic RCCs with either clear-cell (cc) or non-cc histology |
23744542 | Analysis of 138 primary RCCs reveals that E2F1 expression is significantly higher in tumours with a diameter =7 cm and with a favourable American Joint Committee on Cancer (AJCC) stage |
23744542 | Cox regression analysis shows significant prediction of E2F1 expression for disease-free survival and overall survival, implying that E2F1 expression in kidney tumour is a novel prognostic factor for patients with RCC |
23744542 | Cox regression analysis shows significant prediction of E2F1 expression for disease-free survival and overall survival, implying that E2F1 expression in kidney tumour is a novel prognostic factor for patients with RCC |
22955272 | The retinoblastoma protein selectively represses E2F1 targets via a TAAC DNA element during cellular senescence |
22955272 | The retinoblastoma (Rb) protein mediates heterochromatin formation at the promoters of E2 transcription factor 1 (E2F1) target genes, such as proliferating cell nuclear antigen and cyclin A2 (CCNA2), and represses these genes during cellular senescence |
22955272 | Here, we demonstrate that a senescence-associated gene is a direct target of E2F1 and is also repressed by heterochromatin in senescent cells |
22955272 | In contrast, ARF and p27(KIP1), which are also E2F1 targets, are not repressed by Rb and heterochromatin formation |
22955272 | We further determined that TAAC element-mediated Rb association requires the E2F1 binding site, but not E2F1 protein |
22955272 | We further determined that TAAC element-mediated Rb association requires the E2F1 binding site, but not E2F1 protein |
22955272 | These results provide a novel molecular mechanism for the different expression patterns of E2F1 targets and afford new mechanistic insight regarding the selectivity of Rb-mediated heterochromatin formation and gene repression during cellular senescence |
22025288 | Rb is maintained in a hypophosphorylated state resulting in the inhibition of transcription factor E2F1 |
22020331 | BTG3 also binds and inhibits E2F1 |
25961265 | Furthermore, NaBu down-regulates the proto-oncogenes c-Myc, Cyclin D1 and E2F1 mRNA levels |
21223585 | These responses were accompanied by the up-regulation of the cell cycle inhibitor p21 WAF1 and reduced ERK phosphorylation and E2F1 expression |
19656618 | Down-regulation of p16(INK4a) expression by HBx subsequently led to activation of G(1)-CDKs, phosphorylation of Rb, activation of E2F1, and finally evasion from G(1) arrest induced by H(2)O(2) |
19436740 | In contrast, DRIL1 sumoylation impairs its interaction with E2F1 in vitro and modifies its transcriptional activity in vivo, driving transcription of subset of genes regulating leukocyte fate |
19034270 | Furthermore, we show that these miRNAs silence antiproliferative genes, which themselves are E2F1 targets |
18567801 | E2F1 small interfering RNA expression reduced hMSH2 expression and MMR activity in young human primary fibroblast cells |
18567801 | Importantly, expression of E2F1 in quiescent cells restored the MSH2 expression as well as MMR activity, whereas E2F1-infected senescent cells exhibited no restoration of MSH2 expression and MMR activity |
18567801 | These results indicate that the suppression of E2F1 transcriptional activity in senescent cells lead to stable repression of MSH2, followed by a induction of MutS alpha dysfunction, which results in a reduced cellular MMR capacity in senescent cells |
17968325 | Furthermore, such inactivation inhibits p53 but not E2F1 transcriptional activity and impairs DNA-damage-induced transcription of p21 |
17100598 | Studies in the past decade have clearly established a role for the retinoblastoma tumor suppressor protein, Rb, and its primary downstream target E2F1, in the above processes |
16596252 | E2F-1 is a critical modulator of cellular senescence in human cancer |
16596252 | Herein we show that E2F1, a transcription factor essential to a cell cycle progress and a main target of tumor suppressor Rb, is a critical barrier for the induction of senescence |
16596252 | Consistent with the notion of the critical role in senescence of E2F1, cells which overexpressed E2F1 proved to be immune to the induction of senescence |
16596252 | Consistent with the notion of the critical role in senescence of E2F1, cells which overexpressed E2F1 proved to be immune to the induction of senescence |
16596252 | Importantly, it appears that E2F1 depletion-induced cancer cell senescence is not reliant on the integrity of either Rb or p53 |
16596252 | Our results provide a molecular explanation for the selectivity with which senescence induction occurs, and also provides insights into the possibility of using E2F1 as a therapeutic target in the treatment of cancer |
16107878 | C/EBPbeta was unable to inhibit proliferation of MEFs lacking all three RB family proteins or wild-type cells expressing dominant negative E2F-1 and, instead, stimulated their growth |
15811427 | In addition, cells in these two states exhibited quite distinct time course profiles of the proteins, p53, p21WAF1, and E2F1 |
12902982 | Activation of E2F1 induced p14ARF mRNA and protein levels |
12507899 | Induction of p14(ARF) on confluency occurred with low E2F-1 levels |
12362892 | Among them, activated p53 family proteins suppress the function of NF-Y and thereby downregulate a set of cell cycle-related genes, including E2F1, which further leads to downregulation of E2F-regulated genes and cell cycle arrest |
11791184 | A pRb immunoprecipitation demonstrated more binding of E2F-1 to pRb in the high expressing IGFBP-rP1/mac25 clones than in control cells |
11640890 | Expression by recombinant adenovirus of E2F1, E2F2, E2F3, cyclin E/cdk2, and Mdm2 individually resulted in DNA synthesis in 10-30% of cells |
11302695 | Recent studies show that young cells can be induced to develop features of senescence prematurely by damaging agents, chromatin remodeling, and overexpression of ras or the E2F1 gene |
10911949 | Melanin accumulation accelerates melanocyte senescence by a mechanism involving p16INK4a/CDK4/pRB and E2F1 |
10911949 | Here we demonstrate that in melanocytes derived from dark-skinned individuals, CT-induced melanogenesis is associated with accumulation of the tumor suppressor p16INK4a, underphosphorylated retinoblastoma protein (pRb), downregulation of cyclin E, decreased expression of E2F1, and loss of E2F-regulated S-phase gene expression |
10911949 | This delayed senescence may result from reduced association of p16 with CDK4, reduced levels of underphosphorylated pRb, and steady levels of cyclin E and E2F1 |
10585280 | Here we present evidence that activation of a cAMP pathway correlates with multiple cellular changes in these cells: (1) increased expression of the transcription factor microphthalmia; (2) increased melanogenesis; (3) increased association of the cyclin-dependent kinase inhibitors (CDK-Is) p27(KIP1) and p16(INK4) with CDK2 and CDK4, respectively; (4) failure to phosphorylate the retinoblastoma protein (pRB); (5) decreased expression of E2F1, E2F2, and E2F4 proteins; (6) loss of E2F DNA-binding activity; and (7) phenotypic changes characteristic of senescent cells |
9546379 | In contrast, inhibition of RB binding to E2F or ectopic expression of E2F-1 in plaque VSMCs induced massive apoptosis, which required suppression of p53 to rescue cells |
8816912 | Western blot analysis showed that among the E2F-associated proteins, the expression of E2F-1, cyclin A, and cyclin B but not p107 was cell cycle- and senescence-dependent |
8853900 | We show that forced expression of a number of cell cycle-regulatory genes, including erbB-2, v-ras, v-myc, B-myb, ld-1, and E2F-1, alone or in combinations, cannot induce terminally differentiated skeletal muscle cells (myotubes) to synthesize DNA |
8934878 | These included c-fos, c-jun, Id-1, Id-2, E2F-1, and cdc2 |
7616677 | Senescent cells showed the strong transcriptional repressions of early serum responsive genes (c-fos, c-jun, c-myc), late responsive genes of transcription factor E2F1 and cyclin E |
7542356 | Selective repression of growth-regulating cdk2, cyclin E and E2F1 genes in human cell senescence |
7542356 | Transcription factor E2F1 was also completely repressed at the mRNA and protein levels in senescent TIG-1 cells |
7542356 | Therefore, the present results have indicated the selective repressions of cdk2, cyclin E and E2F1 in senescent cells |
8206919 | In presenescent cells, E2F-1 mRNA was cell-cycle regulated, appearing a few hours before S phase |
8206919 | The results suggest that senescent cells may fail to express late G1 genes due to repression of E2F-1, leading to a deficiency of E2F activity |
8206919 | Furthermore, although E2F-1 stimulates DNA synthesis in some cells, other cells, including normal human fibroblasts, require additional factors |
Entries Per Page
Displaying Page of