E2F1 and E2F2 induction in response to DNA damage preserves genomic stability in neuronal cells
E2F transcription factors regulate a wide range of biological processes, including the cellular response to DNA damage. In the present study, we examined whether E2F family members are transcriptionally induced following treatment with several genotoxic agents, and have a role on the cell DNA damage...
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Taylor and Francis Inc.
2015
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| LEADER | 24307caa a22021977a 4500 | ||
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| 001 | PAPER-13469 | ||
| 003 | AR-BaUEN | ||
| 005 | 20230518204350.0 | ||
| 008 | 190411s2015 xx ||||fo|||| 00| 0 eng|d | ||
| 024 | 7 | |2 scopus |a 2-s2.0-84928028362 | |
| 024 | 7 | |2 cas |a caspase 3, 169592-56-7; cycloheximide, 642-81-9, 66-81-9; mitogen activated protein kinase kinase, 142805-58-1; zinostatin, 9014-02-2; dactinomycin, 1402-38-6, 1402-58-0, 50-76-0; histone, 9062-68-4; hydrogen peroxide, 7722-84-1; mitogen activated protein kinase kinase kinase, 146702-84-3; Cycloheximide; Dactinomycin; E2F1 Transcription Factor; E2F2 Transcription Factor; H2AFX protein, human; Histones; Hydrogen Peroxide; MAP Kinase Kinase Kinases; p300-CBP Transcription Factors; p300-CBP-associated factor; Protein Synthesis Inhibitors; Rad51 Recombinase | |
| 040 | |a Scopus |b spa |c AR-BaUEN |d AR-BaUEN | ||
| 100 | 1 | |a Castillo, D.S. | |
| 245 | 1 | 0 | |a E2F1 and E2F2 induction in response to DNA damage preserves genomic stability in neuronal cells |
| 260 | |b Taylor and Francis Inc. |c 2015 | ||
| 270 | 1 | 0 | |m Cánepa, E.T.; Laboratorio de Biología Molecular, Departamento de Química Biológica; Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires; Ciudad de Buenos AiresArgentina; email: ecanepa@qb.fcen.uba.ar |
| 506 | |2 openaire |e Política editorial | ||
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| 520 | 3 | |a E2F transcription factors regulate a wide range of biological processes, including the cellular response to DNA damage. In the present study, we examined whether E2F family members are transcriptionally induced following treatment with several genotoxic agents, and have a role on the cell DNA damage response. We show a novel mechanism, conserved among diverse species, in which E2F1 and E2F2, the latter specifically in neuronal cells, are transcriptionally induced after DNA damage. This upregulation leads to increased E2F1 and E2F2 protein levels as a consequence of de novo protein synthesis. Ectopic expression of these E2Fs in neuronal cells reduces the level of DNA damage following genotoxic treatment, while ablation of E2F1 and E2F2 leads to the accumulation of DNA lesions and increased apoptotic response. Cell viability and DNA repair capability in response to DNA damage induction are also reduced by the E2F1 and E2F2 deficiencies. Finally, E2F1 and E2F2 accumulate at sites of oxidative and UV-induced DNA damage, and interact with gH2AX DNA repair factor. As previously reported for E2F1, E2F2 promotes Rad51 foci formation, interacts with GCN5 acetyltransferase and induces histone acetylation following genotoxic insult. The results presented here unveil a new mechanism involving E2F1 and E2F2 in the maintenance of genomic stability in response to DNA damage in neuronal cells. © 2015 Taylor & Francis Group, LLC |l eng | |
| 593 | |a Laboratorio de Biología Molecular, Departamento de Química Biológica; Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires; Ciudad de Buenos Aires, Argentina | ||
| 593 | |a CEA; Institute of Cellular and Molecular Radiobiology, Fontenay aux Roses, France | ||
| 593 | |a UMR967 INSERM/Universités Paris Diderot et Paris Sud, Fontenay aux Roses, France | ||
| 593 | |a Laboratorio de Genética del Desarrollo Neural, Fundación Instituto Leloir, Ciudad de Buenos Aires, Argentina | ||
| 690 | 1 | 0 | |a DNA DAMAGE RESPONSE |
| 690 | 1 | 0 | |a DNA REPAIR |
| 690 | 1 | 0 | |a E2F TRANSCRIPTION FACTOR |
| 690 | 1 | 0 | |a GENOMIC STABILITY |
| 690 | 1 | 0 | |a NEURONAL CELLS |
| 690 | 1 | 0 | |a ATM PROTEIN |
| 690 | 1 | 0 | |a ATR PROTEIN |
| 690 | 1 | 0 | |a CASPASE 3 |
| 690 | 1 | 0 | |a CYCLOHEXIMIDE |
| 690 | 1 | 0 | |a HISTONE ACETYLTRANSFERASE GCN5 |
| 690 | 1 | 0 | |a HISTONE H2AX |
| 690 | 1 | 0 | |a MESSENGER RNA |
| 690 | 1 | 0 | |a MITOGEN ACTIVATED PROTEIN KINASE KINASE |
| 690 | 1 | 0 | |a RAD51 PROTEIN |
| 690 | 1 | 0 | |a TRANSCRIPTION FACTOR E2F1 |
| 690 | 1 | 0 | |a TRANSCRIPTION FACTOR E2F2 |
| 690 | 1 | 0 | |a ZINOSTATIN |
| 690 | 1 | 0 | |a CYCLOHEXIMIDE |
| 690 | 1 | 0 | |a DACTINOMYCIN |
| 690 | 1 | 0 | |a H2AFX PROTEIN, HUMAN |
| 690 | 1 | 0 | |a HISTONE |
| 690 | 1 | 0 | |a HISTONE ACETYLTRANSFERASE PCAF |
| 690 | 1 | 0 | |a HYDROGEN PEROXIDE |
| 690 | 1 | 0 | |a MITOGEN ACTIVATED PROTEIN KINASE KINASE KINASE |
| 690 | 1 | 0 | |a P300-CBP-ASSOCIATED FACTOR |
| 690 | 1 | 0 | |a PROTEIN SYNTHESIS INHIBITOR |
| 690 | 1 | 0 | |a RAD51 PROTEIN |
| 690 | 1 | 0 | |a TRANSCRIPTION FACTOR E2F1 |
| 690 | 1 | 0 | |a TRANSCRIPTION FACTOR E2F2 |
| 690 | 1 | 0 | |a ANIMAL CELL |
| 690 | 1 | 0 | |a APOPTOSIS |
| 690 | 1 | 0 | |a ARTICLE |
| 690 | 1 | 0 | |a CELL VIABILITY |
| 690 | 1 | 0 | |a CELLULAR STRESS RESPONSE |
| 690 | 1 | 0 | |a CONTROLLED STUDY |
| 690 | 1 | 0 | |a DNA DAMAGE |
| 690 | 1 | 0 | |a DNA REPAIR |
| 690 | 1 | 0 | |a GENE INDUCTION |
| 690 | 1 | 0 | |a GENETIC TRANSCRIPTION |
| 690 | 1 | 0 | |a GENOMIC INSTABILITY |
| 690 | 1 | 0 | |a GENOTOXICITY |
| 690 | 1 | 0 | |a HISTONE ACETYLATION |
| 690 | 1 | 0 | |a HUMAN |
| 690 | 1 | 0 | |a HUMAN CELL |
| 690 | 1 | 0 | |a MOUSE |
| 690 | 1 | 0 | |a NERVE CELL |
| 690 | 1 | 0 | |a NONHUMAN |
| 690 | 1 | 0 | |a OXIDATIVE STRESS |
| 690 | 1 | 0 | |a PROTEIN EXPRESSION |
| 690 | 1 | 0 | |a PROTEIN PROTEIN INTERACTION |
| 690 | 1 | 0 | |a PROTEIN SYNTHESIS |
| 690 | 1 | 0 | |a RADIATION INJURY |
| 690 | 1 | 0 | |a ULTRAVIOLET RADIATION |
| 690 | 1 | 0 | |a UPREGULATION |
| 690 | 1 | 0 | |a CELL SURVIVAL |
| 690 | 1 | 0 | |a CYTOLOGY |
| 690 | 1 | 0 | |a DRUG EFFECTS |
| 690 | 1 | 0 | |a GENETICS |
| 690 | 1 | 0 | |a HEK293 CELL LINE |
| 690 | 1 | 0 | |a METABOLISM |
| 690 | 1 | 0 | |a NERVE CELL |
| 690 | 1 | 0 | |a RADIATION RESPONSE |
| 690 | 1 | 0 | |a TUMOR CELL LINE |
| 690 | 1 | 0 | |a CELL LINE, TUMOR |
| 690 | 1 | 0 | |a CELL SURVIVAL |
| 690 | 1 | 0 | |a CYCLOHEXIMIDE |
| 690 | 1 | 0 | |a DACTINOMYCIN |
| 690 | 1 | 0 | |a DNA DAMAGE |
| 690 | 1 | 0 | |a DNA REPAIR |
| 690 | 1 | 0 | |a E2F1 TRANSCRIPTION FACTOR |
| 690 | 1 | 0 | |a E2F2 TRANSCRIPTION FACTOR |
| 690 | 1 | 0 | |a GENOMIC INSTABILITY |
| 690 | 1 | 0 | |a HEK293 CELLS |
| 690 | 1 | 0 | |a HISTONES |
| 690 | 1 | 0 | |a HUMANS |
| 690 | 1 | 0 | |a HYDROGEN PEROXIDE |
| 690 | 1 | 0 | |a MAP KINASE KINASE KINASES |
| 690 | 1 | 0 | |a NEURONS |
| 690 | 1 | 0 | |a P300-CBP TRANSCRIPTION FACTORS |
| 690 | 1 | 0 | |a PROTEIN SYNTHESIS INHIBITORS |
| 690 | 1 | 0 | |a RAD51 RECOMBINASE |
| 690 | 1 | 0 | |a ULTRAVIOLET RAYS |
| 690 | 1 | 0 | |a UP-REGULATION |
| 700 | 1 | |a Campalans, A. | |
| 700 | 1 | |a Belluscio, L.M. | |
| 700 | 1 | |a Carcagno, A.L. | |
| 700 | 1 | |a Radicell, J.P. | |
| 700 | 1 | |a Cánepa, E.T. | |
| 700 | 1 | |a Pregi, N. | |
| 773 | 0 | |d Taylor and Francis Inc., 2015 |g v. 14 |h pp. 1300-1314 |k n. 8 |p Cell Cycle |x 15384101 |t Cell Cycle | |
| 856 | 4 | 1 | |u https://www.scopus.com/inward/record.uri?eid=2-s2.0-84928028362&doi=10.4161%2f15384101.2014.985031&partnerID=40&md5=f5c9ff8ca7d0c3247a26c2606040cbec |y Registro en Scopus |
| 856 | 4 | 0 | |u https://doi.org/10.4161/15384101.2014.985031 |y DOI |
| 856 | 4 | 0 | |u https://hdl.handle.net/20.500.12110/paper_15384101_v14_n8_p1300_Castillo |y Handle |
| 856 | 4 | 0 | |u https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_15384101_v14_n8_p1300_Castillo |y Registro en la Biblioteca Digital |
| 961 | |a paper_15384101_v14_n8_p1300_Castillo |b paper |c PE | ||
| 962 | |a info:eu-repo/semantics/article |a info:ar-repo/semantics/artículo |b info:eu-repo/semantics/publishedVersion | ||
| 999 | |c 74422 | ||