Cell cycle inhibitor, p19INK4d, promotes cell survival and decreases chromosomal aberrations after genotoxic insult due to enhanced DNA repair

Genome integrity and cell proliferation and survival are regulated by an intricate network of pathways that includes cell cycle checkpoints, DNA repair and recombination, and programmed cell death. It makes sense that there should be a coordinated regulation of these different processes, but the com...

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Autor principal: Scassa, M.E
Otros Autores: Marazita, M.C, Ceruti, J.M, Carcagno, A.L, Sirkin, P.F, González-Cid, M., Pignataro, O.P, Cánepa, E.T
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 2007
Acceso en línea:Registro en Scopus
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Registro en la Biblioteca Digital
Aporte de:Registro referencial: Solicitar el recurso aquí
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024 7 |2 scopus  |a 2-s2.0-34047171404 
024 7 |2 cas  |a phosphorus 32, 14596-37-3; RNA, 63231-63-0; CDKN2D protein, human; Cdkn2d protein, mouse; Cyclin-Dependent Kinase Inhibitor p19; Pyrimidine Dimers; RNA, Messenger; Thymidine, 50-89-5 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
030 |a DRNEA 
100 1 |a Scassa, M.E. 
245 1 0 |a Cell cycle inhibitor, p19INK4d, promotes cell survival and decreases chromosomal aberrations after genotoxic insult due to enhanced DNA repair 
260 |c 2007 
270 1 0 |m Cánepa, E.T.; Laboratorio de Biología Molecular, Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Ciudad Universitaria Pabellon II, 1428 Buenos Aires, Argentina; email: ecanepa@qb.fcen.uba.ar 
506 |2 openaire  |e Política editorial 
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520 3 |a Genome integrity and cell proliferation and survival are regulated by an intricate network of pathways that includes cell cycle checkpoints, DNA repair and recombination, and programmed cell death. It makes sense that there should be a coordinated regulation of these different processes, but the components of such mechanisms remain unknown. In this report, we demonstrate that p19INK4d expression enhances cell survival under genotoxic conditions. By using p19INK4d-overexpressing clones, we demonstrated that p19INK4d expression correlates with the cellular resistance to UV treatment with increased DNA repair activity against UV-induced lesions. On the contrary, cells transfected with p19INK4d antisense cDNA show reduced ability to repair DNA damage and increased sensitivity to genotoxic insult when compared with their p19INK4d-overexpressing counterparts. Consistent with these findings, our studies also show that p19INK4d-overexpressing cells present not only a minor accumulation of UV-induced chromosomal aberrations but a lower frequency of spontaneous chromosome abnormalities than p19INK4d-antisense cells. Lastly, we suggest that p19INK4d effects are dissociated from its role as CDK4/6 inhibitor. The results presented herein support a crucial role for p19INK4d in regulating genomic stability and overall cell viability under conditions of genotoxic stress. We propose that p19INK4d would belong to a protein network that would integrate DNA repair, apoptotic and checkpoint mechanisms in order to maintain the genomic integrity. © 2007 Elsevier B.V. All rights reserved.  |l eng 
536 |a Detalles de la financiación: Agencia Nacional de Promoción Científica y Tecnológica 
536 |a Detalles de la financiación: Universidad de Buenos Aires 
536 |a Detalles de la financiación: Consejo Nacional de Investigaciones Científicas y Técnicas 
536 |a Detalles de la financiación: This work was partially supported by research grants from Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Agencia Nacional de Promoción Científica y Tecnológica (ANPCYT), and Universidad de Buenos Aires. MM, JC, AC and PS are Graduate Fellow and OP, MGC and EC are Research Members of CONICET. The authors would like to thank Zoraida Patrignani and Marcos Besio Moreno for the skillful technical assistance. 
593 |a Laboratorio de Biología Molecular, Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Ciudad Universitaria Pabellon II, 1428 Buenos Aires, Argentina 
593 |a Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina, 1425 Buenos Aires, Argentina 
593 |a Instituto de Biología y Medicina Experimental, CONICET, 1428 Buenos Aires, Argentina 
690 1 0 |a APOPTOSIS 
690 1 0 |a CELL SURVIVAL 
690 1 0 |a CHROMOSOMAL ABERRATIONS 
690 1 0 |a DNA REPAIR 
690 1 0 |a GENOTOXIC 
690 1 0 |a P19INK4D 
690 1 0 |a COMPLEMENTARY DNA 
690 1 0 |a CYCLIN DEPENDENT KINASE INHIBITOR 2D 
690 1 0 |a PHOSPHORUS 32 
690 1 0 |a RNA 
690 1 0 |a ANIMAL CELL 
690 1 0 |a ARTICLE 
690 1 0 |a CELL CYCLE 
690 1 0 |a CELL GROWTH 
690 1 0 |a CELL VIABILITY 
690 1 0 |a CHROMOSOME ABERRATION 
690 1 0 |a CLONOGENIC ASSAY 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a DNA DAMAGE 
690 1 0 |a DNA RECOMBINATION 
690 1 0 |a DNA REPAIR 
690 1 0 |a DNA SYNTHESIS 
690 1 0 |a FLOW CYTOMETRY 
690 1 0 |a GENOTOXICITY 
690 1 0 |a GROWTH INHIBITION 
690 1 0 |a ISOTOPE LABELING 
690 1 0 |a MOUSE 
690 1 0 |a NONHUMAN 
690 1 0 |a NORTHERN BLOTTING 
690 1 0 |a POLYACRYLAMIDE GEL ELECTROPHORESIS 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a PROTEIN CONTENT 
690 1 0 |a TUMOR CELL CULTURE 
690 1 0 |a ULTRAVIOLET IRRADIATION 
690 1 0 |a WESTERN BLOTTING 
690 1 0 |a ANIMALS 
690 1 0 |a BLOTTING, NORTHERN 
690 1 0 |a BLOTTING, WESTERN 
690 1 0 |a CELL SURVIVAL 
690 1 0 |a CHROMOSOME ABERRATIONS 
690 1 0 |a COLONY-FORMING UNITS ASSAY 
690 1 0 |a CYCLIN-DEPENDENT KINASE INHIBITOR P19 
690 1 0 |a DNA DAMAGE 
690 1 0 |a DNA REPAIR 
690 1 0 |a GENOMIC INSTABILITY 
690 1 0 |a HUMANS 
690 1 0 |a IMMUNOPRECIPITATION 
690 1 0 |a MICE 
690 1 0 |a PYRIMIDINE DIMERS 
690 1 0 |a RADIATION TOLERANCE 
690 1 0 |a RNA, MESSENGER 
690 1 0 |a THYMIDINE 
690 1 0 |a ULTRAVIOLET RAYS 
700 1 |a Marazita, M.C. 
700 1 |a Ceruti, J.M. 
700 1 |a Carcagno, A.L. 
700 1 |a Sirkin, P.F. 
700 1 |a González-Cid, M. 
700 1 |a Pignataro, O.P. 
700 1 |a Cánepa, E.T. 
773 0 |d 2007  |g v. 6  |h pp. 626-638  |k n. 5  |p DNA Repair  |x 15687864  |w (AR-BaUEN)CENRE-4426  |t DNA Repair 
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856 4 0 |u https://hdl.handle.net/20.500.12110/paper_15687864_v6_n5_p626_Scassa  |y Handle 
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