Artículo

Sonzogni, S.V.; Ogara, M.F.; Castillo, D.S.; Sirkin, P.F.; Radicella, J.P.; Cánepa, E.T. "Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation" (2015) Molecular and Cellular Biochemistry. 398(1-2):63-72
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Abstract:

DNA is continuously exposed to damaging agents that can lead to changes in the genetic information with adverse consequences. Nonetheless, eukaryotic cells have mechanisms such as the DNA damage response (DDR) to prevent genomic instability. The DNA of eukaryotic cells is packaged into nucleosomes, which fold the genome into highly condensed chromatin, but relatively little is known about the role of chromatin accessibility in DNA repair. p19INK4d, a cyclin-dependent kinase inhibitor, plays an important role in cell cycle regulation and cellular DDR. Extensive data indicate that p19INK4d is a critical factor in the maintenance of genomic integrity and cell survival. p19INK4d is upregulated by various genotoxics, improving the repair efficiency for a variety of DNA lesions. The evidence of p19INK4d translocation into the nucleus and its low sequence specificity in its interaction with DNA prompted us to hypothesize that p19INK4d plays a role at an early stage of cellular DDR. In the present study, we demonstrate that upon oxidative DNA damage, p19INK4d strongly binds to and relaxes chromatin. Furthermore, in vitro accessibility assays show that DNA is more accessible to a restriction enzyme when a chromatinized plasmid is incubated in the presence of a protein extract with high levels of p19INK4d. Nuclear protein extracts from cells overexpressing p19INK4d are better able to repair a chromatinized and damaged plasmid. These observations support the notion that p19INK4d would act as a chromatin accessibility factor that allows the access of the repair machinery to the DNA damage site. © 2014, Springer Science+Business Media New York.

Registro:

Documento: Artículo
Título:Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation
Autor:Sonzogni, S.V.; Ogara, M.F.; Castillo, D.S.; Sirkin, P.F.; Radicella, J.P.; Cánepa, E.T.
Filiación:Laboratorio de Biología Molecular, Departamento de Química Biológica, Universidad de Buenos Aires, Ciudad Universitaria Pabellón II Piso 4, Buenos Aires, 1428, Argentina
CEA, Institute of Cellular and Molecular Radiobiology, Fontenay-aux-Roses, 92265, France
INSERM UMR967, Fontenay-aux-Roses, 92265, France
Universités Paris Diderot et Paris-Sud U967, Fontenay-aux-Roses, 92265, France
Palabras clave:Chromatin relaxation; DNA damage response; Genome integrity; p19INK4d; cyclin dependent kinase inhibitor 2D; nuclear protein; restriction endonuclease; chromatin; cyclin dependent kinase inhibitor 2D; green fluorescent protein; protein binding; animal cell; Article; cell nucleus; cell survival; chromatin structure; controlled study; DNA damage; DNA damage response; DNA repair; genetic stability; genomic instability; human; human cell; intracellular transport; nonhuman; oxidative stress; protein DNA binding; protein DNA interaction; protein function; protein transport; active transport; animal; cell line; cell nucleus; chromatin; confocal microscopy; genetics; HEK293 cell line; HeLa cell line; metabolism; Northern blotting; oxidative stress; Western blotting; Eukaryota; Active Transport, Cell Nucleus; Animals; Blotting, Northern; Blotting, Western; Cell Line; Cell Nucleus; Chromatin; Cyclin-Dependent Kinase Inhibitor p19; DNA Damage; DNA Repair; Green Fluorescent Proteins; HEK293 Cells; HeLa Cells; Humans; Microscopy, Confocal; Oxidative Stress; Protein Binding
Año:2015
Volumen:398
Número:1-2
Página de inicio:63
Página de fin:72
DOI: http://dx.doi.org/10.1007/s11010-014-2205-1
Título revista:Molecular and Cellular Biochemistry
Título revista abreviado:Mol. Cell. Biochem.
ISSN:03008177
CODEN:MCBIB
CAS:Chromatin; Cyclin-Dependent Kinase Inhibitor p19; Green Fluorescent Proteins
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03008177_v398_n1-2_p63_Sonzogni

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Citas:

---------- APA ----------
Sonzogni, S.V., Ogara, M.F., Castillo, D.S., Sirkin, P.F., Radicella, J.P. & Cánepa, E.T. (2015) . Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation. Molecular and Cellular Biochemistry, 398(1-2), 63-72.
http://dx.doi.org/10.1007/s11010-014-2205-1
---------- CHICAGO ----------
Sonzogni, S.V., Ogara, M.F., Castillo, D.S., Sirkin, P.F., Radicella, J.P., Cánepa, E.T. "Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation" . Molecular and Cellular Biochemistry 398, no. 1-2 (2015) : 63-72.
http://dx.doi.org/10.1007/s11010-014-2205-1
---------- MLA ----------
Sonzogni, S.V., Ogara, M.F., Castillo, D.S., Sirkin, P.F., Radicella, J.P., Cánepa, E.T. "Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation" . Molecular and Cellular Biochemistry, vol. 398, no. 1-2, 2015, pp. 63-72.
http://dx.doi.org/10.1007/s11010-014-2205-1
---------- VANCOUVER ----------
Sonzogni, S.V., Ogara, M.F., Castillo, D.S., Sirkin, P.F., Radicella, J.P., Cánepa, E.T. Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation. Mol. Cell. Biochem. 2015;398(1-2):63-72.
http://dx.doi.org/10.1007/s11010-014-2205-1