Publication:
Genomic instability in mice lacking histone H2AX.

dc.contributor.authorCeleste, Arkady
dc.contributor.authorPetersen, Simone
dc.contributor.authorRomanienko, Peter J
dc.contributor.authorFernandez-Capetillo, Oscar
dc.contributor.authorChen, Hua Tang
dc.contributor.authorSedelnikova, Olga A
dc.contributor.authorReina-San-Martin, Bernardo
dc.contributor.authorCoppola, Vincenzo
dc.contributor.authorMeffre, Eric
dc.contributor.authorDifilippantonio, Michael J
dc.contributor.authorRedon, Christophe
dc.contributor.authorPilch, Duane R
dc.contributor.authorOlaru, Alexandru
dc.contributor.authorEckhaus, Michael
dc.contributor.authorCamerini-Otero, R Daniel
dc.contributor.authorTessarollo, Lino
dc.contributor.authorLivak, Ferenc
dc.contributor.authorManova, Katia
dc.contributor.authorBonner, William M
dc.contributor.authorNussenzweig, Michel C
dc.contributor.authorNussenzweig, André
dc.contributor.funderUnited States Department of Health and Human Services
dc.date.accessioned2024-02-09T14:34:59Z
dc.date.available2024-02-09T14:34:59Z
dc.date.issued2002-05-03
dc.descriptionhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721576/es_ES
dc.description.abstractHigher order chromatin structure presents a barrier to the recognition and repair of DNA damage. Double-strand breaks (DSBs) induce histone H2AX phosphorylation, which is associated with the recruitment of repair factors to damaged DNA. To help clarify the physiological role of H2AX, we targeted H2AX in mice. Although H2AX is not essential for irradiation-induced cell-cycle checkpoints, H2AX-/- mice were radiation sensitive, growth retarded, and immune deficient, and mutant males were infertile. These pleiotropic phenotypes were associated with chromosomal instability, repair defects, and impaired recruitment of Nbs1, 53bp1, and Brca1, but not Rad51, to irradiation-induced foci. Thus, H2AX is critical for facilitating the assembly of specific DNA-repair complexes on damaged DNA.es_ES
dc.description.peerreviewedNoes_ES
dc.format.number5569es_ES
dc.format.page922es_ES
dc.format.volume296es_ES
dc.identifier.citationScience . 2002;296(5569):922-7.es_ES
dc.identifier.doi10.1126/science.1069398es_ES
dc.identifier.e-issn1095-9203es_ES
dc.identifier.journalScience (New York, N.Y.)es_ES
dc.identifier.pmchttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721576/
dc.identifier.pubmedID11934988es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/17702
dc.language.isoenges_ES
dc.publisherAmerican Association for the Advancement of Science (AAAS)
dc.relation.publisherversionhttps://doi.org/10.1016/j.isci.2021.103273.es_ES
dc.repisalud.institucionCNIOes_ES
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.meshChromosome Aberrationses_ES
dc.subject.meshDNA Repaires_ES
dc.subject.meshRecombination, Genetices_ES
dc.subject.meshAmino Acid Sequencees_ES
dc.subject.meshAnimalses_ES
dc.subject.meshB-Lymphocyteses_ES
dc.subject.meshBase Sequencees_ES
dc.subject.meshCell Cyclees_ES
dc.subject.meshCells, Culturedes_ES
dc.subject.meshCellular Senescencees_ES
dc.subject.meshDNA Damagees_ES
dc.subject.meshFemalees_ES
dc.subject.meshGene Targetinges_ES
dc.subject.meshHistoneses_ES
dc.subject.meshImmunoglobulin Class Switchinges_ES
dc.subject.meshInfertility, Malees_ES
dc.subject.meshLymphocyte Countes_ES
dc.subject.meshMalees_ES
dc.subject.meshMeiosises_ES
dc.subject.meshMicees_ES
dc.subject.meshMice, Knockoutes_ES
dc.subject.meshMolecular Sequence Dataes_ES
dc.subject.meshMutationes_ES
dc.subject.meshPhosphorylationes_ES
dc.subject.meshSpermatocyteses_ES
dc.subject.meshT-Lymphocyteses_ES
dc.titleGenomic instability in mice lacking histone H2AX.es_ES
dc.typejournal articlees_ES
dc.type.hasVersionAMes_ES
dspace.entity.typePublication
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