http://www.cnr.it/ontology/cnr/individuo/prodotto/ID300650
Histone Methyltransferase DOT1L Drives Recovery of Gene Expression after a Genotoxic Attack (Articolo in rivista)
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- Label
- Histone Methyltransferase DOT1L Drives Recovery of Gene Expression after a Genotoxic Attack (Articolo in rivista) (literal)
- Anno
- 2013-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1371/journal.pgen.1003611 (literal)
- Alternative label
Oksenych V, Zhovmer A, Ziani S, Mari P-O, Eberova J, Nardo T, Stefanini M, Giglia-Mari G, Egly J-M, Coin F. (2013)
Histone Methyltransferase DOT1L Drives Recovery of Gene Expression after a Genotoxic Attack
in PLOS genetics (Online)
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Oksenych V, Zhovmer A, Ziani S, Mari P-O, Eberova J, Nardo T, Stefanini M, Giglia-Mari G, Egly J-M, Coin F. (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url
- http://www.scopus.com/inward/record.url?eid=2-s2.0-84880790091&partnerID=q2rCbXpz (literal)
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- IGBMC, Department of Functional Genomics and Cancer, CNRS/INSERM/Université de Strasbourg, C. U, Strasbourg, France; Université de Toulouse, UPS, IPBS, Toulouse, France; Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche, Pavia, Italy (literal)
- Titolo
- Histone Methyltransferase DOT1L Drives Recovery of Gene Expression after a Genotoxic Attack (literal)
- Abstract
- UV-induced DNA damage causes repression of RNA synthesis. Following the removal of DNA lesions, transcription recovery operates through a process that is not understood yet. Here we show that knocking-out of the histone methyltransferase DOT1L in mouse embryonic fibroblasts (MEF(DOT1L)) leads to a UV hypersensitivity coupled to a deficient recovery of transcription initiation after UV irradiation. However, DOT1L is not implicated in the removal of the UV-induced DNA damage by the nucleotide excision repair pathway. Using FRAP and ChIP experiments we established that DOT1L promotes the formation of the pre-initiation complex on the promoters of UV-repressed genes and the appearance of transcriptionally active chromatin marks. Treatment with Trichostatin A, relaxing chromatin, recovers both transcription initiation and UV-survival. Our data suggest that DOT1L secures an open chromatin structure in order to reactivate RNA Pol II transcription initiation after a genotoxic attack. (literal)
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