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dc.contributor.authorRobbez-Masson, Len_US
dc.contributor.authorTie, CHCen_US
dc.contributor.authorRowe, HMen_US
dc.date.accessioned2020-08-21T14:39:20Z
dc.date.available2017-10-11en_US
dc.date.issued2017-11-06en_US
dc.identifier.urihttps://qmro.qmul.ac.uk/xmlui/handle/123456789/66504
dc.description.abstractCancer cells thrive on genetic and epigenetic changes that confer a selective advantage but also need strategies to avoid immune recognition. In this issue, Cuellar et al. (2017. J. Cell Biol https://doi.org/10.1083/jcb.201612160) find that the histone methyltransferase SETDB1 enables acute myeloid leukemia cells to evade sensing of retrotransposons by innate immune receptors.en_US
dc.format.extent3429 - 3431en_US
dc.languageengen_US
dc.relation.ispartofJ Cell Biolen_US
dc.rightsThis article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).
dc.subjectEpigenesis, Geneticen_US
dc.subjectHistone Codeen_US
dc.subjectHumansen_US
dc.subjectInterferonsen_US
dc.subjectLeukemia, Myeloid, Acuteen_US
dc.subjectProtein Methyltransferasesen_US
dc.subjectRetroelementsen_US
dc.titleCancer cells, on your histone marks, get SETDB1, silence retrotransposons, and go!en_US
dc.typeArticle
dc.rights.holder© 2017 Robbez-Masson et al.
dc.identifier.doi10.1083/jcb.201710068en_US
pubs.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/29066607en_US
pubs.issue11en_US
pubs.notesNot knownen_US
pubs.publication-statusPublisheden_US
pubs.volume216en_US
rioxxterms.funderDefault funderen_US
rioxxterms.identifier.projectDefault projecten_US
qmul.funderHow retrotransposons remodel the genome during early development and reprogramming::European Research Councilen_US
qmul.funderHow retrotransposons remodel the genome during early development and reprogramming::European Research Councilen_US


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