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Griese, M.* ; Seidl, E.* ; Hengst, M.* ; Reu, S.* ; Rock, H.* ; Anthony, G.* ; Kiper, N.* ; Emiralioğlu, N.* ; Snijders, D.* ; Goldbeck, L.* ; Leidl, R. ; Ley-Zaporozhan, J.* ; Krüger-Stollfuss, I.* ; Kammer, B.* ; Wesselak, T.* ; Eismann, C.* ; Schams, A.* ; Neuner, D.* ; MacLean, M.* ; Nicholson, A.G.* ; Lauren, M.* ; Clement, A.B.* ; Epaud, R.* ; de Blic, J.* ; Ashworth, M.* ; Aurora, P.* ; Calder, A.A.* ; Wetzke, M.* ; Kappler, M.* ; Cunningham, S.* ; Schwerk, N.* ; Bush, A.*

International management platform for children's interstitial lung disease (chILD-EU).

Thorax 73, 231-239 (2018)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
It is undeniably one of the greatest findings in biology that (with some very minor exceptions) every cell in the body possesses the whole genetic information needed to generate a complete individual. Today, this concept has been so thoroughly assimilated that we struggle to still see how surprising this finding actually was: all cellular phenotypes naturally occurring in one person are generated from genetic uniformity, and thus are per definition epigenetic. Transcriptional mechanisms are clearly critical for developing and protecting cell identities, because a mis-expression of few or even single genes can efficiently induce inappropriate cellular programmes. However, how transcriptional activities are molecularly controlled and which of the many known epigenomic features have causal roles remains unclear. Today, clarification of this issue is more pressing than ever because profiling efforts and epigenome-wide association studies (EWAS) continuously provide comprehensive datasets depicting epigenomic differences between tissues and disease states. In this commentary, we propagate the idea of a widespread follow-up use of epigenome editing technology in EWAS studies. This would enable them to address the questions of which features, where in the genome, and which circumstances are essential to shape development and trigger disease states.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Paediatric Interstitial Lung Disease ; Rare Lung Diseases ; Paediatric Lung Disaese; Base-resolution Analysis; Dna-methylation; Wide Association; Transcription Factors; Mammalian Genome; Cells; System; Enhancers; Cancer; Genes
ISSN (print) / ISBN 0040-6376
e-ISSN 1468-3296
Zeitschrift Thorax
Quellenangaben Band: 73, Heft: 3, Seiten: 231-239 Artikelnummer: , Supplement: ,
Verlag BMJ Publishing Group
Verlagsort 6-9 Carlton House Terrace, London Sw1y 5ag, England
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Health Economics and Health Care Management (IGM)