Promoter-bound METTL3 maintains myeloid leukaemia by m6A-dependent translation control

Isaia Barbieri, Konstantinos Tzelepis, Luca Pandolfini, Junwei Shi, Gonzalo Millán-Zambrano, Samuel C. Robson, Demetrios Aspris, Valentina Migliori, Andrew J. Bannister, Namshik Han, Etienne De Braekeleer, Hannes Ponstingl, Alan Hendrick, Christopher R. Vakoc, George S. Vassiliou () and Tony Kouzarides ()
Additional contact information
Isaia Barbieri: University of Cambridge
Konstantinos Tzelepis: Haematological Cancer Genetics, Wellcome Trust Sanger Institute
Luca Pandolfini: University of Cambridge
Junwei Shi: Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor
Gonzalo Millán-Zambrano: University of Cambridge
Samuel C. Robson: University of Cambridge
Demetrios Aspris: Haematological Cancer Genetics, Wellcome Trust Sanger Institute
Valentina Migliori: University of Cambridge
Andrew J. Bannister: University of Cambridge
Namshik Han: University of Cambridge
Etienne De Braekeleer: Haematological Cancer Genetics, Wellcome Trust Sanger Institute
Hannes Ponstingl: Haematological Cancer Genetics, Wellcome Trust Sanger Institute
Alan Hendrick: Storm Therapeutics Ltd, Moneta Building (B280), Babraham Research Campus
Christopher R. Vakoc: Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor
George S. Vassiliou: Haematological Cancer Genetics, Wellcome Trust Sanger Institute
Tony Kouzarides: University of Cambridge

Nature, 2017, vol. 552, issue 7683, 126-131

Abstract: The methyltransferase METTL3 promotes the leukaemic state in acute myeloid leukaemia (AML) by catalysing the m6A RNA modification through its recruitment on the transcription start sites of AML-associated genes.

Date: 2017
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DOI: 10.1038/nature24678

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