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Paper Details

The R882H DNMT3A mutation associated with AML dominantly inhibits wild-type DNMT3A by blocking its ability to form active tetramers.
Cancer Cell
322
2014
AML, AML cell genomes, AML cells, CpGs, DNMT3A, R882H, R882H DNMT3A, R882H DNMT3A mutation, acute myeloid leukemia, catalytic, de novo DNA methyltransferase, methyltransferase, normal karyotype, wild-type DNMT3A
Author NameAffiliation
David H SpencerWashington University
Tamara L LamprechtWashington University
Christopher A MillerThe Genome Institute, Washington University
Robert S FultonThe Genome Institute, Washington University
Robert S FultonThe Genome Institute, Washington University
Matthew R MeyerWashington University
Petra Erdmann-GilmoreWashington University, USA Siteman Cancer Center
Reid TownsendWashington University, USA Siteman Cancer Center
Richard K WilsonThe Genome Institute, Washington University, USA Siteman Cancer Center
Richard K WilsonThe Genome Institute, Washington University, USA Siteman Cancer Center
Timothy J LeyWashington University, USA The Genome Institute, USA Siteman Cancer Center
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