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The leukaemia‐associated transcription factors EVI‐1 and MDS1/EVI1 repress transcription and interact with histone deacetylase
Author(s) -
Vinatzer Ursula,
Taplick Jan,
Seiser Christian,
Fonatsch Christa,
Wieser Rotraud
Publication year - 2001
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.2001.02987.x
Subject(s) - trichostatin a , histone deacetylase 2 , histone deacetylase , histone deacetylase 5 , hdac11 , hdac4 , psychological repression , hdac1 , cancer research , histone deacetylase inhibitor , transcription (linguistics) , microbiology and biotechnology , hdac10 , chemistry , histone , biology , genetics , gene , gene expression , linguistics , philosophy
EVI‐1 and its variant form, MDS1/EVI1, have been reported to act in an antagonistic manner and be differentially regulated in samples from patients with acute myeloid leukaemia and rearrangements of the long arm of chromosome 3. Here, we show that both EVI‐1 and MDS1/EVI1 can repress transcription from a reporter construct containing EVI‐1 binding sites and interact with histone deacetylase in mammalian cells. This interaction can be recapitulated in vitro and is mediated by a previously characterized transcription repression domain, whose activity is alleviated by the histone deacetylase inhibitor trichostatin A.