Please use this identifier to cite or link to this item: https://doi.org/10.1038/ncomms10968
Title: Acetylation of C/EBP? inhibits its granulopoietic function
Authors: Bararia, D 
Kwok, H.S 
Welner, R.S
Numata, A 
Sárosi, M.B
Yang, H 
Wee, S
Tschuri, S
Ray, D 
Weigert, O
Levantini, E
Ebralidze, A.K
Gunaratne, J 
Tenen, D.G 
Keywords: CCAAT enhancer binding protein alpha
granulocyte colony stimulating factor
histone acetyltransferase GCN5
lysine
CCAAT enhancer binding protein alpha
granulocyte colony stimulating factor
histone acetyltransferase PCAF
p300-CBP-associated factor
acetylation
acute myeloblastic leukemia
Article
bone marrow cell
cell differentiation
controlled study
DNA binding
down regulation
granulopoiesis
human
human cell
leukemia cell
myeloid leukemia
myeloid leukemia cell line
acetylation
acute myeloid leukemia
cytology
gel mobility shift assay
gene expression regulation
genetics
granulocyte
HEK293 cell line
immunoblotting
immunoprecipitation
liquid chromatography
mass spectrometry
metabolism
myelopoiesis
tumor cell line
Acetylation
CCAAT-Enhancer-Binding Protein-alpha
Cell Differentiation
Cell Line, Tumor
Chromatography, Liquid
Electrophoretic Mobility Shift Assay
Gene Expression Regulation, Neoplastic
Granulocyte Colony-Stimulating Factor
Granulocytes
HEK293 Cells
Humans
Immunoblotting
Immunoprecipitation
Leukemia, Myeloid
Leukemia, Myeloid, Acute
Mass Spectrometry
Myelopoiesis
p300-CBP Transcription Factors
Issue Date: 2016
Publisher: Nature Publishing Group
Citation: Bararia, D, Kwok, H.S, Welner, R.S, Numata, A, Sárosi, M.B, Yang, H, Wee, S, Tschuri, S, Ray, D, Weigert, O, Levantini, E, Ebralidze, A.K, Gunaratne, J, Tenen, D.G (2016). Acetylation of C/EBP? inhibits its granulopoietic function. Nature Communications 7 : 10968. ScholarBank@NUS Repository. https://doi.org/10.1038/ncomms10968
Abstract: CCAAT/enhancer-binding protein alpha (C/EBP?) is an essential transcription factor for myeloid lineage commitment. Here we demonstrate that acetylation of C/EBP? at lysine residues K298 and K302, mediated at least in part by general control non-derepressible 5 (GCN5), impairs C/EBP? DNA-binding ability and modulates C/EBP? transcriptional activity. Acetylated C/EBP? is enriched in human myeloid leukaemia cell lines and acute myeloid leukaemia (AML) samples, and downregulated upon granulocyte-colony stimulating factor (G-CSF)- mediated granulocytic differentiation of 32Dcl3 cells. C/EBP? mutants that mimic acetylation failed to induce granulocytic differentiation in C/EBP?-dependent assays, in both cell lines and in primary hematopoietic cells. Our data uncover GCN5 as a negative regulator of C/EBP? and demonstrate the importance of C/EBP? acetylation in myeloid differentiation.
Source Title: Nature Communications
URI: https://scholarbank.nus.edu.sg/handle/10635/174982
ISSN: 20411723
DOI: 10.1038/ncomms10968
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