Premium
Nuclear transcription factor GATA‐1 is activated during aclacinomycin‐induced erythroid differentiation
Author(s) -
Gillet Reynald,
Bobichon Hélène,
Trentesaux Chantal
Publication year - 2002
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1016/s0248-4900(02)01201-7
Subject(s) - transcription factor , biology , microbiology and biotechnology , gata transcription factor , transcription (linguistics) , cellular differentiation , gata1 , promoter , gene , gene expression , biochemistry , linguistics , philosophy
Anthracycline antitumor drugs induce erythroid differentiation of the K562 erythroleukemic cell line at subtoxic concentrations. Aclacinomycin (ACM) stimulates this process by activating the erythroid transcription factor GATA‐1, that controls genes involved in hemoglobin biosynthesis. To investigate the implication of GATA‐1 in this process, we used a specific anti‐GATA‐1 polyclonal antibody that we produced in our laboratory. The GATA‐1 transcription factor was then monitored during erythroid differentiation induced by aclacinomycin. Here we show that a cellular redistribution and a modification of the phosphorylation state of this transcription factor occurred during ACM‐mediated cell differentiation. It suggests that anthracyclines can induce the erythroid differentiation of neoplastic cells by activating the transcription factor GATA‐1, probably via its clustering into nuclear foci.