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Papers In Press, published online ahead of print June 20, 2005
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan 115
Corresponding Author: bmjyen{at}ibms.sinica.edu.tw
In the interleukin 3-dependent hematopoietic cell line Ba/F3, inhibition of mitogen activated protein kinase, a member of the MAPK/JNK/SAPK kinase family that plays an important role in cell growth and death control, rapidly leads to severe apoptosis. However, most of the anti-apoptotic substrates of MAPK remain to be identified. Here we report that, upon IL-3 stimulation of Ba/F3 cells, the transcription factor GATA-1 is strongly phosphorylated at residue serine-26 (S26) by a MAPK-dependent pathway. Phosphorylation of GATA-1 increases GATA-1-mediated transcription of the E4bp4 survival gene without significantly changing GATA-1’s DNA-binding affinity. Further characterization of GATA-1 phosphorylation site mutants revealed that the anti-apoptotic function of GATA-1 is strongly dependent upon its phosphorylation at the S26 position, and is likely mediated through its up-regulation of Bcl-XL expression. Taken together, our data demonstrate that MAPK-dependent GATA-1 phosphorylation is important for its transactivation of the E4bp4 gene, Bcl-XL expression and cell survival. Therefore, GATA-1 may represent a novel MAPK substrate that plays an essential role in a cytokine-mediated anti-apoptotic response.
J. Biol. Chem, 10.1074/jbc.M506514200
Submitted on June 15, 2005
Accepted on June 20, 2005
MAP kinase-mediated phosphorylation of GATA-1 promotes Bcl-XL expression and cell survival
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