TY  - JOUR
AU  - Ghaffari, Saghi
AU  - Kitidis, C
AU  - Zhao, W
AU  - Marinković, Dragan
AU  - Fleming, MD
AU  - Luo, B
AU  - Marszalek, J
AU  - Lodish, HF
PY  - 2006
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/79
AB  - AKT serine threonine kinase of the protein kinase B (PKB) family plays essential roles in cell survival, growth, metabolism, and differentiation. In the erythroid system, AKT is known to be rapidly phosphorylated and activated in response to erythropoletin (Epo) engagement of Epo receptor (EpoR) and to sustain survival signals in cultured erythroid cells. Here we demonstrate that activated AKT complements EpoR signaling and supports erythroid-cell differentiation in wild-type and JAK2-deficient fetal liver cells. We show that erythroid maturation of AKT-transduced cells is not solely dependent on AKT-induced cell survival or proliferation signals, suggesting that AKT transduces also a differentiation-specific signal downstream of EpoR in erythroid cells. Downregulation of expression of AKT kinase by RNA interference, or AKT activity by expression of dominant negative forms, inhibits significantly fetal liver-derived erythroid-cell colony formation and gene expression, demonstrating that AKT is required for Epo regulation of erythroid-cell maturation.
PB  - Amer Soc Hematology, Washington
T2  - Blood
T1  - AKT induces erythroid-cell maturation of JAK2-deficient fetal liver progenitor cells and is required for Epo regulation of erythroid-cell differentiation
EP  - 1891
IS  - 5
SP  - 1888
VL  - 107
DO  - 10.1182/blood-2005-06-2304
ER  - 

@article{
author = "Ghaffari, Saghi and Kitidis, C and Zhao, W and Marinković, Dragan and Fleming, MD and Luo, B and Marszalek, J and Lodish, HF",
year = "2006",
abstract = "AKT serine threonine kinase of the protein kinase B (PKB) family plays essential roles in cell survival, growth, metabolism, and differentiation. In the erythroid system, AKT is known to be rapidly phosphorylated and activated in response to erythropoletin (Epo) engagement of Epo receptor (EpoR) and to sustain survival signals in cultured erythroid cells. Here we demonstrate that activated AKT complements EpoR signaling and supports erythroid-cell differentiation in wild-type and JAK2-deficient fetal liver cells. We show that erythroid maturation of AKT-transduced cells is not solely dependent on AKT-induced cell survival or proliferation signals, suggesting that AKT transduces also a differentiation-specific signal downstream of EpoR in erythroid cells. Downregulation of expression of AKT kinase by RNA interference, or AKT activity by expression of dominant negative forms, inhibits significantly fetal liver-derived erythroid-cell colony formation and gene expression, demonstrating that AKT is required for Epo regulation of erythroid-cell maturation.",
publisher = "Amer Soc Hematology, Washington",
journal = "Blood",
title = "AKT induces erythroid-cell maturation of JAK2-deficient fetal liver progenitor cells and is required for Epo regulation of erythroid-cell differentiation",
pages = "1891-1888",
number = "5",
volume = "107",
doi = "10.1182/blood-2005-06-2304"
}

Ghaffari, S., Kitidis, C., Zhao, W., Marinković, D., Fleming, M., Luo, B., Marszalek, J.,& Lodish, H.. (2006). AKT induces erythroid-cell maturation of JAK2-deficient fetal liver progenitor cells and is required for Epo regulation of erythroid-cell differentiation. in Blood
Amer Soc Hematology, Washington., 107(5), 1888-1891.
https://doi.org/10.1182/blood-2005-06-2304

Ghaffari S, Kitidis C, Zhao W, Marinković D, Fleming M, Luo B, Marszalek J, Lodish H. AKT induces erythroid-cell maturation of JAK2-deficient fetal liver progenitor cells and is required for Epo regulation of erythroid-cell differentiation. in Blood. 2006;107(5):1888-1891.
doi:10.1182/blood-2005-06-2304 .

Ghaffari, Saghi, Kitidis, C, Zhao, W, Marinković, Dragan, Fleming, MD, Luo, B, Marszalek, J, Lodish, HF, "AKT induces erythroid-cell maturation of JAK2-deficient fetal liver progenitor cells and is required for Epo regulation of erythroid-cell differentiation" in Blood, 107, no. 5 (2006):1888-1891,
https://doi.org/10.1182/blood-2005-06-2304 . .