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dc.creatorGhaffari, Saghi
dc.creatorKitidis, C
dc.creatorZhao, W
dc.creatorMarinković, Dragan
dc.creatorFleming, MD
dc.creatorLuo, B
dc.creatorMarszalek, J
dc.creatorLodish, HF
dc.date.accessioned2021-06-09T13:15:09Z
dc.date.available2021-06-09T13:15:09Z
dc.date.issued2006
dc.identifier.issn0006-4971
dc.identifier.urihttp://rfasper.fasper.bg.ac.rs/handle/123456789/79
dc.description.abstractAKT 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.en
dc.publisherAmer Soc Hematology, Washington
dc.relationUnited States Department of Health & Human Services, National Institutes of Health (NIH), National Cancer Institute (NCI) [K08CA077675]
dc.relationUnited States Department of Health & Human Services, National Institutes of Health (NIH), National Heart Lung & Blood Institute (NHLBI) [P01HL032262]
dc.relationUnited States Department of Health & Human Services, National Institutes of Health (NIH), National Cancer Institute (NCI) [K08CA077675]
dc.relationUnited States Department of Health & Human Services, National Institutes of Health (NIH), National Heart Lung & Blood Institute (NHLBI) [P01HL032262]
dc.rightsopenAccess
dc.sourceBlood
dc.titleAKT induces erythroid-cell maturation of JAK2-deficient fetal liver progenitor cells and is required for Epo regulation of erythroid-cell differentiationen
dc.typearticle
dc.rights.licenseARR
dc.citation.epage1891
dc.citation.issue5
dc.citation.other107(5): 1888-1891
dc.citation.rankaM21
dc.citation.spage1888
dc.citation.volume107
dc.identifier.doi10.1182/blood-2005-06-2304
dc.identifier.fulltexthttp://rfasper.fasper.bg.ac.rs/bitstream/id/662/76.pdf
dc.identifier.pmid16254141
dc.identifier.rcubconv_1096
dc.identifier.scopus2-s2.0-33344458617
dc.identifier.wos000235632700028
dc.type.versionpublishedVersion


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