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http://purl.uniprot.org/citations/23559492http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23559492http://www.w3.org/2000/01/rdf-schema#comment"Neutrophils play an important role in the innate immune response against bacterial and fungal infections. They have a short lifespan in circulation, and their survival can be modulated by several cytokines, including G-CSF. Previous studies have implicated AKT as a critical signaling intermediary in the regulation of neutrophil survival. Our results demonstrate that G-CSF activation of AKT is not sufficient to prolong neutrophil survival. Neutrophils treated with G-CSF undergo apoptosis, even in the presence of high levels of p-AKT. In addition, inhibitors of AKT and downstream targets failed to alter neutrophil survival. In contrast, neutrophil precursors appear to be dependent on AKT signaling pathways for survival, whereas high levels of p-AKT inhibit proliferation. Our data suggest that the AKT/mTOR pathway, although important in G-CSF-driven myeloid differentiation, proliferation, and survival of early hematopoietic progenitors, is less essential in G-CSF suppression of neutrophil apoptosis. Whereas basal AKT levels may be required for the brief life of neutrophils, further p-AKT expression is not able to extend the neutrophil lifespan in the presence of G-CSF."xsd:string
http://purl.uniprot.org/citations/23559492http://purl.org/dc/terms/identifier"doi:10.1189/jlb.1211591"xsd:string
http://purl.uniprot.org/citations/23559492http://purl.uniprot.org/core/author"Silva E."xsd:string
http://purl.uniprot.org/citations/23559492http://purl.uniprot.org/core/author"Cabrera C."xsd:string
http://purl.uniprot.org/citations/23559492http://purl.uniprot.org/core/author"McLemore M.L."xsd:string
http://purl.uniprot.org/citations/23559492http://purl.uniprot.org/core/author"Souza L.R."xsd:string
http://purl.uniprot.org/citations/23559492http://purl.uniprot.org/core/author"Calloway E."xsd:string
http://purl.uniprot.org/citations/23559492http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23559492http://purl.uniprot.org/core/name"J Leukoc Biol"xsd:string
http://purl.uniprot.org/citations/23559492http://purl.uniprot.org/core/pages"883-893"xsd:string
http://purl.uniprot.org/citations/23559492http://purl.uniprot.org/core/title"G-CSF activation of AKT is not sufficient to prolong neutrophil survival."xsd:string
http://purl.uniprot.org/citations/23559492http://purl.uniprot.org/core/volume"93"xsd:string
http://purl.uniprot.org/citations/23559492http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23559492
http://purl.uniprot.org/citations/23559492http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23559492
http://purl.uniprot.org/uniprot/#_P40223-mappedCitation-23559492http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23559492
http://purl.uniprot.org/uniprot/#_Q14AY3-mappedCitation-23559492http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23559492
http://purl.uniprot.org/uniprot/#_Q14BI3-mappedCitation-23559492http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23559492
http://purl.uniprot.org/uniprot/P40223http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/23559492
http://purl.uniprot.org/uniprot/Q14AY3http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/23559492
http://purl.uniprot.org/uniprot/Q14BI3http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/23559492