sub:provenance { sub:assertiondcterms:description "[Although one of these (Y704) has previously been shown to be involved in STAT3 activation from a truncated G-CSF-R derived from a patient with severe chronic neutropenia (SCN), this tyrosine is not required for STAT3 activation by the full-length G-CSF-R. To investigate possible alternative mechanisms of STAT3 activation, we generated a series of Ba/F3 cell transfectants expressing the wild-type G-CSF-R or mutant receptors that either completely lack tyrosines or retain just one of the four cytoplasmic tyrosines of the G-CSF-R. We show that, at saturating G-CSF concentrations, STAT3 activation from the full-length G-CSF-R is efficiently mediated by the C-terminal domain in a manner independent of receptor tyrosines.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine."@en ; wi:evidencedgn-void:source_evidence_literature ; sio:SIO_000772miriam-pubmed:9864153 ; prov:wasDerivedFromdgn-void:BEFREE ; prov:wasGeneratedByeco:ECO_0000203 . dgn-void:BEFREEpav:importedOn "2017-02-19"^^xsd:date . dgn-void:source_evidence_literatureaeco:ECO_0000212 ; rdfs:comment "Gene-disease associations inferred from text-mining the literature."@en ; rdfs:label "DisGeNET evidence - LITERATURE"@en . }