Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
44
pubmed:dateCreated
1996-12-26
pubmed:abstractText
Introduction of erythropoietin receptors (EpoRs) into the interleukin-3 (IL-3)-dependent murine hemopoietic cell line, Ba/F3, enables these cells to not only proliferate, after an initial lag in G1, but also to increase beta-globin mRNA levels in response to erythropoietin (Epo). With IL-3 and Epo costimulation, IL-3-induced signaling appears to be dominant since no increase in beta-globin mRNA occurs. Differentiation and proliferation signals may be uncoupled since EpoRs lacking all eight intracellular tyrosines were compromised in proliferative signaling but retained erythroid differentiation ability. Intriguingly, a chimeric receptor of the extracellular domain of the EpoR and the transmembrane and intracellular domains of IL-3RbetaIL-3 chain (EpoR/IL-3RbetaIL-3) was capable of Epo-induced proliferative and differentiating signaling, suggesting either the existence of a second EpoR subunit responsible for differentiation or that the alpha subunit of the IL-3 receptor (IL-3R) prevents it. Arguing against the former, a truncated EpoR lacking an intracellular domain was incapable of promoting proliferation or differentiation. An EpoR/IL-3Ralpha chimera, in contrast, was capable of transmitting a weak Epo-induced proliferative signal but failed to stimulate accumulation of beta-globin mRNA. Most significantly, coexpression of the EpoR/IL-3Ralpha chimera with either EpoR/IL-3Rbeta or wild-type EpoRs suppressed Epo-induced beta-globin mRNA accumulation. Taken together, these results suggest an active role for the IL-3Ralpha subunit in inhibiting EpoR-specific differentiating signals.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
271
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
27432-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8910323-Animals, pubmed-meshheading:8910323-Cell Differentiation, pubmed-meshheading:8910323-Cell Division, pubmed-meshheading:8910323-Cell Line, pubmed-meshheading:8910323-Clone Cells, pubmed-meshheading:8910323-Erythropoietin, pubmed-meshheading:8910323-Genetic Vectors, pubmed-meshheading:8910323-Globins, pubmed-meshheading:8910323-Hematopoietic Stem Cells, pubmed-meshheading:8910323-Interleukin-3, pubmed-meshheading:8910323-Kinetics, pubmed-meshheading:8910323-Macromolecular Substances, pubmed-meshheading:8910323-Mice, pubmed-meshheading:8910323-Mutagenesis, Site-Directed, pubmed-meshheading:8910323-RNA, Messenger, pubmed-meshheading:8910323-Receptors, Erythropoietin, pubmed-meshheading:8910323-Receptors, Interleukin-3, pubmed-meshheading:8910323-Recombinant Fusion Proteins, pubmed-meshheading:8910323-Retroviridae, pubmed-meshheading:8910323-Transcription, Genetic, pubmed-meshheading:8910323-Transfection
pubmed:year
1996
pubmed:articleTitle
Interleukin-3 (IL-3) inhibits erythropoietin-induced differentiation in Ba/F3 cells via the IL-3 receptor alpha subunit.
pubmed:affiliation
Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia V5Z 1L3, Canada. keith@terryfox.ubc.ca
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't