Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2000-9-7
pubmed:abstractText
The IL-3 family of cytokines transduces signals through Stat5 and regulates myeloid development. Previous studies have determined that a carboxy terminally truncated isoform of Stat5 is activated in immature myeloid cells. This isoform, which lacks a transcriptional activation domain, is generated by a protein-processing event. To determine whether Stat5 cleavage plays an important role in the growth and maturation of myeloid progenitors, the FdCP1 model of myeloid maturation was evaluated. FdCP1 cells are IL-3-dependent myeloid progenitors that differentiate into monocytes when cultured in granulocyte macrophage-colony-stimulating factor (GM-CSF). Consistent with their immature phenotype, when FdCP1 cells are cultured in IL-3 they exhibit robust protease activity and signal through truncated Stat5 isoforms. In contrast, maturation leads to a loss of protease activity and a switch to the expression to full-length Stat5 isoforms. Introduction of a noncleavable, full-length Stat5 mutant into undifferentiated FdCP1 cells leads to a partially differentiated phenotype and prevents further differentiation in response to GM-CSF. These results support our hypothesis that Stat5 processing is important for myeloid maturation. (Blood. 2000;96:1358-1365)
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
96
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1358-65
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Myeloid differentiation of FdCP1 cells is dependent on Stat5 processing.
pubmed:affiliation
Departments of Microbiology and Medicine, Columbia University, New York, NY 10032, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't