Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
44
pubmed:dateCreated
2000-10-26
pubmed:abstractText
Friend erythroleukemia induced in mice by the spleen focus forming virus (SFFV) is a multi-step process. The pre-leukemic phase of the disease results from the abnormal activation of the Erythropoietin (Epo) receptor by the gp55 env gene product of SFFV. Later in disease progression, the emergence of leukemic clones is associated with recurrent genetic events, in particular the activation of the expression of SPI-1, an ETS family transcriptional regulator. We show here that the expression of either SPI-1 or GP55 with the mouse EPOR in avian primary erythroblasts only marginally affects their normal Epo-induced terminal differentiation. In contrast, the co-expression of GP55 and SPI-1 resulted in inhibition of Epo-induced differentiation of EPOR-expressing erythroblasts, promoting instead their proliferation. Co-expression of SPI-1 and GP55 also inhibited the apoptotic cell death program normally induced in response to Epo withdrawal. This cooperation between SPI-1 and GP55 to induce primary erythroblast transformation suggests that progression of Friend erythroleukemia critically depends upon inter-dependent interactions between the molecular events specific of the early and late phase of the disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
19
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5106-10
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
SPI-1 transforming properties depend upon specifically activated forms of the EPOR.
pubmed:affiliation
CNRS UMR146 Institut Curie, Centre Universitaire, Bat. 110, 91405 Orsay, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't