Linked Life Data

2184193

Source:http://linkedlifedata.com/resource/pubmed/id/2184193

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1990-5-25
pubmed:abstractText
The t(14;18) of human follicular B cell lymphoma translocates the Bcl-2 gene into the Ig H chain locus and markedly deregulates Bcl-2 expression. We sought to determine if Bcl-2 could be directly implicated in a growth-factor pathway. Consequently, we introduced a retrovirus containing the murine Bcl-2 gene (N2-M-Bcl-2) or the parental retrovirus (N2) into a series of factor-dependent hemopoietic cell lines. Overexpressed Bcl-2 resulted in no long term IL-2, IL-3, or IL-6 independent clones, indicating that Bcl-2 could not spare the need for a specific ligand-receptor interaction. However, Bcl-2 did extend the short term survival of IL-3-dependent cell lines after factor deprivation. Although viable, IL-3-deprived pro B lymphocytes (FL5.12) bearing N2-M-Bcl-2 were in Go, and deregulated Bcl-2 did not obviously influence cell-cycle progression. Bcl-2 predominant effects were to delay the onset of cell death and to modestly augment viable cell growth in the first 48 h after IL-3 deprivation. This death sparing was associated with increased levels of Bcl-2 RNA and protein in factor-deprived cells possessing N2-M-Bcl-2. This result was not restricted to prolymphocytes because an IL-3-dependent mast cell line (32D) as well as a promyeloid line (FDC-P1) demonstrated the same response to Bcl-2. Moreover, the effect was not limited to the IL-3/IL-3R signal transduction pathway in that promyeloid cells maintained in granulocyte-macrophage-CSF or IL-4 displayed a similar response. Yet, Bcl-2-enhanced cell survival was not universal as an IL-2-dependent T cell line, and an IL-6-dependent myeloma line demonstrated no consistent effect upon IL withdrawal. Thus, Bcl-2 appears to interfere with cell death but in a cell type and/or factor-restricted fashion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
144
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3602-10
pubmed:dateRevised
2006-4-21
pubmed:meshHeading
pubmed-meshheading:2184193-Animals, pubmed-meshheading:2184193-Blotting, Northern, pubmed-meshheading:2184193-Blotting, Southern, pubmed-meshheading:2184193-Cell Line, pubmed-meshheading:2184193-Cell Survival, pubmed-meshheading:2184193-Cloning, Molecular, pubmed-meshheading:2184193-Flow Cytometry, pubmed-meshheading:2184193-Gene Expression, pubmed-meshheading:2184193-Genetic Vectors, pubmed-meshheading:2184193-Growth Substances, pubmed-meshheading:2184193-Hematopoietic Stem Cells, pubmed-meshheading:2184193-Interleukin-2, pubmed-meshheading:2184193-Interleukin-3, pubmed-meshheading:2184193-Interleukin-6, pubmed-meshheading:2184193-Mice, pubmed-meshheading:2184193-Monosaccharide Transport Proteins, pubmed-meshheading:2184193-Proto-Oncogene Proteins, pubmed-meshheading:2184193-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:2184193-Proto-Oncogene Proteins c-myc, pubmed-meshheading:2184193-RNA, Messenger
pubmed:year
1990
pubmed:articleTitle
Deregulated Bcl-2 gene expression selectively prolongs survival of growth factor-deprived hemopoietic cell lines.
pubmed:affiliation
Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110.
pubmed:publicationType
Journal Article