scholarly journals PRODUCTION OF FRIEND LEUKEMIA VIRUS IN A MOUSE LUNG CELL LINE

1967 ◽  
Vol 20 (3) ◽  
pp. 225-236 ◽  
Author(s):  
HIROSHI YOSHIKURA ◽  
YASUKO HIROKAWA ◽  
MASA-ATSU YAMADA ◽  
HARUO SUGANO
Keyword(s):  
Cell Line ◽  
Leukemia Virus ◽  
Mouse Lung ◽  
Friend Leukemia ◽  
Friend Leukemia Virus ◽  
Lung Cell Line

scholarly journals Retroviral insertions downstream of the heterogeneous nuclear ribonucleoprotein A1 gene in erythroleukemia cells: evidence that A1 is not essential for cell growth.

1992 ◽  
Vol 12 (10) ◽  
pp. 4449-4455 ◽  
Author(s):  
Y Ben-David ◽  
M R Bani ◽  
B Chabot ◽  
A De Koven ◽  
A Bernstein
Keyword(s):  
Cell Growth ◽  
Cell Line ◽  
Rna Splicing ◽  
Rna Binding ◽  
Leukemia Virus ◽  
Heterogeneous Nuclear Ribonucleoprotein ◽  
Friend Leukemia ◽  
Erythroleukemia Cell ◽  
Nuclear Ribonucleoprotein ◽  
Friend Leukemia Virus

A large number of novel cellular proto-oncogenes have been identified and cloned by analysis of common integration sites in retrovirally induced malignancies. In the multistage erythroleukemias induced by the various strains of Friend leukemia virus, the analysis of proviral-integration events has led to the identification of two genes, Fli-1 and Spi-1, both novel members of the ets oncogene family of transcription factors. In this report, we describe the identification of another integration site, designated Fli-2 (Friend leukemia virus integration-2), in an erythroleukemia cell line induced by Friend murine leukemia virus (F-MuLV). Rearrangements at the Fli-2 locus were found in two erythroleukemia cell lines independently induced by F-MuLV and one leukemic cell line derived from the spleen of a mouse infected with the polycythemia strain of Friend leukemia virus. The deduced amino acid sequence of a cDNA corresponding to a transcript originating from genomic DNA adjacent to Fli-2 is identical to that of the human heterogeneous nuclear ribonucleoprotein A1 gene, a member of the gene family of RNA-binding proteins involved in RNA splicing. In one erythroleukemia cell line, A1 expression was undetectable as a result of F-MuLV integration in one allele and loss of the other allele. These results suggest that perturbations in RNA splicing mechanisms may contribute to malignant transformation and provide direct evidence that the A1 protein is not required for cell growth.

Retroviral insertions downstream of the heterogeneous nuclear ribonucleoprotein A1 gene in erythroleukemia cells: evidence that A1 is not essential for cell growth

1992 ◽  
Vol 12 (10) ◽  
pp. 4449-4455
Author(s):  
Y Ben-David ◽  
M R Bani ◽  
B Chabot ◽  
A De Koven ◽  
A Bernstein
Keyword(s):  
Cell Growth ◽  
Cell Line ◽  
Rna Splicing ◽  
Rna Binding ◽  
Leukemia Virus ◽  
Heterogeneous Nuclear Ribonucleoprotein ◽  
Friend Leukemia ◽  
Erythroleukemia Cell ◽  
Nuclear Ribonucleoprotein ◽  
Friend Leukemia Virus

A large number of novel cellular proto-oncogenes have been identified and cloned by analysis of common integration sites in retrovirally induced malignancies. In the multistage erythroleukemias induced by the various strains of Friend leukemia virus, the analysis of proviral-integration events has led to the identification of two genes, Fli-1 and Spi-1, both novel members of the ets oncogene family of transcription factors. In this report, we describe the identification of another integration site, designated Fli-2 (Friend leukemia virus integration-2), in an erythroleukemia cell line induced by Friend murine leukemia virus (F-MuLV). Rearrangements at the Fli-2 locus were found in two erythroleukemia cell lines independently induced by F-MuLV and one leukemic cell line derived from the spleen of a mouse infected with the polycythemia strain of Friend leukemia virus. The deduced amino acid sequence of a cDNA corresponding to a transcript originating from genomic DNA adjacent to Fli-2 is identical to that of the human heterogeneous nuclear ribonucleoprotein A1 gene, a member of the gene family of RNA-binding proteins involved in RNA splicing. In one erythroleukemia cell line, A1 expression was undetectable as a result of F-MuLV integration in one allele and loss of the other allele. These results suggest that perturbations in RNA splicing mechanisms may contribute to malignant transformation and provide direct evidence that the A1 protein is not required for cell growth.

Involvement of GER in Friend leukemia virus assembly in high-pressure frozen cells

1990 ◽  
Vol 48 (3) ◽  
pp. 590-591
Author(s):  
W. Djaczenko ◽  
M. Müller ◽  
A. Benedetto ◽  
G. Carbone
Keyword(s):  
High Pressure ◽  
Virus Assembly ◽  
Leukemia Virus ◽  
Leukemia Cells ◽  
Serial Sections ◽  
Myeloma Cells ◽  
Virus Particles ◽  
Friend Leukemia ◽  
Carbon Coated ◽  
Friend Leukemia Virus

A thickening of ER membranes in murine myeloma cells was attributed by de Harven to the assembly of intracisternal virus particles. We observed similar thickening of GER membranes in Friend leukemia cells (FLC) apparently associated with Friend leukemia virus (FLV) assembly. We reinvestigated the problem of GER involvement in FLV assembly using high pressure cryofixed FLC.FLC (745A clone growing in suspension and FF clone growing in monolayer) were immersed in Hexadecene (Fluka, Switzerland) and rapidly frozen in Balzers HPM 010 freezing machine working at 2200 bar. All cells were freeze substituted at -90°C in 2% OsO4 in absolute acetone. Serial sections cut to avoid misinterpretations due to the geometry of sections, were collected on carbon coated 100 mesh grids.

What can we learn from Fli1-deficient mice, new animal models of systemic sclerosis?

2018 ◽  
Vol 3 (1) ◽  
pp. 6-13 ◽  
Author(s):  
Yoshihide Asano
Keyword(s):  
Systemic Sclerosis ◽  
Animal Models ◽  
Leukemia Virus ◽  
Environmental Influences ◽  
Epidemiological Studies ◽  
Potential Candidate ◽  
Predisposing Factor ◽  
Friend Leukemia ◽  
Virus Integration ◽  
Friend Leukemia Virus

Systemic sclerosis is a complex multifactorial disease characterized by autoimmunity, vasculopathy, and selective organ fibrosis. A series of genetic and epidemiological studies have demonstrated that environmental influences play a central role in the onset of systemic sclerosis, while genetic factors determine the susceptibility to and the severity of this disease. Therefore, the identification of predisposing factors related to environmental influences would provide us with an informative clue to better understand the pathological process of this disease. Based on this concept, the deficiency of transcription factor Friend leukemia virus integration 1, which is epigenetically suppressed in systemic sclerosis, seems to be a potential candidate acting as the predisposing factor of this disease. Indeed, Fli1-mutated mice serve as a set of useful disease models to disclose the complex pathology of systemic sclerosis. This article overviews the recent advancement in systemic sclerosis animal models associated with Friend leukemia virus integration 1 deficiency.

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