scholarly journals Dietary lipids and calorie restriction affect mammary tumor incidence and gene expression in mouse mammary tumor virus/v-Ha-ras transgenic mice.

1995 ◽  
Vol 92 (14) ◽  
pp. 6494-6498 ◽  
Author(s):  
G. Fernandes ◽  
B. Chandrasekar ◽  
D. A. Troyer ◽  
J. T. Venkatraman ◽  
R. A. Good
Keyword(s):  
Gene Expression ◽  
Transgenic Mice ◽  
Calorie Restriction ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Dietary Lipids ◽  
Tumor Incidence ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

Multiple regulatory domains in the mouse mammary tumor virus long terminal repeat revealed by analysis of fusion genes in transgenic mice

1988 ◽  
Vol 8 (1) ◽  
pp. 473-479
Author(s):  
T A Stewart ◽  
P G Hollingshead ◽  
S L Pitts
Keyword(s):  
Transgenic Mice ◽  
Long Terminal Repeat ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Terminal Repeat ◽  
Growth Hormone Gene ◽  
Fusion Genes ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

Transcription initiated within the mouse mammary tumor virus (MTV) long terminal repeat (LTR) is regulated by glucocorticoids, androgens, and estrogen. However, expression of the virus in vivo and transcription of MTV LTR fusion genes in transgenic mice are not readily interpretable solely in terms of the influence of these hormones. To investigate whether there is a regulatory role for sequences within the LTR but outside the region known to be responsible for glucocorticoid induction, we have produced transgenic mice carrying genes in which various regions of the LTR have been linked to the human growth hormone gene. Analysis of expression of the fusion genes in these transgenic mice has demonstrated that the 5' end of the LTR can profoundly influence transcription initiated within the MTV LTR.

scholarly journals Transgenic mice carrying the mouse mammary tumor virus ras fusion gene: distinct effects in various tissues.

1989 ◽  
Vol 9 (2) ◽  
pp. 854-859 ◽  
Author(s):  
P J Tremblay ◽  
F Pothier ◽  
T Hoang ◽  
G Tremblay ◽  
S Brownstein ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Mammary Tumor ◽  
Lacrimal Gland ◽  
Mouse Mammary Tumor Virus ◽  
Fusion Gene ◽  
Ras Oncogene ◽  
Mammary Tumor Virus ◽  
Specific Effects ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

Transgenic mice carrying the v-Ha-ras oncogene under the control of the mouse mammary tumor virus long terminal repeat were produced. These mice exhibit several phenotypes: mammary tumors, bilateral hyperplasia of the harderian lacrimal gland, primary bronchio-alveolar lung adenocarcinoma, and splenomegaly. High levels of the transgene RNA were detected in mammary, harderian, and lung tumors. Accumulation of cells of the myeloid lineages was found in enlarged spleens. This phenotype may represent an indirect effect of v-Ha-ras expression on myeloid progenitors. Our data illustrate the cell-specific effects of v-Ha-ras.

Posttranscriptional regulation of cellular gene expression by the c-myc oncogene

1989 ◽  
Vol 9 (1) ◽  
pp. 124-134
Author(s):  
G C Prendergast ◽  
M D Cole
Keyword(s):  
Gene Expression ◽  
Cell Lines ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Cellular Gene ◽  
Mammary Tumor Virus ◽  
Myc Oncogene ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Myc Gene

The c-myc oncogene has been implicated in the development of many different cancers, yet the mechanism by which the c-myc protein alters cellular growth control has proven elusive. We used a cDNA hybridization difference assay to isolate two genes, mr1 and mr2, that were constitutively expressed (i.e., deregulated) in rodent fibroblast cell lines immortalized by transfection of a viral promoter-linked c-myc gene. Both cDNAs were serum inducible in quiescent G0 fibroblasts, suggesting that they are functionally related to cellular proliferative processes. Although there were significant differences in cytoplasmic mRNA levels between myc-immortalized and control cells, the rates of transcription and mRNA turnover of both genes were similar, suggesting that c-myc regulates mr1 and mr2 expression by some nuclear posttranscriptional mechanism. mr1 was also rapidly (within 2 h) and specifically induced by dexamethasone in BALB/c cell lines expressing a mouse mammary tumor virus long terminal repeat-driven myc gene, under conditions where other growth factor-inducible genes were unaffected. A frameshift mutation in the mouse mammary tumor virus myc gene destroyed the dexamethasone stimulation of mr1, indicating that c-myc protein is required for the effect. As in the myc-immortalized cells, the induction of mr1 by c-myc occurred without detectable changes in mr1 transcription or cytoplasmic mRNA stability, implicating regulation, either direct or indirect, through a nuclear posttranscriptional mechanism. These results provide evidence that c-myc can rapidly modulate cellular gene expression and suggest that c-myc may function in gene regulation at the level of RNA export, splicing, or nuclear RNA turnover.

scholarly journals Short communication: Mouse mammary tumor virus driven α-lactalbumin expression effects on lactation and fertility of transgenic mice

2011 ◽  
Vol 94 (5) ◽  
pp. 2418-2424
Author(s):  
S. Le Guillou ◽  
G. Tilly ◽  
B. Passet ◽  
L. Lefèvre ◽  
M. Vilotte ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Short Communication ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus
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