Nucleotide sequences at host–proviral junctions for mouse mammary tumour virus

Nature ◽  
1981 ◽  
Vol 289 (5795) ◽  
pp. 253-258 ◽  
Author(s):  
John E. Majors ◽  
Harold E. Varmus
Keyword(s):  
Nucleotide Sequences ◽  
Mammary Tumour ◽  
Mouse Mammary Tumour Virus

The glucocorticoid receptor binds to defined nucleotide sequences near the promoter of mouse mammary tumour virus

Nature ◽  
1983 ◽  
Vol 304 (5928) ◽  
pp. 749-752 ◽  
Author(s):  
Claus Scheidereit ◽  
Sabine Geisse ◽  
Hannes M. Westphal ◽  
Miguel Beato
Keyword(s):  
Glucocorticoid Receptor ◽  
Nucleotide Sequences ◽  
Mammary Tumour ◽  
Mouse Mammary Tumour Virus

190 EXPRESSION OF GENES ASSOCIATED WITH WINGLESS-RELATED MOUSE MAMMARY TUMOUR VIRUS SIGNALING IN THE PRE-IMPLANTATION BOVINE EMBRYO

2015 ◽  
Vol 27 (1) ◽  
pp. 186
Author(s):  
P. Tribulo ◽  
J. I. Moss ◽  
P. J. Hansen
Keyword(s):  
Embryonic Development ◽  
Blastocyst Stage ◽  
Wnt Signalling ◽  
Mammary Tumour ◽  
Bovine Embryo ◽  
Cell Stage ◽  
Mouse Mammary Tumour Virus ◽  
Ct Value ◽  
Morula Stage ◽  
Canonical Wnt

Wingless-related mouse mammary tumour virus (WNT) signalling participates in early embryonic development to maintain pluripotency, controls cell–cell communication, and modulates cell polarization and migration. To gain an understanding of the regulation of WNT signalling during embryonic development, expression patterns of a variety of molecules involved in WNT signal transduction were evaluated. Specific genes were DKK1, an endogenous inhibitor of canonical WNT signalling, the WNT co-receptors LRP5 and LRP6, WNT-responsive transcription factors, LEF1 and TCF7, and two repressors of WNT-regulated genes, the bovine orthologue of GROUCHO (LOC505120) and AES. Embryos were produced in vitro from oocytes obtained from ovaries collected at a local abattoir. Following oocyte maturation, fertilization was performed with sperm pooled from three randomly selected bulls; a different pool of bulls was used for each replicate. Groups of 30 matured oocytes or embryos at the 2-cell [28–32 h post-insemination (hpi)], 3–4 cell (44–48 hpi), 5–8 cell (50–55 hpi), 9–16 cell (72–75 hpi), morula (120–123 hpi), and blastocyst (168–171 hpi) stages were collected. The zona pellucida was removed with proteinase, RNA was purified, cDNA synthesised using random hexamer primers and real-time qPCR performed. Data analysed were ΔCT values, which were calculated by subtracting the CT value of the geometric mean of the three housekeeping genes (GAPDH, YWHAZ, and SDHA) from the CT value of the sample. The relative transcript abundance was calculated as the 2ΔCT. Data were analysed by least-squares ANOVA using the Proc GLM procedure of SAS (SAS Institute Inc., Cary, NC, USA). A total of 5 replicates were analysed for each developmental stage. Results show significant effects of stage of development for each gene that ranged from P = 0.004 for LRP5 to P ≤ 0.0001 for AES, DKK1, LEF, LOC505120, LRP6, and TCF7. In all cases, expression declined as development advanced. Except for AES, lowest expression occurred at the blastocyst stage. Lowest expression for AES was at the morula stage; expression remained low at the blastocyst stage. For two genes, DKK1 and LEF1, there was no detectable expression at the blastocyst stage. The timing of decline in expression varied between genes, first occurring at the 9–16-cell stage (AES, LEF1, and LOC505120) or morula stage (DKK1, LRP5, LRP6, or TCF7). For DKK1, LEF1, and LRP6, there was also a slight increase in expression from the oocyte to two-cell stage. Results suggest that canonical WNT signalling is reduced at the morula and blastocyst stages relative to earlier stages in development. Research was supported by USDA-NIFA 2011-67015-30688.

Effects of two types of energy restriction on methylation levels of adiponectin receptor 1 and leptin receptor overlapping transcript in a mouse mammary tumour virus-transforming growth factor-α breast cancer mouse model

2019 ◽  
Vol 125 (1) ◽  
pp. 1-9 ◽  
Author(s):  
M. B. Cicekdal ◽  
B. T. Kazan ◽  
B. G. Tuna ◽  
U. Ozorhan ◽  
I. D. Ekici ◽  
...  
Keyword(s):  
Growth Factor ◽  
Leptin Receptor ◽  
Transforming Growth Factor ◽  
Energy Restriction ◽  
The Other ◽  
Adiponectin Receptor ◽  
Mammary Tumour ◽  
Protective Effects ◽  
Mouse Mammary Tumour Virus ◽  
Adiponectin Receptor 1

AbstractThe role of adiponectin and leptin signalling pathways has been suggested to play important roles in the protective effects of energy restriction (ER) on mammary tumour (MT) development. To study the effects of ER on the methylation levels in adiponectin receptor 1 (AdipoR1) and leptin receptor overlapping transcript (Leprot) genes using the pyrosequencing method in mammary fat pad tissue, mouse mammary tumour virus-transforming growth factor-α (MMTV-TGF-α) female mice were randomly assigned to ad libitum (AL), chronic ER (CER, 15 % ER) or intermittent ER (3 weeks AL and 1 week 60 % ER in cyclic periods) groups at 10 weeks of age until 82 weeks of age. The methylation levels of AdipoR1 in the CER group were higher than those in the AL group at week 49/50 (P < 0·05), while the levels of methylation for AdipoR1 and Leprot genes were similar among the other groups. Also, the methylation levels at CpG2 and CpG3 regions of the promoter region of the AdipoR1 gene in the CER group were three times higher (P < 0·05), while CpG1 island of Leprot methylation was significantly lower compared with the other groups (P < 0·05). Adiponectin and leptin gene expression levels were consistent with the methylation levels. We also observed a change with ageing in methylation levels of these genes. These results indicate that different types of ER modify methylation levels of AdipoR1 and Leprot in different ways and CER had a more significant effect on methylation levels of both genes. Epigenetic regulation of these genes may play important roles in the preventive effects of ER against MT development and ageing processes.

Congenital Duplication of the Palm in a Patient with Multiple Anomalies

2003 ◽  
Vol 28 (3) ◽  
pp. 276-279 ◽  
Author(s):  
M. M. AL-QATTAN
Keyword(s):  
Family Member ◽  
Integration Site ◽  
Mammary Tumour ◽  
Mouse Mammary Tumour Virus ◽  
Virus Integration ◽  
Virus Integration Site

In 1995, Parr and McMahon described a syndrome of congenital duplication of footpads in mice which lacked a protein called ‘Wingless-type mouse mammary tumour virus integration site family member 7a” (Wnt-7a). This syndrome has not been described in humans and the following report describes a similar syndrome in a Saudi girl. The role of Wnt-7a in the development of the limb along the dorso-ventral axis is discussed, along with interaction between the Wnt-7a and other axes of limb growth.

Glucocorticoids regulate expression of dihydrofolate reductase cDNA in mouse mammary tumour virus chimaeric plasmids

Nature ◽  
1981 ◽  
Vol 294 (5838) ◽  
pp. 228-232 ◽  
Author(s):  
Frank Lee ◽  
Richard Mulligan ◽  
Paul Berg ◽  
Gordon Ringold
Keyword(s):  
Dihydrofolate Reductase ◽  
Mammary Tumour ◽  
Mouse Mammary Tumour Virus

scholarly journals A Locus affecting Circulating Interferon Levels induced by Mouse Mammary Tumour Virus

1974 ◽  
Vol 23 (2) ◽  
pp. 209-211 ◽  
Author(s):  
E. De Maeyer ◽  
J. De Maeyer-Guignard ◽  
W. T. Hall ◽  
D. W. Bailey
Keyword(s):  
Mammary Tumour ◽  
Mouse Mammary Tumour Virus
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