scholarly journals Leveraging the replication‐competent avian‐like sarcoma virus/tumor virus receptor‐A system for modeling human gliomas

Glia ◽  
2021 ◽  
Author(s):  
Pranjali P. Kanvinde ◽  
Adarsha P. Malla ◽  
Nina P. Connolly ◽  
Frank Szulzewsky ◽  
Pavlos Anastasiadis ◽  
...  
1977 ◽  
Vol 75 (2) ◽  
pp. 593-605 ◽  
Author(s):  
C H Damsky ◽  
J B Sheffield ◽  
G P Tuszynski ◽  
L Warren

Electrophoretic data from both sodium dodecyl sulfate-polyacrylamide gels (SDS-PAGE) and acid-urea gels reveal a protein in purified murine mammary tumor virus (MuMTV) which co-migrates with purified chick skeletal muscle actin. 125I-labeling of intact and disrupted virus preparations shows that the actin-like protein is not artifactually adsorbed to the outside of virions during isolation. Quantitative SDS-PAGE and examination of negatively stained preparations show that the actin cannot be accounted for by a contaminating population of virus-free vesicles. The ultrastructure of mammary epithelial cells and of Rous sarcoma virus-transformed chick embryo fibroblasts shows that virus extrusion is associated with filament-containing cellular processes. In particular, MuMTV is released from the ends of long microvilli which contain a bundle of 6-8-nm microfilaments and share other structural features with intestinal microvilli. We suggest that virus nucleoids require an interaction with host cell contractile proteins for their extrusion from the cell.


1985 ◽  
Vol 5 (9) ◽  
pp. 2204-2211
Author(s):  
F A van der Hoorn ◽  
V Müller

Extremely small quantities of the product of the transforming gene v-mos of Moloney murine sarcoma virus are able to efficiently transform cells. Recent data indicate the existence of a threshold level for v-mos transformation of NIH3T3 cells. Using mouse mammary tumor virus long terminal repeat sequences or hybrid promoters consisting of mouse mammary tumor virus and Moloney murine sarcoma virus long terminal repeat elements to express v-mos in C3H10T1/2 cells, we established cell lines representing different stages of morphological transformation in vitro. The threshold level for v-mos transformation was considerably lower than that for NIH3T3 cells, because no treatment with dexamethasone or primary selection other than transformation was necessary during standard transfection procedures. Using the cell lines mentioned we established an association of the level of v-mos expression with the transformation parameters examined, but not with p53 levels. Furthermore, the characterization of the different promoters showed (i) that the distal binding site confers hormone responsiveness to Moloney murine sarcoma virus promoter elements and (ii) that artifactual transcription initiation sites can be detected in mouse mammary tumor virus-Moloney murine sarcoma virus hybrid promoters which are, however, not regulated by the hormone.


1992 ◽  
Vol 70 (3-4) ◽  
pp. 237-241 ◽  
Author(s):  
Jill E. Parker ◽  
Wendell Winters

Replicate sets of cultures of mouse and of human cells were exposed to cyclic, sine wave, 60-Hz rotating magnetic fields of 1.0 Gs [Formula: see text] for 24-, 48-, or 72-h periods. Total RNA extracted from unexposed control and from magnetic field exposed cells was dot blot hybridized to a number of oncogene probes (including v-myc, v-fos, v-raf, and v-Ha-ras), a probe for 3611 murine sarcoma virus, a probe for the 70 000 dalton heat shock protein (hsp70), and a probe for the long terminal repeat sequence of mouse mammary tumor virus. Comparisons of levels of RNA in unexposed and magnetic field exposed cells measured by densitometer readings of resulting autoradiographs revealed no significant increases or decreases in RNA levels in magnetic field exposed cells with the seven probes tested.Key words: 60 hertz, oncogene, mRNA.


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