Cell surface and other morphological changes accompanying growth inhibition in simian virus 40-transformed 3T3 mouse fibroblasts cells induced by glucocorticoids§

1987 ◽  
Vol 11 (1-4) ◽  
pp. 107-118
Author(s):  
Hasi R. Das ◽  
Robert Baratz ◽  
Delano V. Young
Keyword(s):  
Cell Surface ◽  
Growth Inhibition ◽  
Morphological Changes ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Mouse Fibroblasts

scholarly journals Mechanism of activation of the ret proto-oncogene by multiple endocrine neoplasia 2A mutations.

1995 ◽  
Vol 15 (3) ◽  
pp. 1613-1619 ◽  
Author(s):  
N Asai ◽  
T Iwashita ◽  
M Matsuyama ◽  
M Takahashi
Keyword(s):  
Cell Surface ◽  
Multiple Endocrine Neoplasia ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
3T3 Cells ◽  
Endocrine Neoplasia ◽  
Transforming Activity ◽  
Nih 3T3 ◽  
Men 2A ◽  
Nih 3T3 Cells

Transforming activity of the c-ret proto-oncogene with multiple endocrine neoplasia (MEN) 2A mutations was investigated by transfection of NIH 3T3 cells. Mutant c-ret genes driven by the simian virus 40 or cytomegalovirus promoter induced transformation with high efficiencies. The 170-kDa Ret protein present on the cell surface of transformed cells was highly phosphorylated on tyrosine and formed disulfide-linked homodimers. This result indicated that MEN 2A mutations induced ligand-independent dimerization of the c-Ret protein on the cell surface, leading to activation of its intrinsic tyrosine kinase. In addition to the MEN 2A mutations, we further introduced a mutation (lysine for asparaginic acid at codon 300 [D300K]) in a putative Ca(2+)-binding site of the cadherin-like domain. When c-ret cDNA with both MEN 2A and D300K mutations was transfected into NIH 3T3 cells, transforming activity drastically decreased. Western blot (immunoblot) analysis revealed that very little of the 170-kDa Ret protein with the D300K mutation was expressed in transfectants while expression of the 150-kDa Ret protein retained in the endoplasmic reticulum was not affected. This result also demonstrated that transport of the Ret protein to the plasma membrane is required for its transforming activity.

scholarly journals A recombinant murine retrovirus for simian virus 40 large T cDNA transforms mouse fibroblasts to anchorage-independent growth.

1986 ◽  
Vol 60 (1) ◽  
pp. 290-293 ◽  
Author(s):  
M Brown ◽  
M McCormack ◽  
K G Zinn ◽  
M P Farrell ◽  
I Bikel ◽  
...  
Keyword(s):  
Simian Virus 40 ◽  
Simian Virus ◽  
Anchorage Independent Growth ◽  
Mouse Fibroblasts

scholarly journals Effects of Simian Virus 40-Induced Transformation on Isoaccepting Species of Transfer RNA from Mouse Fibroblasts 1

1973 ◽  
Vol 12 (6) ◽  
pp. 1616-1619 ◽  
Author(s):  
F. H. Portugal ◽  
J. S. Simonds ◽  
D. Twardzik ◽  
M. Oskarsson
Keyword(s):  
Simian Virus 40 ◽  
Simian Virus ◽  
Transfer Rna ◽  
Mouse Fibroblasts

The adenovirus Ela gene induces differentiation of F9 teratocarcinoma cells

1987 ◽  
Vol 7 (5) ◽  
pp. 1782-1790
Author(s):  
X Montano ◽  
D P Lane
Keyword(s):  
Tumor Antigens ◽  
Morphological Changes ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Stem Cell Marker ◽  
Phenotypic Change ◽  
F9 Cells ◽  
Adenovirus E1a ◽  
E1a Gene ◽  
Marker Antigen

Undifferentiated F9 cells transfected with plasmids encoding adenovirus E1a gene products underwent radical morphological changes. They ceased to express the SSEA-1 stem cell marker antigen and started to express a number of the characteristics of the differentiated state that is induced in F9 cells by treatment with retinoic acid. In particular, they expressed keratin intermediate filaments and acquired the ability to synthesise simian virus 40 tumor antigens after virus infection. The transfected cells expressed the E1a proteins, and this expression was necessary to induce the phenotypic changes, since a coisogenic plasmid encoding only a truncated 70-amino-acid E1a polypeptide and the transfection procedure itself did not detectably after the morphology or marker expression of the F9 stem cells. The phenotypic change was induced by both 13S and 12S cDNA plasmids. We discuss these results in the context of known E1a functions and with reference to the other oncogenes and external factors that can cause F9 cell differentiation.

Cell surface binding affinity of Simian virus 40 T-antigen

Virology ◽  
1982 ◽  
Vol 117 (1) ◽  
pp. 173-185 ◽  
Author(s):  
Jutta Lange-Mutschler ◽  
Roland Henning
Keyword(s):  
Cell Surface ◽  
Binding Affinity ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Surface Binding ◽  
Cell Surface Binding
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