Isolation of recessive (mediator-) revertants from NIH 3T3 cells transformed with a c-H-ras oncogene

1990 ◽  
Vol 10 (4) ◽  
pp. 1822-1827
Author(s):  
H Yamada ◽  
T Omata-Yamada ◽  
N Wakabayashi-Ito ◽  
S G Carter ◽  
P Lengyel
Keyword(s):  
Ras Oncogene ◽  
3T3 Cells ◽  
Multiple Copies ◽  
Transforming Activity ◽  
Complementation Groups ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

We have generated two serum- and anchorage-dependent revertants from NIH 3T3 cells transformed with multiple copies of the human c-H-ras oncogene. In both revertants, the c-H-ras oncogene was fully expressed. Fusion of either revertant with untransformed cells or of the two revertants with one another resulted in transformed progeny. These results indicated that the two revertants were recessive and in different complementation groups. We believe that in our two revertants some of the genes mediating the transforming activity of the c-H-ras oncogene are defective; we are attempting to identify these mediator genes.

scholarly journals Isolation of recessive (mediator-) revertants from NIH 3T3 cells transformed with a c-H-ras oncogene.

1990 ◽  
Vol 10 (4) ◽  
pp. 1822-1827 ◽  
Author(s):  
H Yamada ◽  
T Omata-Yamada ◽  
N Wakabayashi-Ito ◽  
S G Carter ◽  
P Lengyel
Keyword(s):  
Ras Oncogene ◽  
3T3 Cells ◽  
Multiple Copies ◽  
Transforming Activity ◽  
Complementation Groups ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

We have generated two serum- and anchorage-dependent revertants from NIH 3T3 cells transformed with multiple copies of the human c-H-ras oncogene. In both revertants, the c-H-ras oncogene was fully expressed. Fusion of either revertant with untransformed cells or of the two revertants with one another resulted in transformed progeny. These results indicated that the two revertants were recessive and in different complementation groups. We believe that in our two revertants some of the genes mediating the transforming activity of the c-H-ras oncogene are defective; we are attempting to identify these mediator genes.

In vitro methylation of the human Ha-ras oncogene (T24) affects its transforming activity on NIH/3T3 cells

1986 ◽  
Vol 10 (3) ◽  
pp. 175-175
Author(s):  
M BORRELLO ◽  
M PIEROTTI ◽  
R DONGHI ◽  
I BONGARZONE ◽  
P MONDELLINI ◽  
...  
Keyword(s):  
Ras Oncogene ◽  
3T3 Cells ◽  
Transforming Activity ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

Metabolism of n-6 fatty acids by NIH-3T3 cells transfected with the ras oncogene

1994 ◽  
Vol 139 (1) ◽  
pp. 71-81 ◽  
Author(s):  
R. J. de Antueno ◽  
R. C. Cantrill ◽  
Y-S. Huang ◽  
G. W. Ells ◽  
M. Elliot ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Ras Oncogene ◽  
3T3 Cells ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

Specific activation of the cellular Harvey-ras oncogene in dimethylbenzanthracene-induced mouse mammary tumors

1986 ◽  
Vol 6 (11) ◽  
pp. 4104-4108
Author(s):  
S Dandekar ◽  
S Sukumar ◽  
H Zarbl ◽  
L J Young ◽  
R D Cardiff
Keyword(s):  
Mammary Tumors ◽  
3T3 Cells ◽  
Mouse Mammary Tumor ◽  
Mouse Mammary Tumors ◽  
Transforming Activity ◽  
Radiation Induced ◽  
Genomic Dnas ◽  
Nih 3T3 ◽  
Adenosine Nucleotide ◽  
Nih 3T3 Cells

Genomic DNAs from dimethylbenzanthracene-induced BALB/c mouse mammary tumors arising from the transplantable hyperplastic outgrowth (HPO) line designated DI/UCD transformed NIH 3T3 cells upon transfection. Transforming activity was attributed to the presence of activated Harvey ras-1 oncogenes containing an A----T transversion at the middle adenosine nucleotide in codon 61. DNAs from untreated DI/UCD HPO cells and radiation-induced and spontaneous mammary tumors from the DI/UCD HPO line failed to transform NIH 3T3 cells. The results indicated that the mutation activation of Harvey ras-1 oncogenes was specific to dimethylbenzanthracene treatment in the mouse mammary tumor system.

scholarly journals A transforming activity not detected by DNA transfer to NIH 3T3 cells is detected by JB6 mouse epidermal cells.

1985 ◽  
Vol 5 (4) ◽  
pp. 890-893 ◽  
Author(s):  
N H Colburn ◽  
M I Lerman ◽  
G A Hegamyer ◽  
T D Gindhart
Keyword(s):  
Tumor Cell ◽  
Cell Lines ◽  
Tumor Cell Lines ◽  
3T3 Cells ◽  
Anchorage Independence ◽  
Transforming Activity ◽  
Mouse Epidermal Cell ◽  
Nih 3T3 ◽  
Transforming Genes ◽  
Nih 3T3 Cells

Transfection of four different mouse epidermal tumor cell DNAs into NIH 3T3 cells yielded neither morphologically altered foci nor anchorage independence. However, promotion-sensitive, but not promotion-insensitive, JB6 mouse epidermal cell lines were permissive for the expression of anchorage independence after transfection of DNA from three of these tumor cell lines. This transforming activity and the promotion-sensitive activity that confers sensitivity to promotion of transformation show differences in restriction enzyme sensitivity. In view of this difference and the differences in both recipient cells and 12-O-tetradecanoyl-phorbol-13-acetate dependence of expression, it appears that the transforming activity and the promotion-sensitive activity are specified by different genes. The JB6 promotion-sensitive cell lines may be useful for detecting and cloning transforming genes that escape detection in the NIH 3T3 cell focus assay.

scholarly journals B-raf, a new member of the raf family, is activated by DNA rearrangement.

1988 ◽  
Vol 8 (6) ◽  
pp. 2651-2654 ◽  
Author(s):  
S Ikawa ◽  
M Fukui ◽  
Y Ueyama ◽  
N Tamaoki ◽  
T Yamamoto ◽  
...  
Keyword(s):  
Ewing Sarcoma ◽  
Dna Rearrangement ◽  
Terminal Portion ◽  
3T3 Cells ◽  
Complementary Dna ◽  
Amino Terminal ◽  
Transforming Activity ◽  
Nih 3T3 ◽  
Transforming Gene ◽  
Nih 3T3 Cells

Complementary DNA clones of a putative transforming gene were isolated from NIH 3T3 cells transformed with human Ewing sarcoma DNA. The gene was termed B-raf because it is related to but distinct from c-raf and A-raf. It appears that substitution in the amino-terminal portion of the normal B-raf protein confers transforming activity to the gene.

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 Alpha B-crystallin expression in mouse NIH 3T3 fibroblasts: glucocorticoid responsiveness and involvement in thermal protection.

1993 ◽  
Vol 13 (3) ◽  
pp. 1824-1835 ◽  
Author(s):  
A Aoyama ◽  
E Fröhli ◽  
R Schäfer ◽  
R Klemenz
Keyword(s):  
Heat Shock ◽  
Thermal Protection ◽  
Cell Clone ◽  
Ectopic Expression ◽  
Small Heat Shock Protein ◽  
Ras Oncogene ◽  
3T3 Cells ◽  
3T3 Fibroblasts ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

alpha B-crystallin, a major soluble protein of vertebrate eye lenses, is a small heat shock protein which transiently accumulates in response to heat shock and other kinds of stress in mouse NIH 3T3 fibroblasts. Ectopic expression of an alpha B-crystallin cDNA clone renders NIH 3T3 cells thermoresistant. alpha B-crystallin accumulates in response to the synthetic glucocorticoid hormone dexamethasone. Dexamethasone-treated NIH 3T3 cells become thermoresistant to the same extent as they accumulate alpha B-crystallin. A cell clone in which alpha B-crystallin is superinduced upon heat shock acquires augmented thermotolerance. Expression of the ras oncogene causes a rapid but transient accumulation of alpha B-crystallin within 1 day. Later, sustained ras oncogene expression suppresses the dexamethasone-mediated alpha B-crystallin accumulation. Thus, oncogenic transformation triggered by the ras oncogene interferes with hormone-mediated accumulation of alpha B-crystallin and concomitant acquisition of thermoresistance. Other known heat shock proteins do not accumulate in response to ectopic alpha B-crystallin expression or to dexamethasone treatment. These results indicate that alpha B-crystallin can protect NIH 3T3 fibroblasts from thermal shock.

Sign in / Sign up

Export Citation Format

Share Document