scholarly journals Reduced hormone-stimulated adenylate cyclase activity in NIH-3T3 cells expressing the EJ human bladder ras oncogene.

1986 ◽  
Vol 83 (11) ◽  
pp. 3703-3707 ◽  
Author(s):  
W. G. Tarpley ◽  
N. K. Hopkins ◽  
R. R. Gorman
Keyword(s):  
Adenylate Cyclase ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Ras Oncogene ◽  
3T3 Cells ◽  
Human Bladder ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

scholarly journals Adenylate cyclase activity of NIH 3T3 cells morphologically transformed byrasgenes

FEBS Letters ◽  
1986 ◽  
Vol 197 (1-2) ◽  
pp. 134-138 ◽  
Author(s):  
Alexander Levitzki ◽  
Joyce Rudick ◽  
Ira Pastan ◽  
William C. Vass ◽  
Douglas R. Lowy
Keyword(s):  
Adenylate Cyclase ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
3T3 Cells ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

scholarly journals Insulin and vasopressin elicit inhibition of cholera-toxin-stimulated adenylate cyclase activity in both hepatocytes and the P9 immortalized hepatocyte cell line through an action involving protein kinase C

1995 ◽  
Vol 312 (3) ◽  
pp. 769-774 ◽  
Author(s):  
L Zeng ◽  
M D Houslay
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Adenylate Cyclase ◽  
Cholera Toxin ◽  
Cell Line ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
3T3 Cells ◽  
Kinase C ◽  
Nih 3T3

Incubation of hepatocytes or the SV40-DNA-immortalized hepatocyte P9 cell line with cholera toxin led to a time-dependent activation of adenylate cyclase activity, which occurred after a defined lag period. When added together with cholera toxin, each of the hormones insulin and vasopressin was capable of attenuating the maximum stimulatory effect achieved by cholera toxin over a period of 60 min through a process which could be blocked by the compounds staurosporine and chelerythrine. Attenuating effects on cholera-toxin-stimulated adenylate cyclase activity could also be elicited by using either the protein kinase C (PKC)-stimulating phorbol ester PMA (phorbol 12-myristate 13-acetate) or the protein phosphatase inhibitor okadaic acid. Alkaline phosphatase treatment of membranes reversed the inhibitory effect of PMA. Cholera toxin also stimulated the adenylate cyclase activity of intact CHO (Chinese-hamster ovary) and NIH-3T3 cells, but this activity was insensitive to the addition of PMA. Overexpression of various PKC isoforms in CHO cell lines did not confer sensitivity to inhibition by PMA upon cholera-toxin-stimulated adenylate cyclase activity. Rather, overexpression of the gamma isoform of PKC allowed PMA to stimulate adenylate cyclase activity in CHO cells. It is suggested that the PKC-mediated phosphorylation of a membrane protein attenuates cholera-toxin-stimulated adenylate cyclase activity in hepatocytes and P9 cells. The cellular selectivity of such an action may be due to the target for this inhibitory action of PKC being a particular isoform of adenylate cyclase which provides the major activity in hepatocytes and P9 cells, but not in either CHO or 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

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.

Identifying the factors and signal pathways necessary for anchorage-independent growth of Ha-ras oncogene-transformed NIH/3T3 cells

Life Sciences ◽  
2003 ◽  
Vol 73 (10) ◽  
pp. 1265-1274 ◽  
Author(s):  
Tsuey-Yu Chang ◽  
Wen-Jiuan Tsai ◽  
Chao-Kai Chou ◽  
Nan-Haw Chow ◽  
Tzeng-Horng Leu ◽  
...  
Keyword(s):  
Signal Pathways ◽  
Ras Oncogene ◽  
3T3 Cells ◽  
Anchorage Independent Growth ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

scholarly journals A human Ki-ras oncogene encodes two transforming p21 proteins.

1986 ◽  
Vol 6 (4) ◽  
pp. 1326-1328 ◽  
Author(s):  
M S McCoy ◽  
R A Weinberg
Keyword(s):  
Ras Oncogene ◽  
3T3 Cells ◽  
Ras Gene ◽  
P21 Protein ◽  
Nih 3T3 ◽  
P21 Proteins ◽  
Nih 3T3 Cells

The human Ki-ras gene was previously reported to contain two alternative fourth exons which encode two distinct p21 proteins differing only at their carboxy termini. The present study shows that either p21 protein is able on its own to transform NIH 3T3 cells to a tumorigenic state.

scholarly journals Depletion of c-myc with specific antisense sequences reverses the transformed phenotype in ras oncogene-transformed NIH 3T3 cells.

1991 ◽  
Vol 11 (7) ◽  
pp. 3699-3710 ◽  
Author(s):  
M D Sklar ◽  
E Thompson ◽  
M J Welsh ◽  
M Liebert ◽  
J Harney ◽  
...  
Keyword(s):  
Nude Mice ◽  
Growth Rates ◽  
Monolayer Culture ◽  
Soft Agar ◽  
Ras Oncogene ◽  
Minimum Level ◽  
3T3 Cells ◽  
Sense Orientation ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

ras oncogene-transformed NIH 3T3 cells expressing glucocorticoid-inducible antisense c-myc cDNA transcripts at levels sufficient to deplete c-myc protein lost their transformed morphology and the ability to grow in soft agar; their ability to form tumors in nude mice was also impaired. These changes were dependent on the continuous expression of the antisense sequences. No major effects on plating efficiencies, growth rates in monolayer culture, or immortalization were observed in the revertant cells, indicating that the observed effects were not a toxic consequence of c-myc protein depletion. Transfection with the same vector expressing c-myc in the sense orientation or other control vectors had no effect on transformation. These results suggest that a certain minimum level of expression of c-myc is required for the maintenance of ras transformation in NIH 3T3 cells.

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