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Research Article

Analysis of the fibroblast transformation potential of GTPase-deficient gip2 oncogenes.

S K Gupta, C Gallego, J M Lowndes, C M Pleiman, C Sable, B J Eisfelder, G L Johnson
S K Gupta
Division of Basic Sciences, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.
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C Gallego
Division of Basic Sciences, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.
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J M Lowndes
Division of Basic Sciences, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.
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C M Pleiman
Division of Basic Sciences, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.
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C Sable
Division of Basic Sciences, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.
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B J Eisfelder
Division of Basic Sciences, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.
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G L Johnson
Division of Basic Sciences, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.
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DOI: 10.1128/MCB.12.1.190
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ABSTRACT

Expression of GTPase-deficient Gi2 alpha subunit (alpha i2) mutant polypeptides and overexpression of the wild-type alpha i2 polypeptide in Rat 1a, Swiss 3T3, and NIH 3T3 fibroblasts altered normal growth regulation and induced a loss of contact inhibition. In Rat 1a cells (but not in NIH 3T3 or Swiss 3T3 cells), expression of the GTPase-deficient alpha i2 mutant polypeptides allowed colony formation in soft agar, which correlated with a loss in anchorage dependence and a decreased serum requirement. The altered growth regulatory properties of Rat 1a cells induced by expression of alpha i2 mutant polypeptides was not significantly inhibited by cotransfection with a dominant negative Ha-ras mutant polypeptide (Asn-17rasH), indicating that the activated Gi2 membrane signal transduction protein is uniquely capable of altering the regulation of Rat 1a cell growth by a predominantly c-ras-independent mechanism. The results show that GTPase-deficient alpha i2 mutant polypeptides have the properties of an oncogene that can induce the phenotypic characteristics of transformation in Rat 1a cells but that only a subset of these changes is observed with NIH 3T3 and Swiss 3T3 cells.

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Analysis of the fibroblast transformation potential of GTPase-deficient gip2 oncogenes.
S K Gupta, C Gallego, J M Lowndes, C M Pleiman, C Sable, B J Eisfelder, G L Johnson
Molecular and Cellular Biology Jan 1992, 12 (1) 190-197; DOI: 10.1128/MCB.12.1.190

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Analysis of the fibroblast transformation potential of GTPase-deficient gip2 oncogenes.
S K Gupta, C Gallego, J M Lowndes, C M Pleiman, C Sable, B J Eisfelder, G L Johnson
Molecular and Cellular Biology Jan 1992, 12 (1) 190-197; DOI: 10.1128/MCB.12.1.190
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