p21(RAS) | ScienceGate

The Kirsten (Ki) and Harvey (Ha) strains of murine sarcoma virus encode a 21,000-dalton protein (p21 ras) which is the product of the transforming gene of these viruses. Normal cells express low levels of p21 ras encoded by cellular genes (Ki-ras and Ha-ras) homologous to the Ki and Ha murine sarcoma virus transformation genes. A bone marrow-derived mouse cell line, 416B, has been shown to express unusually high levels of p21 ras. In this manuscript, we investigated the molecular biology of p21 ras gene expression in 416B and other normal mouse cells. We identified four distinct polyadenylated and polysome-associated RNAs, two related to Ki-ras and two to Ha-ras. The levels in 416B cells of the two Ki-ras RNAs, sized 5.2 and 2.0 kilobases, were both elevated approximately 25-fold over levels found in normal mouse cells; there was no corresponding change in 416B cells in the levels of the two Ha-ras RNAs. We partially purified the two Ki-ras mRNAs and separated them by velocity sedimentation in sucrose density gradients. Both the 5.2- and 2.0-kilobase mRNAs could be translated in vitro into p21 ras. These results show that a cellular onc protein can be translated from two distinct cellular mRNA species.

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The mRNA 5' cap-binding protein, eIF-4E, cooperates with v-myc or E1A in the transformation of primary rodent fibroblasts

Molecular and Cellular Biology ◽

10.1128/mcb.12.3.1234-1238.1992 ◽

1992 ◽

Vol 12 (3) ◽

pp. 1234-1238

Author(s):

A Lazaris-Karatzas ◽

N Sonenberg

Keyword(s):

Signal Transduction ◽

Binding Protein ◽

Signal Transduction Pathway ◽

Transduction Pathway ◽

Rat Embryo ◽

Present Evidence ◽

P21 Ras ◽

Embryo Fibroblasts ◽

Common Signal

We present evidence that eIF-4E, the mRNA 5' cap-binding protein, cooperates with two immortalizing oncogenes, v-myc and E1A, to cause transformation of rat embryo fibroblasts. eIF-4E alone can transform rat embryo fibroblasts when selection is applied. The pattern of transformation by eIF-4E is similar to that of p21 Ras, raising the possibility that eIF-4E shares a common signal transduction pathway with p21 Ras.

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Role of p21 ras in Hormone Signalling and Cell Growth/Transformation

Advances in Experimental Medicine and Biology - Pancreatic Islet Cell Regeneration and Growth ◽

10.1007/978-1-4615-3448-8_15 ◽

1992 ◽

pp. 143-146

Author(s):

Peter F. Blackmore

Keyword(s):

Cell Growth ◽

Growth Transformation ◽

P21 Ras ◽

Hormone Signalling

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Recombinant Adenovirus KGHV500 and CIK Cells Codeliver Anti-p21-Ras scFv for the Treatment of Gastric Cancer with Wild-Type Ras Overexpression

Molecular Therapy — Oncolytics ◽

10.1016/j.omto.2018.10.003 ◽

2018 ◽

Vol 11 ◽

pp. 90-101 ◽

Cited By ~ 2

Author(s):

Mingjuan Wang ◽

Yanling Hong ◽

Qiang Feng ◽

Xinyan Pan ◽

Shuling Song ◽

...

Keyword(s):

Gastric Cancer ◽

Recombinant Adenovirus ◽

Wild Type ◽

Cik Cells ◽

P21 Ras

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Fetal hyperinsulinemia increases farnesylation of p21 Ras in fetal tissues

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.2001.281.2.e217 ◽

2001 ◽

Vol 281 (2) ◽

pp. E217-E223 ◽

Cited By ~ 13

Author(s):

Elizabeth Stephens ◽

Patti J. Thureen ◽

Marc L. Goalstone ◽

Marianne S. Anderson ◽

J. Wayne Leitner ◽

...

Keyword(s):

Growth Factors ◽

Molecular Mechanisms ◽

Fetal Liver ◽

White Blood Cells ◽

Causative Factor ◽

Ras Proteins ◽

Direct Infusion ◽

Fetal Tissues ◽

P21 Ras

Even though the role of fetal hyperinsulinemia in the pathogenesis of fetal macrosomia in patients with overt diabetes and gestational diabetes mellitus seems plausible, the molecular mechanisms of action of hyperinsulinemia remain largely enigmatic. Recent indications that hyperinsulinemia “primes” various tissues to the mitogenic influence of growth factors by increasing the pool of prenylated Ras proteins prompted us to investigate the effect of fetal hyperinsulinemia on the activitiy of farnesyltransferase (FTase) and the amounts of farnesylated p21 Ras in fetal tissues in the ovine experimental model. Induction of fetal hyperinsulinemia by direct infusion of insulin into the fetus and by either fetal or maternal infusions of glucose resulted in significant increases in the activity of FTase and the amounts of farnesylated p21 Ras in fetal liver, skeletal muscle, fat, and white blood cells. An additional infusion of somatostatin into hyperglycemic fetuses blocked fetal hyperinsulinemia and completely prevented these increases, specifying insulin as the causative factor. We conclude that the ability of fetal hyperinsulinemia to increase the size of the pool of farnesylated p21 Ras may prime fetal tissues to the action of other growth factors and thereby constitute one mechanism by which fetal hyperinsulinemia could induce macrosomia in diabetic pregnancies.

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