Literature DB >> 6380758

Microinjection of the oncogene form of the human H-ras (T-24) protein results in rapid proliferation of quiescent cells.

J R Feramisco, M Gross, T Kamata, M Rosenberg, R W Sweet.   

Abstract

Using an E. coli expression-vector system we have efficiently produced, purified, and characterized the full-length, nonfused, protooncogenic and oncogenic (T-24) forms of the human H-ras gene product. These purified ras proteins have been introduced by microinjection into a variety of somatic cells in an effort to examine their function. Within several hours after injection of the oncogenic form of the human H-ras protein into quiescent cells, we observe dramatic morphological changes followed by transient proliferation of the cells. In contrast, microinjection of the normal, protooncogenic form of the ras protein at the same level appears to have only little effect on the cells. Additional experiments indicate that the effect of the ras protein requires entry into the cells, is temporary, is inhibited by cycloheximide or actinomycin D, and is seen only in established cell lines. This experimental approach demonstrates that the bacterially derived and purified human H-ras proteins retain their ability to function when put back into mammalian cells and furthermore, provides a novel assay for transformation induced in established cells by the human H-ras oncogene protein.

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Year:  1984        PMID: 6380758     DOI: 10.1016/0092-8674(84)90531-2

Source DB:  PubMed          Journal:  Cell        ISSN: 0092-8674            Impact factor:   41.582


  119 in total

1.  Effects of inhibitors and ion substitutions on oscillations of cell membrane potential in cells expressing the RAS oncogene.

Authors:  F Lang; S Waldegger; E Woell; M Ritter; K Maly; H Grunicke
Journal:  Pflugers Arch       Date:  1992-08       Impact factor: 3.657

2.  Early regulation of membrane excitability by ras oncogene proteins.

Authors:  C Collin; A G Papageorge; M Sakakibara; P L Huddie; D R Lowy; D L Alkon
Journal:  Biophys J       Date:  1990-09       Impact factor: 4.033

3.  Antisense-fos RNA causes partial reversion of the transformed phenotypes induced by the c-Ha-ras oncogene.

Authors:  B J Ledwith; S Manam; A R Kraynak; W W Nichols; M O Bradley
Journal:  Mol Cell Biol       Date:  1990-04       Impact factor: 4.272

4.  The mammalian mitogen activated protein kinase network.

Authors:  P Lenormand
Journal:  Clin Mol Pathol       Date:  1995-12

Review 5.  Pathobiology of ALK+ anaplastic large-cell lymphoma.

Authors:  Hesham M Amin; Raymond Lai
Journal:  Blood       Date:  2007-05-22       Impact factor: 22.113

6.  p67SRF is a constitutive nuclear protein implicated in the modulation of genes required throughout the G1 period.

Authors:  C Gauthier-Rouvière; J C Cavadore; J M Blanchard; N J Lamb; A Fernandez
Journal:  Cell Regul       Date:  1991-07

7.  Insulin receptor substrate 1 is required for insulin-mediated mitogenic signal transduction.

Authors:  D W Rose; A R Saltiel; M Majumdar; S J Decker; J M Olefsky
Journal:  Proc Natl Acad Sci U S A       Date:  1994-01-18       Impact factor: 11.205

Review 8.  Signal transduction by Ras-like GTPases: a potential target for anticancer drugs.

Authors:  M Spaargaren; J R Bischoff; F McCormick
Journal:  Gene Expr       Date:  1995

9.  Alpha B crystallin accumulation is a specific response to Ha-ras and v-mos oncogene expression in mouse NIH 3T3 fibroblasts.

Authors:  R Klemenz; E Fröhli; A Aoyama; S Hoffmann; R J Simpson; R L Moritz; R Schäfer
Journal:  Mol Cell Biol       Date:  1991-02       Impact factor: 4.272

10.  The human Ha-ras oncogene induces genomic instability in murine fibroblasts within one cell cycle.

Authors:  N C Denko; A J Giaccia; J R Stringer; P J Stambrook
Journal:  Proc Natl Acad Sci U S A       Date:  1994-05-24       Impact factor: 11.205

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