Cellular regulation of mammalian sarcoma virus expression: a gene regulation model for oncogenesis

Porzig, Klaus J.; Robbins, K C; Aaronson, Stuart A.

doi:10.1016/0092-8674(79)90102-8

Cited by 33 publications

(15 citation statements)

References 41 publications

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“…1). Results obtained previously with flat revertants of fibroblasts infected with sarcoma viruses (3,9,29,30,39) are consistent with these conclusions. Although methylation of specific DNA sites could conceivably account for shutdown (24), we were unsuccessful in reverting nonexpressers to expressers with the methylation inhibitor 5-azacytidine.…”

Section: Methodssupporting

confidence: 81%

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Frequent hereditable shutdown of murine retrovirus gene expression in murine cell lines.

Bestwick¹,

Machida²,

Polonoff³

et al. 1984

Mol. Cell. Biol.

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Friend spleen focus-forming virus shuts down its gene expression frequently (ca. 10-3 per generation) in a cis-dominant hereditable fashion in various murine cells but much less frequently in rat cells (less than 10-6 per generation). Thus. nonexpresser variants were isolated at high frequency from murine cell lines by immunoselection directed against virus-encoded cell surface glycoproteins and also simply by subcloning cells from lines which had been cultured for many generations. Studies of independently infected cell clones indicate that shutdown is a property of the cell line rather than of the specific proviral site. Nucleic acid blot analyses suggest that shutdown correlates with decreased transcription. Moreover, preliminary evidence indicates that other murine retroviruses also shut down frequently in murine but not

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Section: Methodssupporting

confidence: 81%

“…(3,9,29,30,39). On the contrary, in other cell lines flat revertants form at a lower frequency due to mutations in the viral src gene or possibly in cellular genes required for expression of the transformed phenotype (3,9,39).…”

Section: Methodsmentioning

confidence: 97%

Frequent hereditable shutdown of murine retrovirus gene expression in murine cell lines.

Bestwick¹,

Machida²,

Polonoff³

et al. 1984

Mol. Cell. Biol.

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Section: Methodsmentioning

confidence: 99%

“…Such revertants exhibit a cellular block to viral gene expression, apparently at the level of transcription (13). Upon continuous passage in tissue culture, one of these revertant clones, designated 82-3, mutates to the transformed state with the concomitant expression of the ST P85 FeSV gene product (13). This biological system offers a series of transformed-revertant-retransformed clones with which to investigate the specificity of the genetic association of an in vttro protein kinase activity with expression of ST P85.…”

Section: Methodsmentioning

confidence: 99%

“…Mink lung-(MvlLu; ATCC 64) cells nonproductively transformed by ST-FeSV, including clones 25a-3 and 61-1 as well as the ST-FeSV NRK transformant clone 52-7, have been described (6,13). The isolation of revertant (clone 82-3) and retransformed (clone 904) mink cells containing the ST-FeSV genome has been reported (13). Feline embryo fibroblasts (FEF-1) were obtained from J. Rhim (National Cancer Institute).…”

Section: Methodsmentioning

confidence: 99%

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Origin and functional properties of the major gene product of the Snyder-Theilen strain of feline sarcoma virus.

Barbacid¹,

Beemon²,

Devare³

1980

Proc. Natl. Acad. Sci. U.S.A.

121

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The only known product of the Snyder-Theilen strain of feline sarcoma virus (ST-FeSV) is a 85,000-dalton protein, designated ST P85, that contains feline leukemia virus gag gene encoded proteins (p15, p12, and a fragment of p30) and a sarcoma virus-specific polypeptide. Antibodies directed against the latter immunoprecipitated a 92,000-dalton phosphoprotein (NCP 92) expressed at low levels in normal feline embryo fibroblasts as well as in feline cells of epithelial or lymphoid origin. Normal cellular proteins crossreactive with ST P85 were also detected in cell lines from various other mammalian species. These results suggest that the ST-FeSV sequences encoding for the sarcoma virus-specific domain of ST P85 originated from an evolutionarily conserved cellular gene expressed in cells of independent differentiation lineage. Immunoprecipitates containing ST-FeSV P85 exhibited a protein kinase activity that specifically phosphorylated tyrosine residues. The physiological significance of this finding is illustrated by the finding that phosphotyrosine is an intrinsic component of ST

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Oncoviral Proteins as Cellular Antigens

Fleissner

Snyder

1982

Current Topics in Microbiology and Immunology

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Cellular regulation of mammalian sarcoma virus expression: a gene regulation model for oncogenesis

Cited by 33 publications

References 41 publications

Frequent hereditable shutdown of murine retrovirus gene expression in murine cell lines.

Frequent hereditable shutdown of murine retrovirus gene expression in murine cell lines.

Origin and functional properties of the major gene product of the Snyder-Theilen strain of feline sarcoma virus.

Oncoviral Proteins as Cellular Antigens

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