Rearrangement of a DNA sequence homologous to a cell-virus junction fragment in several Moloney murine leukemia virus-induced rat thymomas.

Lemay, Guy; Jolicoeur, Paul

doi:10.1073/pnas.81.1.38

Cited by 81 publications

(71 citation statements)

References 23 publications

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“…The size of the 56,000-dalton LSTRA protein is similar to that of nonviral tumor antigen p53, which has been detected in a large number of transformed cells (35 (11,28,49,50). Two of these loci, pMo-1C and Pim-1, have been studied in some detail (11,28) LITERATURE CITED…”

Section: Discussionmentioning

confidence: 99%

Characterization of the protein apparently responsible for the elevated tyrosine protein kinase activity in LSTRA cells.

Voronova¹,

Buss²,

Patschinsky³

et al. 1984

Mol. Cell. Biol.

120

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The LSTRA murine thymoma cell line contains an elevated level of tyrosine protein kinase activity. When a microsomal preparation from these cells is incubated in vitro with ATP, the principal tyrosine protein kinase substrate is a 56,000-dalton protein, p56. We have found that an activity phosphorylating p56 on tyrosine can also be detected at low levels in microsomes from most, but not all, T lymphoma cell lines and from normal thymic tissue. Only 1 of 30 other lymphoma cell lines was found to contain an elevated level of such a tyrosine protein kinase. An activity that phosphorylated p56 in vitro was not detectable in the cells of other hematopoietic lineages. Anti-peptide antibodies reactive with the site of in vitro tyrosine phosphorylation of p56 allowed us to determine that the apparent abundance of the p56 polypeptide parallels closely the level of the tyrosine protein kinase activity in the cell lines examined. This suggests that p56 is the protein kinase responsible for the elevated tyrosine protein kinase activity in LSTRA cells and that the phosphorylation of p56 observed in vitro results from autophosphorylation. Two-dimensional tryptic peptide mapping revealed that p56 is distinct from the proteins encoded by the cellular genes which are the progenitors of retroviral tyrosine protein kinases, src, yes, fgr, abl, fes, and ros. Additionally, none of these proto-oncogenes was found to be transcribed at elevated levels in LSTRA or Thy19 cells. Like the catalytic subunit of the cyclic AMP-dependent protein kinase, the cellular and viral forms of p60src, and the protein phosphatase calcineurin B, p56 contains covalently bound fatty acid.

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Section: Discussionmentioning

confidence: 99%

Characterization of the protein apparently responsible for the elevated tyrosine protein kinase activity in LSTRA cells.

Voronova¹,

Buss²,

Patschinsky³

et al. 1984

Mol. Cell. Biol.

120

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“…DNA from tumor 9 was digested with EcoRI and centrifuged on a sucrose density gradient (15 to 30%) as previously described (29). Fractions containing fragments from 10 to 20 and 2 to 10 kilobase pairs (kbp) were pooled separately and ethanol precipitated.…”

Section: Methodsmentioning

confidence: 99%

“…High-molecular-weight cellular DNA was prepared from primary thymomas or from livers by phenol extraction and was ethanol precipitated and digested with various restriction endonucleases (New England BioLabs, Inc., Beverly, Mass. ; Boehringer Mannheim Biochemicals, Montreal; and P-L Pharmacia, Montreal) under the conditions recommended by the manufacturers as previously described (29). Bacteriophage and plasmid DNAs were prepared essentially as described elsewhere (32).…”

Section: Methodsmentioning

confidence: 99%

“…Recently, the interleukin-2 (6) and interleukin-3 (59) genes were also found to be activated by nearby integration of LTR sequences in gibbon T-lymphoid MLA 144 and in mouse WEH1-3B myelomonocytic leukemia cell lines, respectively. Six other apparently distinct regions, designated Mlvi-1, Mlvi-2, Mlvi-3 (51-54), Misllpvt-J (18,29,57), Pim-1 (8), and Fis-J (47), have been reported to be the sites of common provirus integrations in mouse or rat T-cell or myelogenous leukemic DNA and might represent putative new oncogenes. Among these, provirus insertions have been shown to activate the transcription of Pim-1 (8,44).…”

mentioning

confidence: 99%

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Identification of a new common provirus integration site in gross passage A murine leukemia virus-induced mouse thymoma DNA.

Villemur¹,

Monczak²,

Rassart³

et al. 1987

Mol. Cell. Biol.

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The Gross passage A murine leukemia virus (MuLV) induced T-cell leukemia of clonal (or oligoclonal) origin in inoculated mice. To study the role of the integrated proviruses in these tumor cells, we cloned several newly integrated proviruses (with their flanking cellular sequences) from a single tumor in procaryotic vectors. With each of the five clones obtained, a probe was prepared from the cellular sequences flanking the provirus. With one such probe (SS8), we screened several Gross passage A MuLV-induced SIM.S mouse tumor DNAs and found that, in 11 of 40 tumors, a provirus was integrated into a common region designated Gin-i. A 26-kilobase-pair sequence of Gin-i was cloned from two A libraries, and a restriction map was derived. All proviruses were integrated as a cluster in the same orientation within a 5-kilobase-pair region of Gin-i, and most of them had a recombinant structure of the mink cell focus-forming virus type. The frequency of Gin-i occupancy by provirus was much lower in thymoma induced by other strains of MuLV in other mouse strains.

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“…It is worth mentioning, in this context, the long latency for in vivo induction of neoplasms by such nontransforming retroviruses in birds (Cooper & Neiman, 1980;Hayward et al, 1981;Fung et al, 1982Fung et al, , 1983Payne et al, 1982;Schubach & Groudine, 1984;Steffen, 1984), mice (Lane et al, 1982;Yoshimura & Levine, 1983;Dickson et al, 1984;Lenz et al, 1984;Nusse et al, 1984;, rats (Tsichlis et al, 1983;Lemay & Jolicoeur, 1984) and cats (Neil et al, 1984). This induction results from integration of the viral DNA at a specific site in the cellular genome, which activates aberrant expression of a specific cellular gene by transcriptional control elements located in their long terminal repeats.…”

mentioning

confidence: 99%

Amplification of the Moloney murine leukaemia virus genome and its possible role in facilitation of chemical carcinogenesis in normal rat kidney cells

Priel

Hassan

Huleihel

et al. 1991

Journal of General Virology

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Rearrangement of a DNA sequence homologous to a cell-virus junction fragment in several Moloney murine leukemia virus-induced rat thymomas.

Cited by 81 publications

References 23 publications

Characterization of the protein apparently responsible for the elevated tyrosine protein kinase activity in LSTRA cells.

Characterization of the protein apparently responsible for the elevated tyrosine protein kinase activity in LSTRA cells.

Identification of a new common provirus integration site in gross passage A murine leukemia virus-induced mouse thymoma DNA.

Amplification of the Moloney murine leukaemia virus genome and its possible role in facilitation of chemical carcinogenesis in normal rat kidney cells

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