3Y1 Rat cells are defective in processing of the envelope precursor protein of AKR virus

Hoorn, Frans A. van der; Saris, Christiaan J. M.; Bloemers, H. P. J.

doi:10.1016/0042-6822(83)90361-6

Cited by 5 publications

(4 citation statements)

References 9 publications

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“…(20). Viral proteins were immunoprecipitated from cleared lysates by incubation of portions of the lysates (500,000 cpm) first with antisera directed against Rauscher MLV p30 or gp70 (obtained from the National Cancer Institute) and second with protein A-Sepharose, as described (21). Immunoprecipitates were analyzed by electrophoresis on 10% SDS-polyacrylamide gels and radioactivity was visualized by exposure of EN~HANCE-treated gels to Kodak XAR-5 film.…”

Section: Methodsmentioning

confidence: 99%

Characterization of gP85gag as an antigen recognized by Moloney leukemia virus-specific cytolytic T cell clones that function in vivo.

Hoorn¹,

Lahaye²,

Müller³

et al. 1985

The Journal of Experimental Medicine

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The gag membrane protein gP85gag, encoded by Moloney murine leukemia virus (M-MLV), was identified as a target molecule recognized by Moloney murine sarcoma virus--M-MLV (M-MSV--M-MLV)-specific cytolytic T lymphocyte (CTL) clones. Target cells infected with Ab-X-MLV, an M-MLV-derived mutant virus not encoding gP85gag, were not lysed by the CTL clones. The same CTL clones were shown previously to induce the destruction of M-MLV-induced tumor cells in the peritoneal cavity. We have now characterized CTL-resistant antigen-loss tumor cell variants that have lost the surface antigen, but which retain transcriptionally silent M-MLV genomes. A cloned antigen-loss variant that reverted in vitro to the CTL-susceptible phenotype reexpressed M-MLV genomes that had undergone an insertion event in the region of the viral DNA coding for the gag membrane protein. Intravenous injection of virus-specific CTL clones inhibited tumor formation in mice injected subcutaneously with M-MSV--M-MLV.

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Section: Methodsmentioning

confidence: 99%

Characterization of gP85gag as an antigen recognized by Moloney leukemia virus-specific cytolytic T cell clones that function in vivo.

Hoorn¹,

Lahaye²,

Müller³

et al. 1985

The Journal of Experimental Medicine

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“…For determination of p53, lysates were prepared from cells labeled with [35S]methionine, and p53 was immunoprecipitated with the monoclonal antibody RA3-2C2 (39) and protein A-Sepharose. Analysis of precipitates on sodium dodecyl sulfatepolyacrylamide gels was as described previously (45). The amount of p37mos in cell lines was determined as described previously for p53 with anti-C3 antiserum (36 (11), the v-mos coding sequences located on a 1.16-kb XbaI-HindIII fragment isolated from M-MSV DNA (43), and the viral polyadenylation site present on a 0.5-kb SmaI-PstI fragment (see Fig.…”

Section: Methodsmentioning

confidence: 99%

Differential transformation of C3H10T1/2 cells by v-mos: sequential expression of transformation parameters.

Hoorn¹,

Müller²

1985

Mol. Cell. Biol.

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Extremely small quantities of the product of the transforming gene v-mos of Moloney murine sarcoma virus are able to efficiently transform cells. Recent data indicate the existence of a threshold level for v-mos transformation of NIH3T3 cells. Using mouse mammary tumor virus long terminal repeat sequences or hybrid promoters consisting of mouse mammary tumor virus and Moloney murine sarcoma virus long terminal repeat elements to express v-mos in C3HlOTl/2 cells, we established cell lines representing different stages of morphological transformation in vitro. The threshold level for v-mos transformation was considerably lower than that for NIH3T3 cells, because no treatment with dexamethasone or primary selection other than transformation was necessary during standard transfection procedures. Using the cell lines mentioned we established an association of the level of v-mos expression with the transformation parameters examined, but not with p53 levels. Furthermore, the characterization of the different promoters showed (i) that the distal binding site confers hormone responsiveness to Moloney murine sarcoma virus promoter elements and (ii) that artifactual transcription initiation sites can be detected in mouse mammary tumor virus-Moloney murine sarcoma virus hybrid promoters which are, however, not regulated by the hormone.

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“…The cell surface expression of 68K", in the absence of detectable surface gp52, appears to be a defect in the provirus, rather than in the ability of the cells to correctly process the env precursor. The latter phenomenon has been described for the env gene of AKR virus-infected rat cells (van der Hoorn et aL, 1983) and the gag and env genes of MuLV-infected rat cells (Fitting et al, 1981). In BALB/cV tumor cells, however, the intracellular glycosylated forms of Pr70"", gp52, and gp36 are present (Slagle et aZ., 1984;unpublished observations), suggesting that the cells contain the enzymes necessary to correctly process a normal MMTV env gene.…”

Section: Biological Funandm Of Surface 68k""'mentioning

confidence: 78%

Identification and characterization of a mouse mammary tumor virus protein uniquely expressed on the surface of BALB/cV mammary tumor cells

Slagle

Butel

1985

Virology

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A unique subline of BALB/c mice, designated BALB/cV, exhibits an intermediate mammary tumor incidence (47%) and harbors a distinct milk-transmitted mouse mammary tumor virus (MMTV). The BALB/cV subline was used to study the molecular basis of potential virus-host interactions involving cell surface-expressed MMTV proteins. Cell surface iodination identified virus-specific proteins expressed on BALB/cV primary mammary tumor cells grown in culture. In contrast to (C3H)MMTV-producing cell lines which expressed MMTV gp52, BALB/cV tumor cells lacked gp52 and expressed instead a 68K, env-related protein. The 68Kenv protein was also detected on the surface of metabolically labeled BALB/cV tumor cells by an external immunoprecipitation technique. The expression of 68Kenv was restricted to mammary tissues of BALB/cV mice that also expressed other MMTV proteins. Biochemical analysis established that 68Kenv was not modified by N-linked glycosylation. 125I-labeled 68Kenv was rapidly released into the media of tumor cell cultures and was recovered both in the form of a soluble protein and in a 100,000 g pellet. The biologic function of this cell surface-expressed viral protein remains unknown.

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3Y1 Rat cells are defective in processing of the envelope precursor protein of AKR virus

Cited by 5 publications

References 9 publications

Characterization of gP85gag as an antigen recognized by Moloney leukemia virus-specific cytolytic T cell clones that function in vivo.

Characterization of gP85gag as an antigen recognized by Moloney leukemia virus-specific cytolytic T cell clones that function in vivo.

Differential transformation of C3H10T1/2 cells by v-mos: sequential expression of transformation parameters.

Identification and characterization of a mouse mammary tumor virus protein uniquely expressed on the surface of BALB/cV mammary tumor cells

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