Search PubMed⌕ Search

Biomedical subjects

C J Larsen

Publications and source records attributed to C J Larsen.

At least 127 records · Page 7Linked to original sources
PubMed1984

The expression of the env gene-related gp66 in mouse cells infected with the helper independent Friend leukemia virus is restricted to the myelomonocytic and mastocytic lineages.

The presence of a gp66 closely related to the Friend ecotropic murine leukemia virus gp70 (F-MuLV) has recently been reported (D. Mathieu-Mahul, J. M. Heard, S. Fichelson, S. Gisselbrecht, B. Sola, and C. J. Larsen (1982) virology 119, 59-67). In the present work, characterization of this gp66 was continued. First, immunoprecipitation tests, using cytoplasmic membrane subfractions from one of the myelomonocytic cell lines in which gp66 was first detected, indicated that most of it was associated with rough endoplasmic reticulum. Second, to define the limits of gp66 expression, a variety of hemopoietic cell lines were analyzed for gp66 content. These lines were obtained (a) from various tumors (including erythroleukemias, chloroleukemias, and lymphatic leukemias) induced in susceptible mice by F-MuLV and (b) from long-term bone marrow cultures (LTBMC) infected with F-MuLV. In the latter case, lines of adherent fibroblastoid cells and nonadherent cells with myelomonocytic and mastocytic characteristics were obtained. Although several F-MuLV isolates were used, gp66 was only expressed in myelomonocytic and mastocytic cells. This did not result from in vitro culture conditions as gp66 was also found in fresh cells. These data suggested that a particular processing of the env gene product may exist in both myelomonocytic and mastocytic cell lines. In agreement with this hypothesis, a metabolically unstable gp62 related to MCF gp70 was found in one myelomonocytic cell line expressing MCF virus.

Animals↗
PubMed1984

[A cytoplasmic antigen related to the cell cycle identified by a human autoimmune serum].

A human serum from a patient with an autoimmune disorder, previously characterized for its ability to specifically recognize a chromatin-associated PSL or p55 antigen, was found also to detect a 30-32 K polypeptide in the cytoplasm of human HeLa cells. This molecule is strictly cytoplasmic, does not cross react with nuclear PSL and is synthesized only during the S phase of the cell cycle.

Antigens↗
PubMed1984

[BD-40, intercalating 9-azaellipticine derivative, induces breaks in cellular DNA associated with protein bridges].

The nature of the lesions induced in cell DNA by BD-40, a chemical analog of Ellipticine was analyzed by submitting DNA from drug-treated cells to alkaline sucrose gradient centrifugation. DNA size reduction was only observed when cell lysates were digested by proteolytic enzymes. This result indicates that BD-40 induces DNA breaks which are masked by bridges involving DNA-protein interaction. This is a new type of DNA lesion induced in DNA by an intercalating agent.

Animals↗
PubMed1983

Genesis of a new spleen focus-forming virus: possible role of MCF viruses.

A Friend mink cell focus-inducing (Fr-MCF) virus isolated from a Friend tumor cell line was able to induce acute erythroleukemia associated with polycythemia when injected as a Friend murine ecotropic leukemia virus (F-MuLV) pseudotype into adult Swiss and ICFW mice. One virus isolate recovered from leukemic cells and designated as FV-F3 presented the following properties: (i) persistence of the same leukemogenic power when propagated in vivo and in vitro; (ii) in vivo spleen focus-forming (SFFV) capacity; (iii) presence of erythropoietin (EPO)-independent CFU-E in leukemic animals; (iv) expression of a 32 RNA specifically recognized by a SFFV probe, in FV-F3 infected cells; and (v) expression in FV-F3-infected cell of polypeptides in the range of gp52 SFFV. Peptide analysis of these products revealed close similarities with the parental MCF virus. These data suggest that a SFFV genome arose by genetic recombinational events involving MCF virus.

Animals↗
PubMed1983

Characterization by human autoantibody of a nuclear antigen related to the cell cycle.

Using a serum from a patient with an autoimmune disease, we have recently described a novel 55 000-dalton antigen (p55) in the nucleus of several animal cells including human ones. This antigen, designated PSL, was not related to the previously defined antigens recognized by sera from patients with systemic rheumatic diseases (Sm, n-RNP, SS-B, Scl-70). We have now found that p55 is associated with chromatin structures as it is released from the nucleus of mink cell fibroblasts by saline + DNase treatments. Analysis by sucrose gradient centrifugation of the nuclear material released in these conditions indicated that p55 co-migrated with core histones. Meanwhile, p55 was absent from the residual nuclear matrices (achromatinic nuclei). Localization of p55 in synchronized cells was performed by indirect immunofluorescence and immunoprecipitation. P55 appeared to accumulate in the nucleus during the S phase. Finally, it was not recognized by an anti-SV40 tumor serum that specifically precipitated the protein p53, which has been recently related to cell proliferation. Thus, PSL an p53, although apparently not antigenically related, appear to be implicated in the same step of the cell cycle.

Animals↗
PubMed1982

Possible relationship between pyrido-pyrrolo-isoquinoline derivative (BD-40) cell uptake and cell viability.

BD-40 is a pyrido-pyrrolo-isoquinoline derivative which possesses an heterocyclic nucleus very closely related to ellipticine and a diethylaminopropyl amino lateral chain (Rivalle et al., 1979). Cellular effects of the drug have been studied. Viability and morphology of the cells were irreversibly impaired by 24 hours drug treatments at concentrations exceeding 0.10 micro M. Spectrofluorimetric determinations of the drug repartition between cytoplasm and nucleus showed that 10 per cent of BD-40 was found in the nucleus for external drug concentrations lower than 0.10 micro M. On the other hand, for cytotoxic doses exceeding 0.10 micro M, 40 to 50 per cent of the total intracellular BD-40 were found in the nuclear fraction. Although possible exchange phenomena during the course of the cell fractionation cannot be excluded, these results suggest that a direct relationship exists between BD-40 nuclear content and cell lethality. Comparisons of intracellular drug contents in the absence and the presence of a metabolic inhibitor, sodium azide, indicated that drug content of azide-treated cells was approximately twice that of untreated cells. Besides, sodium azide blocked the release of the drug when previously loaded cells were placed in BD-40-free medium. These results are in agreement with the existence of an active outward transport (efflux), which is sodium azide-sensitive.

Animals↗
PubMed1981

[Effect of toyocamycin on the biosynthesis of viral glycoproteins in a cell line chronically infected with a murine retrovirus].

Toyocamycin (TMC), an adenosine analog has been previously reported to inhibit both number and infectivity of retrovirus particles released by chronically infected cells (Bonar et al., 1970; Riman, 1971; Mauchauffé et al., 1979). We have previously shown that loss of infectivity could result from the incorporation of TMC in place of adenosine in the genomic 35S RNA (Larsen et al., 1979). This phenomenon is likely to impair the structure of the viral genome in such a way that reverse transcriptase cannot properly copy the template. Another consequence of the Toyocamycin action on the retrovirus particles released by analog-treated cells was their reduced content in envelope glycoprotein or gp70 (Mathieu - Mahul et al., 1979). In order to find the origin of this defect, which could also explain the loss of infectivity, viral polypeptides present in the cytoplasm of Toyocamycin-treated cells were analyzed by immunoprecipitation with specific antisera. The results indicated a diminution of the biosynthesis of the envelope glycoprotein and other GAG gene-related polypeptides. However, the gpr85env precursor was normally synthesized and processed into its final products (gp70 + p15E), which accumulated in the cells. These result make it likely that Toyocamycin has no specific effect on the virus replicative process in chronically infected cells but acts by deteriorating cellular functions, which are necessary to virus assembly. Indeed, it was found that a membrane fraction corresponding to smooth endoplasmic reticulum and Golgi apparatus was severely reduced if not totally suppressed in TMC-treated cells.

Animals↗
PubMed1980

[Characterization of viral RNA in Friend tumor cells having lost their capacity to produce viral particles].

Cytoplasmic RNA from Friend tumoral cells which had lost their ability to produce viral particles was analyzed for its viralRNA content. A major 32S RNA corresponding to the genome of the defective SFFV virus was detected by hybridization with a synthetic DNA complementary to the Rauscher virus genome. Very low amounts of a 34S species were also found. No 38S RNA with the size of the helper virus genome was present in the cells. It was concluded that the cessation of virus production resulted from a disappearance of the helper provirus from these cells or from a block in the transcriptional process of this provirus.

Animals↗
PubMed1979

[Change in the envelope of a murine retrovirus produced in the presence of toyocamycin].

Toyocamycin (TMC), an adenosine analog, impairs qualitatively and quantitatively virus production in a cellular system chronically infected by Friend Virus. Viral particles released by cell cultures treated with 0.2 microgram/ml of the drug have lost most of their glycoprotein (gp 70) content. This phenomenon is likely to modify the viral envelope and could explain the loss of infectivity of the virus.

Animals↗
PubMed1979

Effect of toyocamycin on the synthesis of the 70S RNA of a murine retrovirus.

The murine Eveline cell line chronically infected by Friend virus was treated with Toyocamycin (TMC), an adenosin analog and the virions released in the presence of the drug were examined for their RNA. It was found that 70S RNA which was synthesized incorporated Toyocamycin. However, its subunit structure and its poly (A) content were apparently preserved. This incorporation may explain loss of endogenous reverse transcriptase activity.

Animals↗