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M Vignal

Publications and source records attributed to M Vignal.

30 records · Page 2Linked to original sources
PubMed1975

Chromosomal localization of human genes governing the interferon-induced antiviral state.

Interferon sensitivity of different normal and aneusomic human cells and of different mouse-human hybrids cells has been compared. G21 trisomic cells are more sensitive than diploid cells; whereas, on the contrary, triploid cells are normal in their human interferon sensitivity. Among other aneusomic cell lines tested, E16 trisomic cells are significantly less sensitive. These data are in favor of the hypotheses that the G21 chromosome carries genetic information for structural proteins involved in the receptor system for interferon, that there is a regulatory mechanism governing the antiviral state, and that the E16 chromosome is a possible candidate for carrying information for such a depressive regulatory mechanism. None of the chromosome abnormalities studies are involved with interferon synthesis.

Cell Line↗
PubMed1973

Mechanism of interferon uptake in parental and somatic monkey-mouse hybrid cells.

Dose-response curves of interferons in different sensitive cells are regularly sigmoidal. In somatic monkey-mouse hybrid cells, however, a significant decrease in the slope of the curve for primate interferon was observed, while the dose-response effect was unaltered for mouse interferon. High concentrations of primate interferon were 10- to 100-times less effective in hybrid clones than in parental monkey CV-1 cells; at low concentrations the antiviral effect was 10- to 20-times higher in hybrid clones than in the parental cells. The receptor(s) for primate interferon located on the cell membrane was destroyed by trypsin but not by EDTA. Similarly, acid pH inactivated these receptor sites. We, thus, postulate that the antiviral effect is, at least partially, related to the amount of interferon taken up by the cells. Uptake could be conditioned by active cooperation of two cell-specific factors: a receptor and an activator. The activator might be missing or inactivated for primate interferon in the hybrid cells. We suggest that the putative antiviral protein is not cell-species specific, and that information for its synthesis in the hybrid cells might be located on a mouse rather than a monkey chromosome.

Animals↗
PubMed1971

Use of monkey-mouse hybrid cells for the study of the cellular regualtion of interferon production and action.

Four clones of a somatic monkey-mouse hybrid cell line were studied. One of these clones produced both mouse and monkey interferon, while the three others produced only mouse interferon. All four were, however, sensitive to both mouse and monkey (or human) interferon. The karyotype analysis of these four hybrid clones and the parental cell lines enabled us to locate the possible genetic site governing the synthesis of monkey interferon on a small subtelocentric monkey chromosome. The genetic site responsible for the synthesis of the antiviral protein is located on a different (monkey or mouse) chromosome.

Animals↗
PubMedDate not supplied

Interferon inhibits transformation of mouse cells by exogenous cellular or viral genes.

Specific genes can be introduced into cultured mammalian cells by DNA transfer, sometimes to be stably integrated and expressed. Because interferon inhibits the transformation initiated by DNA viruses, we wondered if it might also affect transformation induced by recombinant plasmids and cellular genes. We show here that in mouse L cells interferon treatment prevents stable integration and expression of the transfected plasmids containing the cloned herpesvirus thymidine kinase (tk) gene, or the dihydrofolate reductase (dhfr) gene from hamster ovary cells. In contrast, interferon does not prevent transient expression of the tk gene in unintegrated form.

Animals↗