Physical, morphological, and biochemical alterations in the membrane of AKR mouse cells after interferon treatment.

Chang, Esther H.; Jay, Francis T.; Friedman, Robert M.

doi:10.1073/pnas.75.4.1859

Cited by 73 publications

(15 citation statements)

References 27 publications

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“…IFN (and especially IFN-'y) thus have been reported to modulate the expression of surface antigens. IFN treatment has also been shown to alter cell surface properties, for example, charge (38), mobility of ligand receptors (39), binding of lectins (40), architecture (41), and exposure ofgangliosides (42 …”

Section: Discussionmentioning

confidence: 99%

Interferons modulate the expression of hormone receptors on the surface of murine melanoma cells.

Kameyama¹,

Tanaka²,

Ishida³

et al. 1989

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 99%

Interferons modulate the expression of hormone receptors on the surface of murine melanoma cells.

Kameyama¹,

Tanaka²,

Ishida³

et al. 1989

J. Clin. Invest.

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“…Inhibition was maximum at 24 h after treatment with 1,000 U of interferon per ml and was dose dependent and reversible with time. Pinocytosis was inhibited when human and chicken embryo cells were treated with homologous, but not heterologous, interferons.In addition to inhibiting viral replication, interferon treatment of cells produces a variety of effects on the plasma membrane (2,3,7,9,12,15) 91:238a, 1981) reported that interferon treatment of thioglycollate-elicited mouse peritoneal macrophages caused a marked change in the distribution of microtubules and 10-nm filaments in a major fraction of the cells; this alteration was correlated with an inhibition of pinocytosis. The results reported here describe some details of the inhibition of pinocytosis in cells treated with interferon.…”

mentioning

confidence: 99%

Interferon treatment inhibits pinocytosis.

Wilcox¹,

Whitaker-Dowling²,

Youngner³

et al. 1983

Mol. Cell. Biol.

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Treating mouse L cells with crude or purified mouse interferon inhibited fluidphase pinocytosis. Inhibition was maximum at 24 h after treatment with 1,000 U of interferon per ml and was dose dependent and reversible with time. Pinocytosis was inhibited when human and chicken embryo cells were treated with homologous, but not heterologous, interferons.In addition to inhibiting viral replication, interferon treatment of cells produces a variety of effects on the plasma membrane (2,3,7,9,12,15) 91:238a, 1981) reported that interferon treatment of thioglycollate-elicited mouse peritoneal macrophages caused a marked change in the distribution of microtubules and 10-nm filaments in a major fraction of the cells; this alteration was correlated with an inhibition of pinocytosis. The results reported here describe some details of the inhibition of pinocytosis in cells treated with interferon.Mouse L cells were pretreated with 1,000 U of crude mouse interferon per ml for 24 h before the uptake of horseradish peroxidase (HRP) was measured. Untreated control cells and interferon-treated cells both internalized HRP at a rate which was linear with respect to time and to the HRP concentration in the medium (Fig. 1A and B). However, the rate of HRP uptake in the interferon-treated cells was only about 20% of the control rate (Fig. 1A). The uptake of fluorescein-dextran was also inhibited, and examination by fluorescence microscopy (8) suggested that all the cells in the population were inhibited to a similar extent (data not shown).To determine whether interferon treatment inhibits pinocytosis by altering the interaction between pinocytic vesicles and lysosomes, the subcellular distribution of internalized HRP was analyzed. Confluent monolayers of L cells were treated with crude mouse interferon (1,000 U/ml) for 24 h before HRP was added. The cells were then homogenized, and the postnuclear supernatants were centrifuged in isopycnic sucrose density gradients. The distribution of the HRP internalized by interferon-treated and untreated cells paralleled the distribution of the lysosomal marker N-acetyl-p-glucosaminidase (Fig. 2).When L cells were treated for 24 h with increasing concentrations of crude mouse interferon, slight inhibition of HRP uptake was apparent at concentrations of 1 and 10 U/ml, and 50% inhibition was observed at 100 U/ml. At the highest dose tested (1,000 U/ml), HRP uptake was inhibited by 75% (Fig. 3). Similar doseresponse data were obtained when L cells were treated with a purified mouse interferon preparation (Fig. 3).HRP uptake was analyzed as a function of time after the addition of 1,000 U of interferon per ml to L cells. There was no detectable effect on HRP uptake at 4 h; however, by 8 h after the addition of the inhibitor, a 25% reduction was seen. By 14 h the rate of uptake had decreased to 1.3 ng/mg per min, a 50% reduction. The greatest inhibition (a decrease to 28% of control levels) was observed at 24 h (Fig. 4).Cells which had been treated with 1,000 U of interferon per ml for 24 h were th...

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“…BFA also blocks transport from the ER, and from the trans-Golgi complex to the plasma membrane E4, 7,15]. The proteins within and beyond the trans-Golgi network (TGN) do not return to the ER in the presence of BFA and the transport from post trans-GC compartment to the plasma membrane is not inhibited by BFA [1][2][3]13]. In the present study we have used BFA to further characterize the effect of IFN on intracellular transport of VSV-G and to determine more precisely the site at which transport of G protein to the cell surface in IFN pretreated cell is blocked.…”

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confidence: 96%

“…The inhibitory effect of IFNs on some enveloped viruses appears to be quite unique, inducing also the release of virus particles with low infectivity and deficient in glycoproteins. Reduced amounts of glycoproteins on released viruses have been described for murine leukemia viruses (MLV), vesicular stomatitis virus (VSV), herpes simplex virus-1 (HSV-1) and bovine parainfluenza-3 virus (PI-3V) [1,2,5,6,12].Mouse LB cells pretreated with IFN (30U/ml) release 10-fold less VSV particles than untreated controls; however, under the same conditions there was observed as much as a 200-fold decrease of viral infectivity [9]. These results suggested that in the presence of IFN not only the production of VSV particles is inhibited, but also the production of noninfectious viruses is enhanced.…”

mentioning

confidence: 99%

Use of Brefeldin A to localize block in intracellular transport of vesicular stomatitis virus G protein on interferon-treated cells

Poláková

Russ

1992

Archives of Virology

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Brefeldin A (BFA) induced a rapid redistribution of vesicular stomatitis virus G protein (VSV-G) to the endoplasmatic reticulum (ER) in interferon (IFN)-pretreated cells. This result is consistent with accumulation of VSV-G in the trans-Golgi (GC) complex in cells pretreated with IFN and implies that IFN does not interfere with the ability of BFA to induce redistribution of proteins from GC to ER.

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Physical, morphological, and biochemical alterations in the membrane of AKR mouse cells after interferon treatment.

Cited by 73 publications

References 27 publications

Interferons modulate the expression of hormone receptors on the surface of murine melanoma cells.

Interferons modulate the expression of hormone receptors on the surface of murine melanoma cells.

Interferon treatment inhibits pinocytosis.

Use of Brefeldin A to localize block in intracellular transport of vesicular stomatitis virus G protein on interferon-treated cells

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