Interferon mouse

Experiment was carried out as described in Figure 1, using 20 lU/mL of both interferons. , Mouse fibroblast interferon , T-cell interferon , T-cell interferon after passage through a Sepharose—ganglioside column (see Figure 8). T EMC titer in the absence of interferon (19). 

Several of these IFNs of mouse and human lymphocytes and fibroblasts are available commercially and have been best prepared in quantity by recombinant DNA procedures because they are produced in very small amounts by the cells. The commercial materials do not generally require further purification for their intended purposes. [Pestkas, Interferons and Interferon standards and general abbreviations. Methods Enzymol, Wiley Sons, 119 1986, ISBN 012182019X Lengyel, Biochemistry of interferons and their actions, Ann Bev Biochem 51 251-282 7982 De Maeyer and De Maeyer-Guignard, Interferons in The Cytokine Handbook, 3rd Edn, Thomson et al. Eds, pp. 491-516 7998 Academic Press, San Diego, ISBN 0126896623.]... 

Dubois, M.F., Mezger, V., Morange, M., Ferrieux, C., Lebon, P., Bensaude, O. (1988). Regulation of the heat-shock response by interferon in mouse L cells. J. Cell Physiol. 137, 102—109. 

In addition, stndies evaluating interferon alpha/beta and interlenkin-16 expression have shown snbstantial antiviral effects against HlV-1 in vitro and in a humanized mouse model (Cremer et al. 2000 Lanret et al. 1994 Sanhadji et al. 1997 Zhou etal. 1997). 

Mouse peritoneal macrophages that have been activated to produce nitric oxide by 7-interferon and lipopolysac-charide were shown to oxidize LDL less readily than unactivated macrophages. Inhibition of nitric oxide synthesis in the same model was shown to enhance LDL oxidation (Jessup etal., 1992 Yates a al., 1992). It has recently been demonstrated that nitric oxide is able to inhibit lipid peroxidation directly within LDL (Ho etal., 1993c). Nitric oxide probably reacts with the propagating peroxyl radicals thus terminating the chain of lipid peroxidation. The rate constant for the reaction between nitric oxide and peroxyl radicals has recently been determined to be 1-3 X10 M" s (Padmaja and Huie, 1993). This... 

Gentz, R., Hayes, A., Grau, N. et al. (1992) Analysis of soluble human and mouse interferon-gamma receptors expressed in eukaryotic cells. European Journal of Biochemistry, 210 (2), 545-554. 

This approach appears somewhat irrational and without much scientific merit, since many of these new molecules are minimally toxic or nontoxic by this sort of acute evaluation. As in the case of interferons or monoclonal antibodies, the toxic effects observed in humans might not be predicted from safety assessments in rodents. An appropriate test species should be selected. Is the rat or mouse the appropriate species to evaluate a species-specific rDNA protein such as human growth hormone or interferons, or would nonhuman primates be more suitable Does the nonhuman primate really offer any advantages There is some consensus that the nonhuman primate may be a more appropriate species for testing some rDNA human proteins. 

S6, and SlOb) and two 20S a-subunits (C8 and C9) are known to be phosphoryl-ated. Phosphorylation appears to be particularly important for 26S proteasome assembly and stability. The kinase inhibitor staurosporine reduces 26S proteasome levels in mouse lymphoma cells [135] and interferon y results in reduced phosphorylation of 20S proteasome a-subunits and decreased 26S proteasome levels [141]. 

Zie QW, Whisnant R, Nathan C. Promoter of the mouse gene encoding calcium-independent nitric oxide synthase confers inducibility by interferon gamma and bacterial lipopolysaccharide. J Exp Med 1993 177 1779-1784. 

Lucas, M., Mashimo, T, Frenkiel, M. P., et al. (2003) Infection of mouse neurones by West Nile virus is modulated by the interferon-inducible 2 -5" oligoadenylate synthetase lb protein. Immunol. Cell Biol. 81, 230-236. 

Asherson GL, Dieli F. 1992. Immune deviation in the mouse transfer of selective depression of contact sensitivity and interleukin-2 response with retension of interferon-gamma production requires CD8+ T cells. Immunology 76 427-432. 

The following cell cultures and virus have shown to be suitable MDBK cells (ATCC No. CCL22), or Mouse L cells (NCTC clone 929 ATCC No. CCL I) as the cell culture and vesicular stomatitis virus VSV Indiana strain (ATCC No. VR-158) as the infective agent or human diploid fibroblast FS-71 cells responsive to interferon as the cell culture, and encephalomyocarditis virus (ATCC No. VR-129B) as the infective agent. 

Misaki IL, Nagaya H., Fujiyama K., Yanagihara I., Honda T. and Seki T. (2003) N-Hnked glycan structures of mouse interferon-p produced by Bombyx mori larvae. Biochem. Biophys. Res. Commun. 311,979-986. 

Slepnev et al. [313] presented a simple method for protein radio-labeling with Bolten-Hunter reagent (iV-hydroxy succinimide ester of 3-(p-hydroxy di-iodophenyl)) propionic acid) in AOT/octane-RMs using mouse IgG, human transferrin, protein A, and a2-interferon as labeling examples. The yield of radio-labeling in RMs was found to be higher than that achieved in homogeneous aqueous solution. 

In 1985, Stuehr and Marietta demonstrated that the macrophage is the major source of N02 and NO, in response to LPS, at least in the mouse. Subsequently, this group showed that addition of LPS and the immune cytokine interferon-y (cytokines are discussed in more detail below) to macrophages results in N-nitrosation of morpholine the N-nitrosamine was not formed by addition of NO2 and morpholine to the macrophages, and the highest levels of N-nitrosamine occurred many hours prior to the peak NO2" formation (Miwa et al., 1987). Thus, treated macrophages are stimulated to produce a reactive precursor to N02 and NO,, which is capable of N-nitrosamine formation. 

Lorsbach, R. B., Murphy, W. J., Lowenstein, C. J., Snyder, S. H., and Russell, S. W. (1993). Expression of the nitric oxide synthase gene in mouse macrophages activated for tumor cell killing. Molecular basis for the synergy between interferon-gamma and lipopolysaccharide. J. Biol. Chem. 268, 1908-1913. 

In this communication we extend our earlier observations, which primarily dealt with the antiviral action of mouse fibroblast interferon, to its antigrowth activity and to antiviral and antigrowth activities of mouse T-cell interferon. We will show that inhibition by common gangiiosides Is restricted to both activities of fibroblast interferon alone. T-cell interferon, although its biological activities are analogous to those of fibroblast Interferon, neither binds to nor Is inhibited by these glycol ipids. Furthermore we demonstrate that mouse leukemia L—1210 cells that were selected for resistance to fibroblast interferon (6), respond equally well to T-cell Interferon as the parent cells which are responsive to both Interferons. 

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