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Titlebook: Biological Response Modifiers — Interferons, Double-Stranded RNA and 2′,5′-Oligoadenylates; W. E. G. Müller,H. C. Schröder Book 1994 Sprin

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https://doi.org/10.1007/978-3-642-78549-8Doppelstrang-RNA; HIV; Immunantwort; RNA; Virusinfektion; Zytokine; cancer; cancer therapy; cytokine; cytokin
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978-3-642-78551-1Springer-Verlag Berlin Heidelberg 1994
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2-5A and Virus Infection,ately, cells and living organisms are provided with various defense mechanisms against viral infection. The most important of these is interferon (IFN), which performs a multitude of functions, particularly in the regulation of cell growth, cell differentiation and immune responses (Gastl and Huber 1988).
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Zusammenfassende Diskussion und Ausblick,ulation of host factors during initial host-pathogen interactions is initiated by host recognition of viral signals, and disease development is conditioned by the subsequent response to these signals. The identity and function of host proteins involved in the recognition and response to pathogen sig
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D. Hölzel,G. Schubert-Fritschle,Ch. Thiemes, see Petska et al. 1987; Sen and Lengyel 1992). In this review, we will discuss the regulation of the double-stranded (ds) RNA-activated protein kinase which is one of more than 30 proteins induced by interferon. The dsRNA-activated protein kinase will be referred to as the P68 kinase (Katze et al
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D. Hölzel,G. Schubert-Fritschle,Ch. Thiemeosynthesis of interferon (IFN), production of 2′,5′-oligoadenylate (2-5A), ribonuclease L (RNase L) activity and different cell-mediated immune functions. A restriction of available bioactive dsRNA (or of dsRNA-dependent enzymes) may play an important role in the disease progression. The results sum
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Klinisch angewandte Immunologieogenic, and specific for viral functions. Effective viral chemotherapy has been hindered because viruses employ host cell systems to replicate. Recent advances in molecular virology provide a rational basis for the development of antiviral compounds that will interfere with biochemically defined, vi
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