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Titlebook: Cytokine Knockouts; Scott K. Durum,Kathrin Muegge Book 19981st edition Springer Science+Business Media New York 1998 Colon.Vivo.cytokine.c

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書目名稱Cytokine Knockouts
編輯Scott K. Durum,Kathrin Muegge
視頻videohttp://file.papertrans.cn/243/242629/242629.mp4
叢書名稱Contemporary Immunology
圖書封面Titlebook: Cytokine Knockouts;  Scott K. Durum,Kathrin Muegge Book 19981st edition Springer Science+Business Media New York 1998 Colon.Vivo.cytokine.c
描述My personal history in the field of cytokines had an initial period of several years during which my student and then colleague, Werner Muller, tried in vain to attract me to them. My interest always vanished when I was confronted with complex data pointing to func- tional redundancy of cytokines in cell culture systems. When gene targeting in the mouse germline became possible, this frustration came to an end. We and others immediately embarked on analyzing the in vivo function of cytokines and the problem of functional redundancy with this powerful new approach. The early cytokine gene knockouts performed by colleagues in Wiirzburg (IL-2) and by ourselves (IL-4 and IL-l 0) seemed to give clear answers and at the same time led to surprises: Each of these cytokines apparently had its own special and irreplaceable function, and this function could be quite distinct from what had been anticipated from functional experiments in vitro. Al- though the latter finding is of course a wonderful incentive for fur- ther research, the former is pleasing in a general sense since it highlights the value of each of those one hundred thousand genes or so in our genome, cherished by evolution to be
出版日期Book 19981st edition
關(guān)鍵詞Colon; Vivo; cytokine; cytokines; development; enzyme; enzymes; genes; immunodeficiency; interferon; metabolis
版次1
doihttps://doi.org/10.1007/978-1-4757-2753-1
isbn_ebook978-1-4757-2753-1
copyrightSpringer Science+Business Media New York 1998
The information of publication is updating

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Russell L. Ciochon,Gregg F. Gunnells to TNF receptor-mediated effects tends to be obscured in single gene knockout mice, because the loss of one ligand may be compensated by the remaining one. Since both genes are very closely linked and map within the major histo compatibility complex (MHC), single mutations cannot be crossed togeth
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https://doi.org/10.1057/978-1-137-54786-6, oncostatin M (OSM) and ciliary neurotrophic factor (CNTF) display overlapping activities with IL-6 that may be explained by a common receptor signal transducing component (gp 130). In order to clarify the unique functions of IL-6 in vivo, we have disrupted the murine IL-6 gene in the second exon b
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https://doi.org/10.1007/978-3-030-26376-8e receptor complexes for IL-11, leukemia inhibitory factor (LIF), oncostatin M (OSM), ciliary neurotrophic factor (CNTF), and cardiotrophin-1 (CT-1) .. The discovery of this shared signal transducer, gp 130, helps to explain how these different cytokines can mediate overlapping biological functions
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The IL-2 Deficiency Syndrome,e excluded, and the different sources of the two lymphokines, i.e., mainly activated T-cells for IL-2 versus a wide variety of non-lymphocytic cells for IL-15 . predict that in vivo, the two cytokines will play quite distinct roles in the regulation of lymphocyte activation. Therefore, it will be im
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