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Titlebook: Nuclear Factor кB; Regulation and Role Rudi Beyaert Book 2003 Kluwer Academic Publishers 2003 Mammalia.apoptosis.biology.biomedicine.cell.

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發(fā)表于 2025-3-21 18:38:45 | 只看該作者 |倒序瀏覽 |閱讀模式
書目名稱Nuclear Factor кB
副標題Regulation and Role
編輯Rudi Beyaert
視頻videohttp://file.papertrans.cn/669/668546/668546.mp4
圖書封面Titlebook: Nuclear Factor кB; Regulation and Role  Rudi Beyaert Book 2003 Kluwer Academic Publishers 2003 Mammalia.apoptosis.biology.biomedicine.cell.
描述Seventeen years after its initial description, nuclear factor-KB (NF-KB) endures as one of the most studied transcription factors. NF-KB has attracted widespread interest based on the variety of stimuli that activate it, the diverse genes and bio- logical responses that it controls, the striking evolutionary conservation of struc- ture and function among species, and its involvement in a variety of human diseases. The biochemical basis by which several stimuli converge to activate NF-KB has been largely elucidated during recent years. While first discovered as a key regulatory factor of the immune system, NF-KB is now recognized as an important player in the functioning of many organs and cell types. The ongoing examination of NF-KB signaling has revealed its ever expanding role in immune and inflammatory responses, but also in cancer and development. For this reason, numerous efforts are underway to develop safe inhibitors of NF-KB to be used in the treatment of both chronic and acute disease situations. The present book is the first to review and synthesize our knowledge of this interesting transcription factor. As such, the choice of subjects to review was daunting. To set the s
出版日期Book 2003
關(guān)鍵詞Mammalia; apoptosis; biology; biomedicine; cell; cell biology; cellular differentiation; diseases; inflammat
版次1
doihttps://doi.org/10.1007/978-94-010-0163-2
isbn_softcover978-94-010-3983-3
isbn_ebook978-94-010-0163-2
copyrightKluwer Academic Publishers 2003
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發(fā)表于 2025-3-21 23:58:06 | 只看該作者
The Role of Ubiquitin In NF-,B Signaling,tin-protein ligase (E3), ubiquitin is conjugated to a lysine residue of the protein substrate through an isopeptide linkage. Ubiquitin itself has seven lysines. One of these lysines, typically Lys48, can be further conjugated by another ubiquitin to form a polyubiquitin chain through the processive
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Regulation of NF-,B by Glucocorticoids,e action of several messenger molecules called cytokines, chemokines and adhesion molecules, including TNF, IL-1, IL-2, IL-6, MCP-1, IL-8, GM-CSF, ICAM-1 and E-selectin (Cato & Wade, 1996; Barnes & Karin, 1997). These cytokines are produced by (and in turn activate) different surrounding cell types,
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Genetic Analysis of NF-,B-Dependent Signaling Pathways in Mammalian Cells,proach has also been successfully applied to study the TGF. receptor (Hocevar & Howe, 1996) and T-cell receptor-mediated signaling (Goldsmith & Weiss, 1987; Serafini et al., 1995; Williams et al., 1998). While biochemical studies and reverse genetics have tremendously advanced our understanding of t
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Delineation of NF-,B Signaling by Gene Targeting,uding proinflammatory cytokines and products of viral and bacterial infections, induce the serine phosphorylation of I.B proteins. Phosphorylated I.B proteins become targets for ubiquitination and proteosome-mediated degradation, a process that releases NF-.B and promotes its translocation to the nu
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Control of Immunity by Rel Proteins in Drosophila,ers of the hematopoietic lineage have been recently described in Drosophila; they exhibit strong conservation with molecules involved in mammalian hematopoiesis (Lebestky et al., 2000). Even if these studies have demonstrated the role of the Toll pathway for proper hemocyte proliferation (Qiu et al.
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