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

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NF-,B Activation by Card Proteins, Deregulation of this process, resulting in too much or too little cell death, can cause both developmental defects and a wide variety of diseases such as cancer and neurodegenerative disorders (Mullauer et al., 2001). At the heart of this complex machinery is a conserved family of cysteine protease

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Viruses as Intruders in the Rel/NF-,B Signaling Pathway, related at the level of sequence and structure and in their regulation by subcellular localization. When bound to DNA, Rel/NF-.B proteins influence the expression of hundreds of cellular genes and, as discussed in this review, many viral genes. Many of the Rel/NF-.B cellular target genes control im

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The I,B Kinase (IKK) Complex,al, chemical and biological activators, activates cytoplasmic NF-.B indirectly via phosphorylation of its inhibitor protein I.B. Phosphorylated I.Bs rapidly undergo ubiquitin-dependent degradation and subsequently free NF-.B dimers enter the nucleus to regulate transcription of target genes. This in

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Genetic Analysis of NF-,B-Dependent Signaling Pathways in Mammalian Cells,n unknown gene, based on its function. In using forward genetics, one can knockout or gain gene expression by random mutagenesis or by introducing expression libraries, followed by selection based on function (Stark & Gudkov, 1999). As a result, a collection of mutant cell lines and cDNA reagents wi

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Delineation of NF-,B Signaling by Gene Targeting,65), RelB, c-Rel, NF-.B1 (p105, the precursor for p50) and NF-.B2 (p100, the precursor for p52) (Karin & Ben-Neriah, 2000). Among these, RelA and c-Rel contain potent transcriptional activation domains. Thus the transcriptionally active forms of NF-.B are dimers of c-Rel/p50, c-Rel/RelA, RelA/RelA a