[PDF][PDF] NF-κB: a lesson in family values

D Thanos, T Maniatis - Cell, 1995 - core.ac.uk
Cell, 1995core.ac.uk
NF-KB and the other members of the Rel family of transcriptional activator proteins have
been a focal point for understanding how extracellular signals induce the expression of
specific sets of genes in higher eukaryotes. Unlike most transcriptional activators, this family
of proteins resides in the cytoplasm and must therefore translocate into the nucleus to
function. The nuclear translocation of Rel proteins is induced by an extraordinarily large
number of agents ranging from bacterial and viral pathogens to immune and inflammatory …
NF-KB and the other members of the Rel family of transcriptional activator proteins have been a focal point for understanding how extracellular signals induce the expression of specific sets of genes in higher eukaryotes. Unlike most transcriptional activators, this family of proteins resides in the cytoplasm and must therefore translocate into the nucleus to function. The nuclear translocation of Rel proteins is induced by an extraordinarily large number of agents ranging from bacterial and viral pathogens to immune and inflammatory cytokines to a variety of agents that damage cells. Remarkably, an even larger number of genes appear to be targets for the activation by Rel proteins. As a result of these properties, we are confronted with two intriguing questions: how do multiple signal transduction pathways lead to the activation of NFKB, and how does a particular inducer lead to the activation of only one or a subset of the genes targeted by NFKB? Answers to these questions require a detailed understanding of the pathways of Rel protein activation and the mechanisms by which the genes targeted by Rel proteins are turned on. Here, we review recent progress in understanding the mechanisms involved in the activation of NF-KB, the function of individual Rel family proteins, and synergistic interactions between Rel proteins and other families of transcription factors, leading to specific gene activation.
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