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Crosstalk via the NF-kappaB signaling system Basak S; Hoffmann ACytokine Growth Factor Rev 2008[Jun]; 19 (3-4): 187-97The nuclear factor kappaB (NF-kappaB) family of transcription factors consists of 15 possible dimers whose activity is controlled by a family of inhibitor proteins, known as IkappaBs. A variety of cellular stimuli, many of them transduced by members of the tumor necrosis factor receptor (TNFR) superfamily, induce degradation of IkappaBs to activate an overlapping subset of NF-kappaB dimers. However, generation and stimulus-responsive activation of NF-kappaB dimers are intimately linked via various cross-regulatory mechanisms that allow crosstalk between different signaling pathways through the NF-kappaB signaling system. In this review, we summarize these mechanisms and discuss physiological and pathological consequences of crosstalk between apparently distinct inflammatory and developmental signals. We argue that a systems approach will be valuable for understanding questions of specificity and emergent properties of highly networked cellular signaling systems.|*Signal Transduction[MESH]|Animals[MESH]|Growth and Development[MESH]|Immunity[MESH]|Inflammation/metabolism[MESH]|Lymphoid Tissue/embryology/metabolism[MESH]|Mice[MESH]|NF-kappa B p50 Subunit/metabolism[MESH]|NF-kappa B/*metabolism[MESH]|Receptors, Tumor Necrosis Factor/metabolism[MESH]|Transcription Factor RelA/metabolism[MESH] |
