298
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Regulation and function of NF-kappaB transcription factors in the immune system.

      Annual review of immunology
      Animals, Humans, I-kappa B Proteins, metabolism, Immune System, Lymphocytes, immunology, Lymphoproliferative Disorders, genetics, Myeloid Cells, NF-kappa B, antagonists & inhibitors, Receptors, Antigen, T-Cell, Receptors, Interleukin-1, Signal Transduction, Toll-Like Receptors, Tumor Necrosis Factor-alpha

      Read this article at

      ScienceOpenPublisherPubMed
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The mammalian Rel/NF-kappaB family of transcription factors, including RelA, c-Rel, RelB, NF-kappaB1 (p50 and its precursor p105), and NF-kappaB2 (p52 and its precursor p100), plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation. The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2. A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers. Although work over the past two decades has shed significant light on the regulation of NF-kappaB transcription factors and their functions, much progress has been made in the past two years revealing new insights into the regulation and functions of NF-kappaB. This recent progress is covered in this review.

          Related collections

          Author and article information

          Comments

          Comment on this article