Abstract
NF-κB comprises a family of transcription factors that are critically involved in various inflammatory processes. In this paper, the role of NF-κB in inflammation and atherosclerosis and the regulation of the NF-κB signaling pathway are summarized. The structure, function, and regulation of the NF-κB inhibitors, IκBα and IκBβ, are reviewed. The regulation of NF-κB activity by glucocorticoid receptor (GR) signaling and IκBα sumoylation is also discussed. This paper focuses on the recently reported regulatory function that adipocyte enhancer-binding protein 1 (AEBP1) exerts on NF-κB transcriptional activity in macrophages, in which AEBP1 manifests itself as a potent modulator of NF-κB via physical interaction with IκBα and a critical mediator of inflammation. Finally, we summarize the regulatory roles that recently identified IκBα-interacting proteins play in NF-κB signaling. Based on its proinflammatory roles in macrophages, AEBP1 is anticipated to serve as a therapeutic target towards the treatment of various inflammatory conditions and disorders.
Highlights
NF-κB comprises a family of transcription factors that are critically involved in various inflammatory processes
This paper focuses on the recently reported regulatory function that adipocyte enhancer-binding protein 1 (AEBP1) exerts on NF-κB transcriptional activity in macrophages, in which AEBP1 manifests itself as a potent modulator of NF-κB via physical interaction with IκBα and a critical mediator of inflammation
NF-κB comprises a family of ubiquitously expressed, eukaryotic transcription factors that participate in the regulation of multiple immediate genes that are expressed at the onset of many vital biological processes such as cell growth, immunoregulation, apoptosis, and inflammation [2, 3]
Summary
The ability to sense external stimuli that could be lethal to cells coupled with the potential to respond to such cytotoxic signals by switching on defensive genes to sustain cell growth and survival is a remarkable facet of nuclear factor kappa B (NF-κB). Since NF-κB is ubiquitously expressed in almost all types of cells and is a transcription factor that is sequestered in an inactive state in the cytosol but can become activated by a wide range of diverse internal and external stimuli, NFκB has long been considered an ideal safeguard to defend the cell against countless stimuli and maintain its homeostasis [1]. NF-κB comprises a family of ubiquitously expressed, eukaryotic transcription factors that participate in the regulation of multiple immediate genes that are expressed at the onset of many vital biological processes such as cell growth, immunoregulation, apoptosis, and inflammation [2, 3]. NF-κB exists in cells as a heterodimer of members of the Rel family of proteins, including p50, p52, p65 (RelA), RelB, and c-Rel, which share a high degree of structural similarity (Figure 1)
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