Abstract
Nuclear factor κB (NF-κB) is a family of inducible transcription factors that plays a vital role in different aspects of immune responses. NF-κB is normally sequestered in the cytoplasm as inactive complexes via physical association with inhibitory proteins termed IκBs. In response to immune and stress stimuli, NF-κB members become activated via two major signaling pathways, the canonical and noncanonical pathways, and move to the nucleus to exert transcriptional functions. NF-κB is vital for normal immune responses against infections, but deregulated NF-κB activation is a major cause of inflammatory diseases. Accumulated studies suggest the involvement of NF-κB in the pathogenesis of renal inflammation caused by infection, injury, or autoimmune factors. In this review, we discuss the current understanding regarding the activation and function of NF-κB in different types of kidney diseases.
Highlights
Nuclear factor κB (NF-κB) was initially discovered as a B cell nuclear protein binding to the κ enhancer of the immunoglobulin κ light chain gene [1, 2]
It subsequently became clear that NF-κB is a ubiquitously expressed transcription factor that mediates signal-induced expression of numerous genes involved in different biological processes, including immune responses, inflammation, cell growth and survival [3, 4]
Concluding remarks NF-κB has been well established as a pivotal mediator of inflammation, its role in mediating inflammation in specific organs is less well understood
Summary
Nuclear factor κB (NF-κB) was initially discovered as a B cell nuclear protein binding to the κ enhancer of the immunoglobulin κ light chain gene [1, 2]. It subsequently became clear that NF-κB is a ubiquitously expressed transcription factor that mediates signal-induced expression of numerous genes involved in different biological processes, including immune responses, inflammation, cell growth and survival [3, 4]. The major IκB member regulating canonical NF-κB pathway is IκBα, a protein characterized by its dynamic changes along with signal-induced NF-κB activation.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
