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Front Biol    2012, Vol. 7 Issue (4) : 277-291    https://doi.org/10.1007/s11515-012-1233-z
REVIEW
NFκB signaling regulates embryonic and adult neurogenesis
Yonggang ZHANG, Wenhui HU()
Department of Neuroscience, Temple University School of Medicine, Philadelphia, PA 19140, USA
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Abstract

Both embryonic and adult neurogenesis involves the self-renewal/proliferation, survival, migration and lineage differentiation of neural stem/progenitor cells. Such dynamic process is tightly regulated by intrinsic and extrinsic factors and complex signaling pathways. Misregulated neurogenesis contributes much to a large range of neurodevelopmental defects and neurodegenerative diseases. The signaling of NFκB regulates many genes important in inflammation, immunity, cell survival and neural plasticity. During neurogenesis, NFκB signaling mediates the effect of numerous niche factors such as cytokines, chemokines, growth factors, extracellular matrix molecules, but also cross-talks with other signaling pathways such as Notch, Shh, Wnt/β-catenin. This review summarizes current progress on the NFκB signaling in all aspects of neurogenesis, focusing on the novel role of NFκB signaling in initiating early neural differentiation of neural stem cells and embryonic stem cells.
Keywords neural stem cells      transcriptional factors      NFκB      neurogenesis      embryonic stem cells      signal transduction     
Corresponding Author(s): HU Wenhui,Email:whu@temple.edu   
Issue Date: 01 August 2012
 Cite this article:   
Yonggang ZHANG,Wenhui HU. NFκB signaling regulates embryonic and adult neurogenesis[J]. Front Biol, 2012, 7(4): 277-291.
 URL:  
https://academic.hep.com.cn/fib/EN/10.1007/s11515-012-1233-z
https://academic.hep.com.cn/fib/EN/Y2012/V7/I4/277
Fig.1  Signaling cascade of NFκB activation and identified members of each family. The red highlighted text denotes the best-studied original member(s) for each family.
Fig.2  Signaling pathways of NFκB activation. In the classical pathway, the classical stimulators like TNFα bind to receptor, leading to recruitment of the adaptor molecule TRADD and the signaling proteins TRAF2 and RIP1. TRAF2 recruits the IKK complex that phosphorylates IκBα at serine residue 32 and 36, leading to its ubiquitination and degradation by the proteasome, allowing the release of the classical heterodimer of p65/p50, which then translocate to the nucleus to regulate the transcription of target genes. In the non-classical pathway, NIK-induced phosphorylation of IKKα leads to the phosphorylation of p100 and proteasome-mediated processing of p100 into p52, allowing the nuclear translocation of RelB/p52 to regulate target gene expression. In the atypical pathway, the p38-activated casein kinase 2 (CK2) phosphorylates IκBα at a cluster of serine residues within C-terminal domain, while oxidative stress induces spleen tyrosine kinase (Syk)-mediated phosphorylation of IκBα at tyrosine residue (Y-42) within N-terminal domain.
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