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Please use this identifier to cite or link to this item:
https://nccur.lib.nccu.edu.tw/handle/140.119/111921
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| Title: | NF-kappaB signaling pathways in neurological inflammation: A mini review |
| Authors: | Shih, Ruey-Horng
Wang, Chen-Yu
Yang, Chuen-Mao |
| Contributors: | 神科所 |
| Keywords: | autacoid;immunoglobulin enhancer binding protein;transcription factor Rel;transcription factor RelA;apoptosis;brain damage;cell cycle;cell proliferation;cell survival;genetic transcription;human;immune response;nervous system inflammation;neurotoxicity;pain;protein degradation;protein expression;protein phosphorylation;Review;signal transduction |
| Date: | 2015-12 |
| Issue Date: | 2017-08-10 17:03:02 (UTC+8) |
| Abstract: | The NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells) transcription factor family is a pleiotropic regulator of many cellular signaling pathways, providing a mechanism for the cells in response to a wide variety of stimuli linking to inflammation. The stimulated cells will be regulated by not only the canonical but also non-canonical NF-κB pathways. To initiate both of these pathways, κB-degradation triggers NF-κB release and the nuclear translocated-heterodimer (or homodimer) can associate with the lκB sites of promoter to regulate the gene transcriptions. NF--κB ubiquitously expresses in neurons and the constitutive NF-κB activation is associated with processing of neuronal information. NF-κB can regulate the transcription of genes such as chemokines, cytokines, proinflammatory enzymes, adhesion molecules, proinflammatory transcription factors, and other factors to modulate the neuronal survival. In neuronal insult, NF-κB constitutively active in neuron cell bodies can protect neurons against different injuries and regulate the neuronal inflammatory reactions. Besides neurons, NF-κB transcription factors are abundant in glial cells and cerebral blood vessels and the diverse functions of NF-κB also regulate the inflammatory reaction around the neuronal environment. NF-κB transcription factors are abundant in the brain and exhibit diverse functions. Several central nerve system (CNS) diseases are linked to NF-κB activated by inflammatory mediators. The RelA and c-Rel expression produce opposite effects on neuronal survival. Importantly, c-Rel expression in CNS plays a critical role in anti-apoptosis and reduces the age-related behaviors. Moreover, the different subunits of NF-κB dimer formation can modulate the neuroninflammation, neuronal protection, or neurotoxicity. The diverse functions of NF-κB depend on the subunits of the NF-κB dimer-formation which enable us to develop a therapeutic approach to neuroinflammation based on a new concept of inflammation as a strategic tool in neuronal cells. However, the detail role of NF-κB in neuroinflammation, remains to be clarified. In the present article, we provide an updated review of the current state of our knowledge about relationship between NF-κB and neuroinflammation. © 2015 Shih, Wang and Yang. |
| Relation: | Frontiers in Molecular Neuroscience, 8(DEC) |
| Data Type: | article |
| DOI 連結: | http://dx.doi.org/10.3389/fnmol.2015.00077 |
| DOI: | 10.3389/fnmol.2015.00077 |
| Appears in Collections: | [企業管理學系] 期刊論文
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