Please use this identifier to cite or link to this item:
https://ah.lib.nccu.edu.tw/handle/140.119/111921
DC Field | Value | Language |
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dc.contributor | 神科所 | zh_Tw |
dc.creator | Shih, Ruey-Horng | en_US |
dc.creator | Wang, Chen-Yu | en_US |
dc.creator | Yang, Chuen-Mao | en_US |
dc.date | 2015-12 | en_US |
dc.date.accessioned | 2017-08-10T09:03:02Z | - |
dc.date.available | 2017-08-10T09:03:02Z | - |
dc.date.issued | 2017-08-10T09:03:02Z | - |
dc.identifier.uri | http://nccur.lib.nccu.edu.tw/handle/140.119/111921 | - |
dc.description.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. | en_US |
dc.format.extent | 921265 bytes | - |
dc.format.mimetype | application/pdf | - |
dc.relation | Frontiers in Molecular Neuroscience, 8(DEC) | en_US |
dc.subject | 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 | en_US |
dc.title | NF-kappaB signaling pathways in neurological inflammation: A mini review | en_US |
dc.type | article | |
dc.identifier.doi | 10.3389/fnmol.2015.00077 | |
dc.doi.uri | http://dx.doi.org/10.3389/fnmol.2015.00077 | |
item.grantfulltext | restricted | - |
item.cerifentitytype | Publications | - |
item.fulltext | With Fulltext | - |
item.openairetype | article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
Appears in Collections: | 期刊論文 |
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