學術產出-期刊論文
| 題名 | NF-kappaB signaling pathways in neurological inflammation: A mini review |
| 作者 | Shih, Ruey-Horng Wang, Chen-Yu Yang, Chuen-Mao |
| 貢獻者 | 神科所 |
| 關鍵詞 | 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 |
| 日期 | 2015-12 |
| 上傳時間 | 10-八月-2017 17:03:02 (UTC+8) |
| 摘要 | 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. |
| 關聯 | Frontiers in Molecular Neuroscience, 8(DEC) |
| 資料類型 | article |
| DOI | http://dx.doi.org/10.3389/fnmol.2015.00077 |
| dc.contributor | 神科所 | zh_Tw |
| dc.creator (作者) | Shih, Ruey-Horng | en_US |
| dc.creator (作者) | Wang, Chen-Yu | en_US |
| dc.creator (作者) | Yang, Chuen-Mao | en_US |
| dc.date (日期) | 2015-12 | en_US |
| dc.date.accessioned | 10-八月-2017 17:03:02 (UTC+8) | - |
| dc.date.available | 10-八月-2017 17:03:02 (UTC+8) | - |
| dc.date.issued (上傳時間) | 10-八月-2017 17:03:02 (UTC+8) | - |
| dc.identifier.uri (URI) | http://nccur.lib.nccu.edu.tw/handle/140.119/111921 | - |
| dc.description.abstract (摘要) | 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 (關聯) | Frontiers in Molecular Neuroscience, 8(DEC) | en_US |
| dc.subject (關鍵詞) | 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 (題名) | NF-kappaB signaling pathways in neurological inflammation: A mini review | en_US |
| dc.type (資料類型) | article | |
| dc.identifier.doi (DOI) | 10.3389/fnmol.2015.00077 | |
| dc.doi.uri (DOI) | http://dx.doi.org/10.3389/fnmol.2015.00077 |