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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-Aug-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-Aug-2017 17:03:02 (UTC+8) - dc.date.available 10-Aug-2017 17:03:02 (UTC+8) - dc.date.issued (上傳時間) 10-Aug-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
