DC Field | Value | Language |
---|---|---|
dc.contributor.author | J H Lee | - |
dc.contributor.author | Jeong Hoon Kim | - |
dc.contributor.author | Sunhong Kim | - |
dc.contributor.author | K S Cho | - |
dc.contributor.author | S B Lee | - |
dc.date.accessioned | 2018-04-19T05:18:52Z | - |
dc.date.available | 2018-04-19T05:18:52Z | - |
dc.date.issued | 2018 | - |
dc.identifier.issn | 1570-159X | - |
dc.identifier.uri | 10.2174/1570159X15666170601124220 | ko |
dc.identifier.uri | https://oak.kribb.re.kr/handle/201005/17704 | - |
dc.description.abstract | Background: The transcriptional control of neuronal specification and early development has been intensively studied over the past few decades. However, relatively little is known about transcriptional programs associated with the maintenance of terminally differentiated neuronal cells with respect to their functions, structures, and cell type-specific identity features. Methods: Notably, largely because of the recent advances in related techniques such as next generation sequencing and chromatin immunoprecipitation sequencing, the physiological implications of system-wide regulation of gene expression through changes in chromatin states have begun to be extensively studied in various contexts and systems, including the nervous system. Results: Here, we attempt to review our current understanding of the link between chromatin changes and neuronal maintenance in the period of life after the completion of neuronal development. Perturbations involving chromatin changes in the system-wide transcriptional control are believed to be closely associated with diverse aspects of neuronal aging and neurodegenerative conditions. Conclusion: In this review, we focused on heterochromatin and epigenetic dysregulation in neurodegenerative conditions as well as neuronal aging, the most important risk factor leading to neuronal degeneration, in order to highlight the close association between chromatin changes and neuronal maintenance. Lastly, we reviewed the currently available and potential future applications of pharmacological control of the chromatin states associated with neuronal maintenance | - |
dc.publisher | Bentham Science Publ Ltd | - |
dc.title | Chromatin changes associated with neuronal maintenance and their pharmacological application | - |
dc.title.alternative | Chromatin changes associated with neuronal maintenance and their pharmacological application | - |
dc.type | Article | - |
dc.citation.title | Current Neuropharmacology | - |
dc.citation.number | 2 | - |
dc.citation.endPage | 125 | - |
dc.citation.startPage | 118 | - |
dc.citation.volume | 16 | - |
dc.contributor.affiliatedAuthor | Jeong Hoon Kim | - |
dc.contributor.affiliatedAuthor | Sunhong Kim | - |
dc.contributor.alternativeName | 이장호 | - |
dc.contributor.alternativeName | 김정훈 | - |
dc.contributor.alternativeName | 김선홍 | - |
dc.contributor.alternativeName | 조경상 | - |
dc.contributor.alternativeName | 이성배 | - |
dc.identifier.bibliographicCitation | Current Neuropharmacology, vol. 16, no. 2, pp. 118-125 | - |
dc.identifier.doi | 10.2174/1570159X15666170601124220 | - |
dc.subject.keyword | Epigenetic changes | - |
dc.subject.keyword | heterochromatin formation | - |
dc.subject.keyword | histone | - |
dc.subject.keyword | neurodegenerative disease | - |
dc.subject.keyword | neuronal maintenance | - |
dc.subject.keyword | neuronal aging | - |
dc.subject.local | Epigenetic change | - |
dc.subject.local | Epigenetic changes | - |
dc.subject.local | heterochromatin formation | - |
dc.subject.local | histone | - |
dc.subject.local | Histone | - |
dc.subject.local | neurodegenerative disease | - |
dc.subject.local | Neurodegenrative disease | - |
dc.subject.local | Neurodegenerative diseases | - |
dc.subject.local | Neurodegenerative disease | - |
dc.subject.local | neuronal maintenance | - |
dc.subject.local | neuronal aging | - |
dc.description.journalClass | Y | - |
There are no files associated with this item.
Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.