Comparative gene expression profiling reveals the mechanisms of axon regeneration
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, Jinyoung | - |
dc.contributor.author | Cho, Yongcheol | - |
dc.date.accessioned | 2021-12-07T15:42:11Z | - |
dc.date.available | 2021-12-07T15:42:11Z | - |
dc.date.created | 2021-08-30 | - |
dc.date.issued | 2021 | - |
dc.identifier.issn | 1742-464X | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/130119 | - |
dc.description.abstract | Axons are vulnerable to injury, potentially leading to degeneration or neuronal death. While neurons in the central nervous system fail to regenerate, neurons in the peripheral nervous system are known to regenerate. Since it has been shown that injury-response signal transduction is mediated by gene expression changes, expression profiling is a useful tool to understand the molecular mechanisms of regeneration. Axon regeneration is regulated by injury-responsive genes induced in both neurons and their surrounding non-neuronal cells. Thus, an experimental setup for the comparative analysis between regenerative and nonregenerative conditions is essential to identify ideal targets for the promotion of regeneration-associated genes and to understand the mechanisms of axon regeneration. Here, we review the original research that shows the key factors regulating axon regeneration, in particular by using comparative gene expression profiling in diverse systems. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | WILEY | - |
dc.subject | LOCAL PROTEIN-SYNTHESIS | - |
dc.subject | MESSENGER-RNA TRANSLATION | - |
dc.subject | WALLERIAN DEGENERATION | - |
dc.subject | MAMMALIAN TARGET | - |
dc.subject | SELF-DESTRUCTION | - |
dc.subject | RAPAMYCIN MTOR | - |
dc.subject | ADULT NEURONS | - |
dc.subject | INJURY | - |
dc.subject | INHIBITION | - |
dc.subject | NOGO | - |
dc.title | Comparative gene expression profiling reveals the mechanisms of axon regeneration | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Cho, Yongcheol | - |
dc.identifier.doi | 10.1111/febs.15646 | - |
dc.identifier.scopusid | 2-s2.0-85097285425 | - |
dc.identifier.wosid | 000597166500001 | - |
dc.identifier.bibliographicCitation | FEBS JOURNAL, v.288, no.16, pp.4786 - 4797 | - |
dc.relation.isPartOf | FEBS JOURNAL | - |
dc.citation.title | FEBS JOURNAL | - |
dc.citation.volume | 288 | - |
dc.citation.number | 16 | - |
dc.citation.startPage | 4786 | - |
dc.citation.endPage | 4797 | - |
dc.type.rims | ART | - |
dc.type.docType | Review; Early Access | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.subject.keywordPlus | LOCAL PROTEIN-SYNTHESIS | - |
dc.subject.keywordPlus | MESSENGER-RNA TRANSLATION | - |
dc.subject.keywordPlus | WALLERIAN DEGENERATION | - |
dc.subject.keywordPlus | MAMMALIAN TARGET | - |
dc.subject.keywordPlus | SELF-DESTRUCTION | - |
dc.subject.keywordPlus | RAPAMYCIN MTOR | - |
dc.subject.keywordPlus | ADULT NEURONS | - |
dc.subject.keywordPlus | INJURY | - |
dc.subject.keywordPlus | INHIBITION | - |
dc.subject.keywordPlus | NOGO | - |
dc.subject.keywordAuthor | axon regeneration | - |
dc.subject.keywordAuthor | comparative analysis | - |
dc.subject.keywordAuthor | differential gene expression | - |
dc.subject.keywordAuthor | gene expression profiling | - |
dc.subject.keywordAuthor | nerve injury | - |
dc.subject.keywordAuthor | transcriptome | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
(02841) 서울특별시 성북구 안암로 14502-3290-1114
COPYRIGHT © 2021 Korea University. All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.