Selective PCAF inhibitor ameliorates cognitive and behavioral deficits by suppressing NF-kappa B-mediated neuroinflammation induced by A beta in a model of Alzheimer's disease
DC Field | Value | Language |
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dc.contributor.author | Park, Soo-Yeon | - |
dc.contributor.author | Kim, Mi-Jeong | - |
dc.contributor.author | Kim, Young Jun | - |
dc.contributor.author | Lee, Yoo-Hyun | - |
dc.contributor.author | Bae, Donghyuk | - |
dc.contributor.author | Kim, Sunoh | - |
dc.contributor.author | Na, Younghwa | - |
dc.contributor.author | Yoon, Ho-Geun | - |
dc.date.accessioned | 2021-09-04T17:55:18Z | - |
dc.date.available | 2021-09-04T17:55:18Z | - |
dc.date.created | 2021-06-18 | - |
dc.date.issued | 2015-04 | - |
dc.identifier.issn | 1107-3756 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/94029 | - |
dc.description.abstract | Several recent studies have reported an association between neurodegeneration and histone modifications, such as acetylation, deacetylation and methylation. In addition, questions have been raised regarding a potential functional role for the histone acetylation enzymes in b-amyloid (A beta)-mediated neurotoxicity, particularly the p300/CBP-associated factor (PCAF) enzyme. We recently reported the potential utility of a PCAF inhibitor in the suppression of A beta-induced neuronal cell death, although the in vivo effectiveness of the PCAF inhibitor remained unclear. In this study, we modified the PCAF inhibitor by chemical derivatization and selected compound C-30-27 as the most potent PCAF inhibitor. We demonstrated that C-30-27 selectively inhibited acetylation-dependent nuclear factor-kappa B (NF-kappa B) at Lys-122 and suppressed the NF-kappa B-mediated inflammatory response induced by lipopolysaccharide (LPS) or Aa in both BV2 and Neuro-2A (N2A) cells. Finally, we demonstrated that C-30-27 improved cognitive deficits, as well as the capacity for locomotion and the damaged cholinergic system in the A beta-treated rats. In conclusion, our results demonstrate that this selective PCAF inhibitor has the potential to reduce the neuroinflammatory response induced by A beta. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | SPANDIDOS PUBL LTD | - |
dc.subject | HISTONE ACETYLTRANSFERASE INHIBITOR | - |
dc.subject | LONG-TERM-MEMORY | - |
dc.subject | TRANSCRIPTION FACTOR | - |
dc.subject | SYSTEMIC INFLAMMATION | - |
dc.subject | AMYLOID NEUROTOXICITY | - |
dc.subject | BRAIN INFLAMMATION | - |
dc.subject | ACETYLCHOLINESTERASE | - |
dc.subject | MICROGLIA | - |
dc.subject | ACETYLATION | - |
dc.subject | ACTIVATION | - |
dc.title | Selective PCAF inhibitor ameliorates cognitive and behavioral deficits by suppressing NF-kappa B-mediated neuroinflammation induced by A beta in a model of Alzheimer's disease | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Young Jun | - |
dc.identifier.doi | 10.3892/ijmm.2015.2099 | - |
dc.identifier.scopusid | 2-s2.0-84923668985 | - |
dc.identifier.wosid | 000351764800033 | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, v.35, no.4, pp.1109 - 1118 | - |
dc.relation.isPartOf | INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE | - |
dc.citation.title | INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE | - |
dc.citation.volume | 35 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 1109 | - |
dc.citation.endPage | 1118 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Research & Experimental Medicine | - |
dc.relation.journalWebOfScienceCategory | Medicine, Research & Experimental | - |
dc.subject.keywordPlus | HISTONE ACETYLTRANSFERASE INHIBITOR | - |
dc.subject.keywordPlus | LONG-TERM-MEMORY | - |
dc.subject.keywordPlus | TRANSCRIPTION FACTOR | - |
dc.subject.keywordPlus | SYSTEMIC INFLAMMATION | - |
dc.subject.keywordPlus | AMYLOID NEUROTOXICITY | - |
dc.subject.keywordPlus | BRAIN INFLAMMATION | - |
dc.subject.keywordPlus | ACETYLCHOLINESTERASE | - |
dc.subject.keywordPlus | MICROGLIA | - |
dc.subject.keywordPlus | ACETYLATION | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordAuthor | Alzheimer&apos | - |
dc.subject.keywordAuthor | s disease | - |
dc.subject.keywordAuthor | P300/CBP-associated factor | - |
dc.subject.keywordAuthor | inflammation | - |
dc.subject.keywordAuthor | nuclear factor-kappa B | - |
dc.subject.keywordAuthor | neurotoxicity | - |
dc.subject.keywordAuthor | beta-amyloid | - |
dc.subject.keywordAuthor | cognitive deficit | - |
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