DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, KC | - |
dc.contributor.author | Kim, HG | - |
dc.contributor.author | Roh, TY | - |
dc.contributor.author | Park, J | - |
dc.contributor.author | Jung, KM | - |
dc.contributor.author | Lee, JS | - |
dc.contributor.author | Choi, SY | - |
dc.contributor.author | Kim, SS | - |
dc.contributor.author | Choi, BS | - |
dc.date.accessioned | 2016-04-01T02:24:23Z | - |
dc.date.available | 2016-04-01T02:24:23Z | - |
dc.date.created | 2011-03-10 | - |
dc.date.issued | 2011-01-14 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.other | 2011-OAK-0000022841 | - |
dc.identifier.uri | https://oasis.postech.ac.kr/handle/2014.oak/25071 | - |
dc.description.abstract | HIV-1 can establish a latent infection in memory CD4 + T cells to evade the host immune response. CD4 molecules can act not only as the HIV-1 receptor for entry but also as the trigger in an intracellular signaling cascade for T-cell activation and proliferation via protein tyrosine kinases. Novel chronic HIV-1-infected A3.01-derived (NCHA) cells were used to examine the involvement of CD4 downstream signaling in HIV-1 latency. CD4 receptors in NCHA cells were dramatically downregulated on its surface but were slightly decreased in whole-cell lysates. The expression levels of CD4 downstream signaling molecules, including P56(Lck), ZAP-70, LAT, and c-Jun, were sharply decreased in NCHA cells. The lowered histone modifications of H3K4me3 and H3K9ac correlated with the downregulation of P56(Lck), ZAP-70, and LAT in NCHA cells. AP-1 binding activity was also reduced in NCHA cells. LAT and c-Jun suppressed in NCHA cells were highly induced after PMA treatment. In epigenetic analysis, other signal transduction molecules which are associated with active and/or latent HIV-1 infection showed normal states in HIV-1 latently infected cells compared to A3.01 cells. In conclusion, we demonstrated that the HIV-1 latent state is sustained by the reduction of downstream signaling molecules via the downregulation of CD4 and the attenuated activity of transcription factor as AP-1. The HIV-1 latency model via T-cell deactivation may provide some clues for the development of the new antireservoir therapy. (C) 2010 Elsevier Inc. All rights reserved. | - |
dc.description.statementofresponsibility | X | - |
dc.language | English | - |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | - |
dc.relation.isPartOf | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.subject | NCHA cells | - |
dc.subject | CD4 receptor | - |
dc.subject | Signaling molecular | - |
dc.subject | ZAP-70 | - |
dc.subject | AP-1 | - |
dc.subject | Deactivation | - |
dc.subject | T-CELL ACTIVATION | - |
dc.subject | SYNAPSE FORMATION | - |
dc.subject | GENE-EXPRESSION | - |
dc.subject | HUMAN GENOME | - |
dc.subject | TRANSCRIPTION | - |
dc.subject | METHYLATIONS | - |
dc.title | The effect of CD4 receptor downregulation and its downstream signaling molecules on HIV-1 latency | - |
dc.type | Article | - |
dc.contributor.college | 융합생명공학부 | - |
dc.identifier.doi | 10.1016/J.BBRC.2010.12.032 | - |
dc.author.google | Kim, KC | - |
dc.author.google | Kim, HG | - |
dc.author.google | Roh, TY | - |
dc.author.google | Park, J | - |
dc.author.google | Jung, KM | - |
dc.author.google | Lee, JS | - |
dc.author.google | Choi, SY | - |
dc.author.google | Kim, SS | - |
dc.author.google | Choi, BS | - |
dc.relation.volume | 404 | - |
dc.relation.issue | 2 | - |
dc.relation.startpage | 646 | - |
dc.relation.lastpage | 651 | - |
dc.contributor.id | 10138348 | - |
dc.relation.journal | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.relation.index | SCI급, SCOPUS 등재논문 | - |
dc.relation.sci | SCI | - |
dc.collections.name | Journal Papers | - |
dc.type.rims | ART | - |
dc.identifier.bibliographicCitation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.404, no.2, pp.646 - 651 | - |
dc.identifier.wosid | 000286543800012 | - |
dc.date.tcdate | 2019-02-01 | - |
dc.citation.endPage | 651 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 646 | - |
dc.citation.title | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.citation.volume | 404 | - |
dc.contributor.affiliatedAuthor | Roh, TY | - |
dc.identifier.scopusid | 2-s2.0-78651360646 | - |
dc.description.journalClass | 1 | - |
dc.description.journalClass | 1 | - |
dc.description.wostc | 6 | - |
dc.description.scptc | 7 | * |
dc.date.scptcdate | 2018-05-121 | * |
dc.type.docType | Article | - |
dc.subject.keywordPlus | T-CELL ACTIVATION | - |
dc.subject.keywordPlus | SYNAPSE FORMATION | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | HUMAN GENOME | - |
dc.subject.keywordPlus | TRANSCRIPTION | - |
dc.subject.keywordPlus | METHYLATIONS | - |
dc.subject.keywordAuthor | NCHA cells | - |
dc.subject.keywordAuthor | CD4 receptor | - |
dc.subject.keywordAuthor | Signaling molecular | - |
dc.subject.keywordAuthor | ZAP-70 | - |
dc.subject.keywordAuthor | AP-1 | - |
dc.subject.keywordAuthor | Deactivation | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biophysics | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Biophysics | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.
library@postech.ac.kr Tel: 054-279-2548
Copyrights © by 2017 Pohang University of Science ad Technology All right reserved.