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The effect of CD4 receptor downregulation and its downstream signaling molecules on HIV-1 latency SCIE SCOPUS

Title
The effect of CD4 receptor downregulation and its downstream signaling molecules on HIV-1 latency
Authors
Kim, KCKim, HGRoh, TYPark, JJung, KMLee, JSChoi, SYKim, SSChoi, BS
Date Issued
2011-01-14
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
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.
Keywords
NCHA cells; CD4 receptor; Signaling molecular; ZAP-70; AP-1; Deactivation; T-CELL ACTIVATION; SYNAPSE FORMATION; GENE-EXPRESSION; HUMAN GENOME; TRANSCRIPTION; METHYLATIONS
URI
https://oasis.postech.ac.kr/handle/2014.oak/25071
DOI
10.1016/J.BBRC.2010.12.032
ISSN
0006-291X
Article Type
Article
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, vol. 404, no. 2, page. 646 - 651, 2011-01-14
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노태영ROH, TAE YOUNG
Dept of Life Sciences
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