PMID- 21181272
OWN - NLM
STAT- MEDLINE
DCOM- 20120217
LR  - 20211020
IS  - 1573-4978 (Electronic)
IS  - 0301-4851 (Linking)
VI  - 38
IP  - 8
DP  - 2011 Nov
TI  - Histonedeacetylase inhibitor Oxamflatin increase HIV-1 transcription by inducing 
      histone modification in latently infected cells.
PG  - 5071-8
LID - 10.1007/s11033-010-0653-6 [doi]
AB  - HIV-1 latency represents a major problem in the eradication of HIV-1 in infected 
      individuals treated with highly active anti-retroviral therapy. Histone 
      deacetylase (HDAC) inhibits HIV-1 gene expression and virus production and may 
      contribute to quiescence of HIV-1 within resting CD4+ T cells. Here, we evaluated 
      the effect of Oxamflatin, a class I HDAC inhibitor, on the epigenetic change at 
      HIV-1 long terminal repeat (LTR) and the induction of the latent viruses in the 
      latency Jurkat T cell line. Flow cytometry assay showed that Oxamflatin activate 
      HIV-1 gene expression in these latently infected cells by 2-17 fold than 
      background levels. Chromatin immunoprecipitation (ChIP) assays further revealed 
      that Oxamflatin increase the acetylation level of histone H3 and histone H4 at 
      the nucleosome 1(nuc-1) site of the HIV-1 LTR compared to mock treatment. We also 
      found that Oxamflatin had a synergization with prostratin, or 5-azacytidine or 
      tumor necrosis factor-alpha to activate the HIV-1 promoter. Taken together, our 
      results suggest that the histone acetylation plays an important role in 
      regulating HIV-1 LTR gene expression, and Oxamflatin has potential as drug 
      candidates as antilatency therapies.
FAU - Yin, Hao
AU  - Yin H
AD  - State Key Laboratory of Genetic Engineering, Institute of Genetics, School of 
      Life Sciences, Fudan University, Shanghai 200433, China.
FAU - Zhang, Yuhao
AU  - Zhang Y
FAU - Zhou, Xin
AU  - Zhou X
FAU - Zhu, Huanzhang
AU  - Zhu H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20101223
PL  - Netherlands
TA  - Mol Biol Rep
JT  - Molecular biology reports
JID - 0403234
RN  - 0 (Histone Deacetylase Inhibitors)
RN  - 0 (Histones)
RN  - 0 (Hydroxamic Acids)
RN  - 0 (oxamflatin)
RN  - 3X2S926L3Z (trichostatin A)
SB  - IM
MH  - Acetylation/drug effects
MH  - Cell Death/drug effects
MH  - Cell Survival/drug effects
MH  - Chromatin Immunoprecipitation
MH  - Dose-Response Relationship, Drug
MH  - Drug Synergism
MH  - HEK293 Cells
MH  - HIV Infections/drug therapy/*virology
MH  - HIV Long Terminal Repeat/genetics
MH  - HIV-1/drug effects/*genetics
MH  - Histone Deacetylase Inhibitors/*pharmacology/therapeutic use
MH  - Histones/*metabolism
MH  - Humans
MH  - Hydroxamic Acids/*pharmacology/therapeutic use
MH  - Jurkat Cells
MH  - Promoter Regions, Genetic/genetics
MH  - Protein Processing, Post-Translational/*drug effects
MH  - Time Factors
MH  - Transcription, Genetic/*drug effects
MH  - Virus Latency/drug effects/genetics
EDAT- 2010/12/25 06:00
MHDA- 2012/02/18 06:00
CRDT- 2010/12/25 06:00
PHST- 2010/06/28 00:00 [received]
PHST- 2010/12/04 00:00 [accepted]
PHST- 2010/12/25 06:00 [entrez]
PHST- 2010/12/25 06:00 [pubmed]
PHST- 2012/02/18 06:00 [medline]
AID - 10.1007/s11033-010-0653-6 [doi]
PST - ppublish
SO  - Mol Biol Rep. 2011 Nov;38(8):5071-8. doi: 10.1007/s11033-010-0653-6. Epub 2010 
      Dec 23.