Alteration in the simian virus 40 maturation pathway after butyrate-induced hyperacetylation of histones

Roman, Ann

doi:10.1128/jvi.44.3.958-962.1982

Cited by 9 publications

(3 citation statements)

References 21 publications

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“…The fact that the HDAC inhibitors also cause a reduction in the size of the pool of replicating SV40 minichromosomes at late times suggests that HDAC activity may play a role in determining the biological fate of newly replicated SV40 minichromosomes. This suggestion that the fate of newly replicated SV40 minichromosomes may be determined in part by HDAC function is consistent with previous work which showed that treatment of SV40 infected cells late in infection with NaBu reduced the fraction of newly replicated minichromosomes which became committed to the encapsidation pathway [ 24 ].…”

Section: Discussionsupporting

confidence: 92%

HDAC inhibitors stimulate viral transcription by multiple mechanisms

Balakrishnan

Milavetz

2008

Virol J

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Section: Discussionsupporting

confidence: 92%

HDAC inhibitors stimulate viral transcription by multiple mechanisms

Balakrishnan

Milavetz

2008

Virol J

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“…Butyrate has been reported to exert additional cytostatic effects such as G2/M blockage and antiviral activity against RNA viruses (12,20,52,53,63). We have not examined the possible differences in chromatin structure between large and small DNA viruses in the presence and absence of butyrate to study the potential butyrate-mediated alterations of chromatin structure (33,58) that might contribute to the observed differences in replication patterns among DNA viruses.…”

Section: Discussionmentioning

confidence: 99%

n-Butyrate, a cell cycle blocker, inhibits the replication of polyomaviruses and papillomaviruses but not that of adenoviruses and herpesviruses

Shadan

Cowsert

Villarreal

1994

J Virol

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Small DNA viruses are dependent on the interaction of early proteins (such as large T antigen) with host p53 and Rb to bring about the G,-to-S cell cycle transition. The large DNA viruses are less dependent on host regulatory genes since additional early viral proteins (such as viral DNA polymerase, DNA metabolic enzymes, and other replication proteins) are involved in DNA synthesis. A highly conserved domain of large T antigen (similar to the p53-binding region) exclusively identifies papovavirus, parvovirus, and papillomaviruses from all other larger DNA viruses and implies a conserved interaction with host regulatory genes. In this report, we show that 3 to 6 mM butyrate, a general cell cycle blocker implicated in inhibition of the G1-to-S transition, inhibits DNA replication of polyomavirus and human papillomavirus type 11 but not the replication of larger DNA viruses such as adenovirus types 2 and 5, herpes simplex virus type 1, Epstein-Barr virus, and cytomegalovirus, which all bypass the butyrate-mediated cell cycle bloclk This butyrate effect on polyomavirus replication is not cell type specific, nor does it depend on the p53 or Rb gene, as inhibition was seen in fibroblasts with intact or homozygous deleted p53 or Rb, 3T6 cells, keratinocytes, C2C12 myoblasts, and 3T3-L1 adipocytes. In addition, butyrate did not inhibit expression of polyomavirus T antigen. The antiviral elfect of butyrate involves a form of imprinted state, since pretreatment of cells with 3 mM butyrate inhibits human papillomavirus type 11 DNA replication for at least 96 h after its removal. Butyrate, therefore, serves as a molecular tool in dissecting the life cycle of smaller DNA viruses from that of the larger DNA viruses in relation to the cell cycle.

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“…Since cellular DNA and viral replication can be inhibited by butyrate (8,11) we chose nonreplicating recombinant plasaids (12) for our studies.…”

Section: Introductionmentioning

confidence: 99%

Expression of recombinant plasmids in mammalian cells Is enhanced by sodium butyrate

1983

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We have studied the effects of sodium butyrate on DNA-mediated gene transfer in an effort to investigate interrelationships between chromatin structure and expression of recombinant plasmids. Our results demonstrate that butyrate affects the early stages of gene activity following DNA uptake at least two levels. First, the number of cells able to express foreign DNA increases from 10% to up to 40%. Second, there is an increase in enhancer-dependent transcription, approximately 30 fold in HeLa cells, involving the SV40 early promoter. Stable transformation efficiencies increase to 4% and 10% in HeLa S3 and monkey kidney CV-1 cells, respectively. Finally, expression of integrated recombinant plasmid genes is reinducible by a second treatment five weeks after initial exposure to this agent.

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Alteration in the simian virus 40 maturation pathway after butyrate-induced hyperacetylation of histones

Cited by 9 publications

References 21 publications

HDAC inhibitors stimulate viral transcription by multiple mechanisms

HDAC inhibitors stimulate viral transcription by multiple mechanisms

n-Butyrate, a cell cycle blocker, inhibits the replication of polyomaviruses and papillomaviruses but not that of adenoviruses and herpesviruses

Expression of recombinant plasmids in mammalian cells Is enhanced by sodium butyrate

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