Evidence map›Paper›PMID 18959802›Full record

ArticleBMC genomics2008

Histone deacetylase inhibitors: a new mode for inhibition of cholesterol metabolism.

Sridar V Chittur, Niquiche Sangster-Guity, Paulette J McCormick

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 65 citations in OpenAlex.

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  6. Transcriptional and epigenetic landscape of CaJournal of cell communication and signaling · 2021
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  11. Model-based clustering of multi-tissue gene expression data.Bioinformatics (Oxford, England) · 2020
    Article
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  15. Article
  16. Epigenetics of Lipid Phenotypes.Current cardiovascular risk reports · 2016
    Article
  17. Article
  18. Article
  19. Article
  20. Emerging regulation and function of betatrophin.International journal of molecular sciences · 2014
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Sridar V ChitturCenter for Functional Genomics, University at Albany, State University of New York, Cancer Research Center, One Discovery Drive, Rm 310, Rensselaer, NY 12144, USA. schittur@albany.edu
Niquiche Sangster-Guity
Paulette J McCormick
University at Albany, State University of New York · USJohns Hopkins Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEukaryotic gene expression is a complex process involving multiple cis and trans activating molecules to either facilitate or inhibit transcription. In recent years, many studies have focused on the role of acetylation of histone proteins in modulating transcription, whereas deacetylation of these same proteins is associated with inactivation or repression of gene expression. This study explores gene expression in HepG2 and F9 cell lines treated with Trichostatin A (TSA), a potent histone deacetylase inhibitor.

resultsThese experiments show that TSA treatment results in clear repression of genes involved in the cholesterol biosynthetic pathway as well as other associated pathways including fatty acid biosynthesis and glycolysis. TSA down regulates 9 of 15 genes in this pathway in the F9 embryonal carcinoma model and 11 of 15 pathway genes in the HepG2 cell line. A time course study on the effect of TSA on gene expression of various enzymes and transcription factors involved in these pathways suggests that down regulation of Srebf2 may be the triggering factor for down regulation of the cholesterol biosynthesis pathway.

conclusionOur results provide new insights in the effects of histone deacetylases on genes involved in primary metabolism. This observation suggests that TSA, and other related histone deacetylase inhibitors, may be useful as potential therapeutic entities for the control of cholesterol levels in humans.

Indexed as

Gene Expression RegulationHistone Deacetylase InhibitorsAcetylationAnticholesteremic AgentsCell LineCholesterolEnzyme InhibitorsHumansHydroxamic AcidsMetabolic Networks and PathwaysSterol Regulatory Element Binding Protein 2Anticholesteremic AgentsCholesterolEnzyme InhibitorsHistone Deacetylase InhibitorsHydroxamic AcidsSREBF2 protein, humanSterol Regulatory Element Binding Protein 2trichostatin A

Identifiers

PMID18959802
PMCPMC2613157
OpenAlexW2088666810

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.