Evidence map›Paper›PMID 16914722›Full record

ArticleMolecular and cellular biology2006

Histone H3 acetylation and H3 K4 methylation define distinct chromatin regions permissive for transgene expression.

Chunhong Yan, Douglas D Boyd

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

81 citing papers in PubMed, 171 citations in OpenAlex.

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  12. Parasitology · 2021
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21 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Chunhong YanDepartment of Cancer Biology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030, USA. cyan@mdanderson.org
Douglas D Boyd
The University of Texas MD Anderson Cancer Center · US

Funding

UROKINASE RECEPTOR EXPRESSION--COLON CANCERR01CA058311 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BOYD, DOUGLAS D. · 1994 to 2010
$2.2M
Regulation of type IV collagenase expressionR01DE010845 · NIDCR · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BOYD, DOUGLAS D. · 1994 to 2007
$1.7M
Regulation of urokinase receptor expression in colon cancerR56CA058311 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BOYD, DOUGLAS D. · 2008 to 2008
$288k
NCI NIH HHS R01 CA058311NCI NIH HHS R01 CA58311NCI NIH HHS R56 CA058311NIDCR NIH HHS R01 DE010845NIDCR NIH HHS R01 DE10845
6 · The paper itself

Abstract

Histone modifications are associated with distinct transcription states and serve as heritable epigenetic markers for chromatin structure and function. While H3 K9 methylation defines condensed heterochromatin that is able to silence a nearby gene, how gene silencing within euchromatin regions is achieved remains elusive. We report here that histone H3 K4 methylation or K9/K14 acetylation defines distinct chromatin regions permissive or nonpermissive for transgene expression. A permissive chromatin region is enriched in H3 K4 methylation and H3 acetylation, while a nonpermissive region is poor in or depleted of these two histone modifications. The histone modification states of the permissive chromatin can spread to transgenic promoters. However, de novo histone H3 acetylation and H3 K4 methylation at a transgenic promoter in a nonpermissive chromatin region are stochastic, leading to variegated transgene expression. Moreover, nonpermissive chromatin progressively silences a transgene, an event that is accompanied by the reduction of H3 K4 methylation and H3 acetylation levels at the transgenic promoter. These repressive effects of nonpermissive chromatin cannot be completely countered by strong transcription activators, indicating the dominance of the chromatin effects. We therefore propose a model in which histone H3 acetylation and H3 K4 methylation localized to discrete sites in the mammalian genome mark distinct chromatin functions that dictate transgene expression or silencing.

Indexed as

Gene ExpressionAcetylationCells, CulturedChromatinGene SilencingGenome, HumanGreen Fluorescent ProteinsHistonesHumansMethylationModels, GeneticMosaicismPromoter Regions, GeneticRecombination, GeneticRegulatory Sequences, Nucleic AcidTransgenesChromatinenhanced green fluorescent proteinGreen Fluorescent ProteinsHistones

Identifiers

PMID16914722
PMCPMC1592829
OpenAlexW2131229011

What OpenQuestion holds

Textmetadata
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.