Evidence map›Paper›PMID 16055715›Full record

ArticleMolecular and cellular biology2005

Synergistic and additive properties of the beta-globin locus control region (LCR) revealed by 5'HS3 deletion mutations: implication for LCR chromatin architecture.

Xiangdong Fang, Jin Sun, Ping Xiang, Man Yu, Patrick A Navas, Kenneth R Peterson, George Stamatoyannopoulos, Qiliang Li

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed, 28 citations in OpenAlex.

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  16. Methyl binding domain protein 2 mediates gamma-globin gene silencing in adult human betaYAC transgenic mice.Proceedings of the National Academy of Sciences of the United States of America · 2006
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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

8 authors at 2 institutions in 1 country.

Xiangdong FangMedical Genetics, University of Washington, Seattle, 98195, USA.
Jin Sun
Ping Xiang
Man Yu
Patrick A Navas
Kenneth R Peterson
George Stamatoyannopoulos
Qiliang Li
University of Washington Medical Center · USUniversity of Kansas Medical Center · US

Funding

MOLECULAR CONTROL OF GLOBIN GENE SWITCHINGR37DK045365 · NIDDK · UNIVERSITY OF WASHINGTON · PI STAMATOYANNOPOULOS, GEORGE · 1998 to 2006
$3.8M
Molecular Mechanism of Human g-Globin Gene SilencingR01HL073439 · NHLBI · UNIVERSITY OF WASHINGTON · PI LI, QILIANG · 2003 to 2011
$2.8M
MOLECULAR CONTROL OF HUMAN GLOBIN GENE SWITCHINGR01DK045365 · NIDDK · UNIVERSITY OF WASHINGTON · PI STAMATOYANNOPOULOS, GEORGE · 1992 to 2011
$1.6M
Mechanism of Gamma-Globin Gene Activation in the AdultR01DK061805 · NIDDK · UNIVERSITY OF WASHINGTON · PI LI, QILIANG · 2001 to 2004
$1.5M
Molecular control of fetal G-globin gene expressionR01DK061804 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI PETERSON, KENNETH R · 2001 to 2004
$1.2M
Globin Gene Switching: Molecular ControlR56DK045365 · NIDDK · UNIVERSITY OF WASHINGTON · PI STAMATOYANNOPOULOS, GEORGE · 2007 to 2007
$78k
NHLBI NIH HHS HL73439NHLBI NIH HHS R01 HL073439NIDDK NIH HHS DK45365NIDDK NIH HHS DK61804NIDDK NIH HHS DK61805NIDDK NIH HHS R01 DK045365NIDDK NIH HHS R01 DK061804NIDDK NIH HHS R01 DK061805NIDDK NIH HHS R37 DK045365NIDDK NIH HHS R56 DK045365
6 · The paper itself

Abstract

Deletion of the 234-bp core element of the DNase I hypersensitive site 3 (5'HS3) of the locus control region (LCR) in the context of a human beta-globin locus yeast artificial chromosome (beta-YAC) results in profound effects on globin gene expression in transgenic mice. In contrast, deletion of a 2.3-kb 5'HS3 region, which includes the 234-bp core sequence, has a much milder phenotype. Here we report the effects of these deletions on chromatin structure in the beta-globin locus of adult erythroblasts. The 234-bp 5'HS3 deletion abolished histone acetylation throughout the beta-globin locus; recruitment of RNA polymerase II (pol II) to the LCR and beta-globin gene promoter was reduced to a basal level; and formation of all the 5' DNase I hypersensitive sites of the LCR was disrupted. The 2.3-kb 5'HS3 deletion mildly reduced the level of histone acetylation but did not change the profile across the whole locus; the 5' DNase I hypersensitive sites of the LCR were formed, but to a lesser extent; and recruitment of pol II was reduced, but only marginally. These data support the hypothesis that the LCR forms a specific chromatin structure and acts as a single entity. Based on these results we elaborate on a model of LCR chromatin architecture which accommodates the distinct phenotypes of the 5'HS3 and HS3 core deletions.

Indexed as

Gene DeletionLocus Control RegionAcetylationAnimalsChromatinChromatin ImmunoprecipitationDeoxyribonuclease IDNADNA-Binding ProteinsDNA PrimersErythroblastsErythroid-Specific DNA-Binding FactorsGlobinsHistonesMiceMice, TransgenicChromatinDeoxyribonuclease IDNADNA-Binding ProteinsDNA PrimersErythroid-Specific DNA-Binding FactorsGlobinsHistonesRNA Polymerase IITranscription Factors

Identifiers

PMID16055715
PMCPMC1190234
OpenAlexW2165504805

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.