Evidence map›Paper›PMID 26124638›Full record

ArticleDrug design, development and therapy2015

Histone demethylase LSD1-mediated repression of GATA-2 is critical for erythroid differentiation.

Yidi Guo, Xueqi Fu, Yue Jin, Jing Sun, Ye Liu, Bo Huo, Xiang Li, Xin Hu

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

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  16. Epigenetic Regulation of Hematopoietic Stem Cells.International journal of stem cells · 2016
    Review
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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 1 institution in 1 country.

Yidi GuoSchool of Life Sciences, Jilin University, Changchun, People's Republic of China.
Xueqi FuSchool of Life Sciences, Jilin University, Changchun, People's Republic of China ; Key Laboratory for Molecular Enzymology and Engineering of Ministry of Education, Jilin University, Changchun, People's Republic of China.
Yue JinSchool of Life Sciences, Jilin University, Changchun, People's Republic of China.
Jing SunSchool of Life Sciences, Jilin University, Changchun, People's Republic of China.
Ye LiuSchool of Life Sciences, Jilin University, Changchun, People's Republic of China.
Bo HuoSchool of Life Sciences, Jilin University, Changchun, People's Republic of China.
Xiang LiSchool of Life Sciences, Jilin University, Changchun, People's Republic of China.
Xin HuSchool of Life Sciences, Jilin University, Changchun, People's Republic of China ; Key Laboratory for Molecular Enzymology and Engineering of Ministry of Education, Jilin University, Changchun, People's Republic of China ; National Engineering Laboratory of AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, People's Republic of China.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe transcription factor GATA-2 is predominantly expressed in hematopoietic stem and progenitor cells and counteracts the erythroid-specific transcription factor GATA-1, to modulate the proliferation and differentiation of hematopoietic cells. During hematopoietic cell differentiation, GATA-2 exhibits dynamic expression patterns, which are regulated by multiple transcription factors.

methodsStable LSD1-knockdown cell lines were established by growing murine erythroleukemia (MEL) or mouse embryonic stem cells together with virus particles, in the presence of Polybrene(®) at 4 μg/mL, for 24-48 hours followed by puromycin selection (1 μg/mL) for 2 weeks. Real-time polymerase chain reaction (PCR)-based quantitative chromatin immunoprecipitation (ChIP) analysis was used to test whether the TAL1 transcription factor is bound to 1S promoter in the GATA-2 locus or whether LSD1 colocalizes with TAL1 at the 1S promoter. The sequential ChIP assay was utilized to confirm the role of LSD1 in the regulation of H3K4me2 at the GATA-2 locus during erythroid differentiation. Western blot analysis was employed to detect the protein expression. The alamarBlue(®) assay was used to examine the proliferation of the cells, and the absorbance was monitored at optical density (OD) 570 nm and OD 600 nm.

resultsIn this study, we showed that LSD1 regulates the expression of GATA-2 during erythroid differentiation. Knockdown of LSD1 results in increased GATA-2 expression and inhibits the differentiation of MEL and embryonic stem cells. Furthermore, we demonstrated that LSD1 binds to the 1S promoter of the GATA-2 locus and suppresses GATA-2 expression, via histone demethylation.

conclusionOur data revealed that LSD1 mediates erythroid differentiation, via epigenetic modification of the GATA-2 locus.

Indexed as

ErythropoiesisAnimalsBasic Helix-Loop-Helix ProteinsBinding SitesCell Line, TumorCell ProliferationDNA MethylationDown-RegulationEmbryonic Stem CellsEpigenesis, GeneticErythroid CellsGATA2 Transcription FactorGene Knockdown TechniquesHistone DemethylasesHistonesLeukemia, Erythroblastic, AcuteBasic Helix-Loop-Helix ProteinsGata2 protein, mouseGATA2 Transcription FactorHistone DemethylasesHistonesKDM1a protein, mouseProto-Oncogene ProteinsTal1 protein, mouseT-Cell Acute Lymphocytic Leukemia Protein 1GATA factor switchinghistone demethylationLSD1

Identifiers

PMID26124638
PMCPMC4482369
OpenAlexW1485310459

What OpenQuestion holds

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LicenceCC BY-NC
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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.