Evidence map›Paper›PMID 22801367›Full record

ArticleMolecular and cellular biology2012

Negative regulation of JAK2 by H3K9 methyltransferase G9a in leukemia.

Hye-Ju Son, Ji-Young Kim, Yoonsoo Hahn, Sang-Beom Seo

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Hye-Ju SonDepartment of Life Science, College of Natural Sciences, Research Center for Biomolecules and Biophysics, Chung-Ang University, Seoul, Republic of Korea.
Ji-Young Kim
Yoonsoo Hahn
Sang-Beom Seo
Chung-Ang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone methylation at specific lysine residues is a crucial regulatory process in transcriptional regulation. Using chromatin immunoprecipitation with microarray technology (ChIP-chip) analysis, we found that the H3K9-me2 target gene JAK2 was an important factor during differentiation of the HL-60 promyelocytic leukemia cell line by all-trans-retinoic acid (ATRA) treatment. Here, we report that the H3K9 methyltransferase G9a negatively regulated JAK2 transcription in histone methyltransferase activity and in a YY1-dependent manner during ATRA-mediated leukemia cell differentiation. We found that G9a knockdown repressed ATRA-mediated HL-60 cell differentiation. We demonstrated that G9a interacts with YY1 and is recruited to the JAK2 promoter along with corepressors, including histone deacetylase, that induced H3K9-me2. Repression of JAK2 transcription by G9a decreased H3Y41 phosphorylation and promoted inhibition of the recently identified JAK2-H3Y41P-HP1α pathway-mediated leukemogenesis.

Indexed as

Adaptor Proteins, Signal TransducingCell DifferentiationChromobox Protein Homolog 5Gene Expression Regulation, NeoplasticHistocompatibility AntigensHistone-Lysine N-MethyltransferaseHL-60 CellsHumansJanus Kinase 2K562 CellsLeukemiaLIM Domain ProteinsMethylationPhosphorylationPromoter Regions, GeneticProto-Oncogene ProteinsAdaptor Proteins, Signal TransducingCBX5 protein, humanChromobox Protein Homolog 5EHMT2 protein, humanHistocompatibility AntigensHistone-Lysine N-MethyltransferaseJAK2 protein, humanJanus Kinase 2LIM Domain ProteinsLMO2 protein, humanProto-Oncogene ProteinsTretinoinYY1 protein, humanYY1 Transcription Factor

Identifiers

PMID22801367
PMCPMC3430193
OpenAlexW2122694008

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.