Evidence map›Paper›PMID 24395799›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Analysis of chromatin-state plasticity identifies cell-type-specific regulators of H3K27me3 patterns.

Luca Pinello, Jian Xu, Stuart H Orkin, Guo-Cheng Yuan

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 76 citations in OpenAlex.

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  18. Epigenetic Changes Induced byInfection and immunity · 2019
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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 2 institutions in 1 country.

Luca PinelloDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer Institute and Harvard School of Public Heath, Boston, MA 02215.
Jian Xu
Stuart H Orkin
Guo-Cheng Yuan
Dana-Farber Cancer Institute · USBoston Children's Hospital · US

Funding

CORE--VECTOR PRODUCTIONP30DK056465 · NIDDK · FRED HUTCHINSON CANCER RESEARCH CENTER · PI TOROK-STORB, BEVERLY J. · 1999 to 2014
$14.9M
MOLECULAR ANALYSIS OF NORMAL AND TYHALASSEMIC DNAR01HL032259 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI ORKIN, STUART H · 1985 to 2022
$8.8M
Toward a systematic understanding of targeting mechanisms for epigenetic factorsR01HG005085 · NHGRI · DANA-FARBER CANCER INST · PI YUAN, GUO-CHENG · 2011 to 2014
$1.7M
Mechanistic roles of BCL11A in globin switching and fetal hemoglobin silencingK01DK093543 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI XU, JIAN · 2011 to 2015
$732k
A guided approach to interrogating genome-wide chromatin interactionsR21HG006778 · NHGRI · DANA-FARBER CANCER INST · PI YUAN, GUO-CHENG · 2012 to 2013
$481k
Howard Hughes Medical InstituteNHGRI NIH HHS R01 HG005085NHGRI NIH HHS R01HG005085NHGRI NIH HHS R21 HG006778NHLBI NIH HHS P01HL03262NHLBI NIH HHS R01 HL032259NHLBI NIH HHS R01HL32259NIDDK NIH HHS K01 DK093543NIDDK NIH HHS K01DK093543NIDDK NIH HHS P30 DK056465
6 · The paper itself

Abstract

Chromatin states are highly cell-type-specific, but the underlying mechanisms for the establishment and maintenance of their genome-wide patterns remain poorly understood. Here we present a computational approach for investigation of chromatin-state plasticity. We applied this approach to investigate an ENCODE ChIP-seq dataset profiling the genome-wide distributions of the H3K27me3 mark in 19 human cell lines. We found that the high plasticity regions (HPRs) can be divided into two functionally and mechanistically distinct subsets, which correspond to CpG island (CGI) proximal or distal regions, respectively. Although the CGI proximal HPRs are typically associated with continuous variation across different cell-types, the distal HPRs are associated with binary-like variations. We developed a computational approach to predict putative cell-type-specific modulators of H3K27me3 patterns and validated the predictions by comparing with public ChIP-seq data. Furthermore, we applied this approach to investigate mechanisms for poised enhancer establishment in primary human erythroid precursors. Importantly, we predicted and experimentally validated that the principal hematopoietic regulator T-cell acute lymphocytic leukemia-1 (TAL1) is involved in regulating H3K27me3 variations in collaboration with the transcription factor growth factor independent 1B (GFI1B), providing fresh insights into the context-specific role of TAL1 in erythropoiesis. Our approach is generally applicable to investigate the regulatory mechanisms of epigenetic pathways in establishing cellular identity.

Indexed as

Gene Expression RegulationAmino Acid MotifsArea Under CurveBasic Helix-Loop-Helix ProteinsCell LineChromatinComputational BiologyCpG IslandsEpigenesis, GeneticErythroid CellsGenetic VariationHematopoiesisHistonesHumansPolycomb-Group ProteinsProto-Oncogene ProteinsBasic Helix-Loop-Helix ProteinsChromatinGFI1B protein, humanHistonesPolycomb-Group ProteinsProto-Oncogene ProteinsRepressor ProteinsTAL1 protein, humanT-Cell Acute Lymphocytic Leukemia Protein 1Transcription Factorshematopoiesishistone modificationsmotifspolycomb

Identifiers

PMID24395799
PMCPMC3903219
OpenAlexW1997151052

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.