Evidence map›Paper›PMID 39337329›Full record

ArticleInternational journal of molecular sciences2024

Network Analysis of Enhancer-Promoter Interactions Highlights Cell-Type-Specific Mechanisms of Transcriptional Regulation Variation.

Justin Koesterich, Jiayi Liu, Sarah E Williams, Nan Yang, Anat Kreimer

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Justin KoesterichGraduate Programs in Molecular Biosciences, Rutgers The State University of New Jersey, 604 Allison Rd., Piscataway, NJ 08854, USA.ORCID 0000-0001-8195-5666
Jiayi LiuGraduate Programs in Molecular Biosciences, Rutgers The State University of New Jersey, 604 Allison Rd., Piscataway, NJ 08854, USA.ORCID 0000-0001-6432-0124
Sarah E WilliamsNash Family Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.ORCID 0000-0003-3624-611X
Nan YangNash Family Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Anat KreimerGraduate Programs in Molecular Biosciences, Rutgers The State University of New Jersey, 604 Allison Rd., Piscataway, NJ 08854, USA.ORCID 0000-0002-3066-5498

Funding

Functional mapping of noncoding regulatory variants in human neuronal subtypes3.R01MH129372 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Nan Yang · 2022 to 2026
$3.4M
Early Epigenetic Footprint of Neurological DiseasesR00MH117393 · NIMH · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI KREIMER, ANAT · 2020 to 2022
$747k
Cell-type specific and activity-dependent characterization of non-coding autism de novo variants in human stem cell-derived neuronsF31MH133365 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI WILLIAMS, SARAH ELIZABETH · 2023 to 2025
$146k
NIMH NIH HHS F31 MH133365NIMH NIH HHS F31MH133365NIMH NIH HHS R00MH117393-05NIMH NIH HHS R01 MH129372NIMH NIH HHS R01MH129372Simons Foundation 1012863NY
6 · The paper itself

Abstract

Gene expression is orchestrated by a complex array of gene regulatory elements that govern transcription in a cell-type-specific manner. Though previously studied, the ability to utilize regulatory elements to identify disrupting variants remains largely elusive. To identify important factors within these regions, we generated enhancer-promoter interaction (EPI) networks and investigated the presence of disease-associated variants that fall within these regions. Our study analyzed six neuronal cell types across neural differentiation, allowing us to examine closely related cell types and across differentiation stages. Our results expand upon previous findings of cell-type specificity of enhancer, promoter, and transcription factor binding sites. Notably, we find that regulatory regions within EPI networks can identify the enrichment of variants associated with neuropsychiatric disorders within specific cell types and network sub-structures. This enrichment within sub-structures can allow for a better understanding of potential mechanisms by which variants may disrupt transcription. Together, our findings suggest that EPIs can be leveraged to better understand cell-type-specific regulatory architecture and used as a selection method for disease-associated variants to be tested in future functional assays. Combined with these future functional characterization assays, EPIs can be used to better identify and characterize regulatory variants' effects on such networks and model their mechanisms of gene regulation disruption across different disorders. Such findings can be applied in practical settings, such as diagnostic tools and drug development.

Indexed as

Enhancer Elements, GeneticGene Expression RegulationGene Regulatory NetworksPromoter Regions, GeneticBinding SitesCell DifferentiationHumansNeuronsTranscription FactorsTranscription, GeneticTranscription Factorsautismcell networksdisease geneticsenhancer–promoter interactionepigenetics

Identifiers

PMID39337329
PMCPMC11432627

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Registered trials

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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.