Evidence map›Paper›PMID 28855250›Full record

ReviewThe Journal of cell biology2017

Crossed wires: 3D genome misfolding in human disease.

Heidi K Norton, Jennifer E Phillips-Cremins

Abstract readReview
In one paragraph

Review in The Journal of cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing 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

37 citing papers in PubMed.

  1. Polymorphic 3D genome architecture mediated by transposable elements.bioRxiv : the preprint server for biology · 2026
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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

2 authors.

Heidi K NortonDepartment of Bioengineering, University of Pennsylvania, Philadelphia, PA.
Jennifer E Phillips-CreminsDepartment of Bioengineering, University of Pennsylvania, Philadelphia, PA jcremins@seas.upenn.edu.ORCID 0000-0002-4702-0450

Funding

Engineering and visualizing genome folding at high spatiotemporal resolutionU01HL129998 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI BLOBEL, GERD A, PHILLIPS-CREMINS, JENNIFER ELIZABETH · 2015 to 2019
$4.2M
NHLBI NIH HHS U01 HL129998
6 · The paper itself

Abstract

Mammalian genomes are folded into unique topological structures that undergo precise spatiotemporal restructuring during healthy development. Here, we highlight recent advances in our understanding of how the genome folds inside the 3D nucleus and how these folding patterns are miswired during the onset and progression of mammalian disease states. We discuss potential mechanisms underlying the link among genome misfolding, genome dysregulation, and aberrant cellular phenotypes. We also discuss cases in which the endogenous 3D genome configurations in healthy cells might be particularly susceptible to mutation or translocation. Together, these data support an emerging model in which genome folding and misfolding is critically linked to the onset and progression of a broad range of human diseases.

Indexed as

Chromosomes, HumanGenome, HumanNucleic Acid ConformationAnimalsCCCTC-Binding FactorCell NucleusEnhancer Elements, GeneticGene DeletionGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseHumansMutationNeoplasmsPhenotypePromoter Regions, GeneticProtein BindingCCCTC-Binding Factor

Identifiers

PMID28855250
PMCPMC5674879

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.