Evidence map›Paper›PMID 33176162›Full record

ArticleMolecular cell2020

Poison Exon Splicing Regulates a Coordinated Network of SR Protein Expression during Differentiation and Tumorigenesis.

Nathan K Leclair, Mattia Brugiolo, Laura Urbanski, Shane C Lawson, Ketan Thakar, Marina Yurieva, Joshy George, John Travis Hinson, Albert Cheng, Brenton R Graveley and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

106 citing papers in PubMed, 154 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Predicting human mRNA isoform levels from site-specific splicing kineticsbioRxiv : the preprint server for biology · 2026
    Article
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  7. Article
  8. Article
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  13. Review
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  15. Article
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  17. Review
  18. Review
  19. Article
  20. Ultra-Conserved Poison Exons Enable Rapid and Safe Splicing Factor Gene Expression Switches: A Hypothesis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review

46 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 1 country.

Nathan K LeclairThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA; Graduate Program in Genetics and Development, UConn Health, Farmington, CT, USA.
Mattia BrugioloThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA.
Laura UrbanskiThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA; Graduate Program in Genetics and Development, UConn Health, Farmington, CT, USA.
Shane C LawsonGraduate Program in Genetics and Development, UConn Health, Farmington, CT, USA; Department of Genetics and Genome Sciences, UConn Health, Farmington, CT, USA.
Ketan ThakarThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA.
Marina YurievaThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA.
Joshy GeorgeThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA; Institute for Systems Genomics, UConn Health, Farmington, CT, USA.
John Travis HinsonThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA; Department of Genetics and Genome Sciences, UConn Health, Farmington, CT, USA.
Albert ChengThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA; Department of Genetics and Genome Sciences, UConn Health, Farmington, CT, USA; Institute for Systems Genomics, UConn Health, Farmington, CT, USA.
Brenton R GraveleyDepartment of Genetics and Genome Sciences, UConn Health, Farmington, CT, USA; Institute for Systems Genomics, UConn Health, Farmington, CT, USA.
Olga AnczukówThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA; Department of Genetics and Genome Sciences, UConn Health, Farmington, CT, USA; Institute for Systems Genomics, UConn Health, Farmington, CT, USA. Electronic address: olga.anczukow@jax.org.
Jackson Laboratory · USUConn Health · US

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI Anna Karolina Palucka · 1985 to 2026
$61.9M
Genomic Analysis of Nucleic Acid TransactionsR35GM118140 · NIGMS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI GRAVELEY, BRENTON R. · 2016 to 2025
$6.8M
Modular Platform for Combinatorial Epigenome ManipulationR01HG009900 · NHGRI · JACKSON LABORATORY · PI ADAMS, MARK D · 2018 to 2022
$3.7M
Comprehensive Analysis of Allelic, Cellular and Molecular Heterogeneity in Human 3-Dimensional Cardiac Microtissues with MYH7 MutationsR01HL142787 · NHLBI · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI HINSON, JOHN TRAVIS · 2018 to 2021
$2.1M
Mechanisms of post-transcriptional regulation of splicing factorsR01GM138541 · NIGMS · JACKSON LABORATORY · PI ANCZUKOW-CAMARDA, OLGA · 2020 to 2024
$2.1M
Human cardiac microtissues with innate immune sensing to study adverse consequences of genome editingU01EB028898 · NIBIB · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI HINSON, JOHN TRAVIS · 2019 to 2019
$752k
Role of Splicing Factors in Breast CancerR00CA178206 · NCI · JACKSON LABORATORY · PI ANCZUKOW-CAMARDA, OLGA · 2016 to 2018
$747k
NCI NIH HHS P30 CA034196NCI NIH HHS R00 CA178206NHGRI NIH HHS R01 HG009900NHLBI NIH HHS R01 HL142787NIBIB NIH HHS U01 EB028898NIGMS NIH HHS R01 GM138541NIGMS NIH HHS R35 GM118140
6 · The paper itself

Abstract

The RNA isoform repertoire is regulated by splicing factor (SF) expression, and alterations in SF levels are associated with disease. SFs contain ultraconserved poison exon (PE) sequences that exhibit greater identity across species than nearby coding exons, but their physiological role and molecular regulation is incompletely understood. We show that PEs in serine-arginine-rich (SR) proteins, a family of 14 essential SFs, are differentially spliced during induced pluripotent stem cell (iPSC) differentiation and in tumors versus normal tissues. We uncover an extensive cross-regulatory network of SR proteins controlling their expression via alternative splicing coupled to nonsense-mediated decay. We define sequences that regulate PE inclusion and protein expression of the oncogenic SF TRA2β using an RNA-targeting CRISPR screen. We demonstrate location dependency of RS domain activity on regulation of TRA2β-PE using CRISPR artificial SFs. Finally, we develop splice-switching antisense oligonucleotides to reverse the increased skipping of TRA2β-PE detected in breast tumors, altering breast cancer cell viability, proliferation, and migration.

Indexed as

Cell DifferentiationExonsRNA SplicingBreast NeoplasmsFemaleHumansMyelodysplastic SyndromesNerve Tissue ProteinsProtein IsoformsSerine-Arginine Splicing FactorsTumor Cells, CulturedNerve Tissue ProteinsProtein IsoformsSerine-Arginine Splicing FactorsTRA2B protein, humanRNA splicing, SR proteins, differentiation, cancer, cross-regulation, antisense oligonucleotides, CRISPR/Cas13, CRISPR-Artificial Splicing Factors, alternative splicing, oncogene

Identifiers

PMID33176162
PMCPMC7680420
OpenAlexW3100281265

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.