Evidence map›Paper›PMID 32615442›Full record

ArticleDNA repair2020

TREX1 - Apex predator of cytosolic DNA metabolism.

Sean R Simpson, Wayne O Hemphill, Teesha Hudson, Fred W Perrino

Open access · greenAbstract read
In one paragraph

Article in DNA repair, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 54 citations in OpenAlex.

  1. Autoinflammatory syndromes of STING and TREX1 dysfunction.The Journal of clinical investigation · 2026
    Review
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  16. How Does cGAS Avoid Sensing Self-DNA under Normal Physiological Conditions?International journal of molecular sciences · 2023
    Review
  17. Article
  18. Multiple RNA- and DNA-binding proteins exhibit direct transfer of polynucleotides with implications for target-site search.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  19. Article
  20. Article
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.

Sean R SimpsonDepartment of Biochemistry, Center for Structural Biology, Wake Forest School of Medicine, Winston-Salem, NC 27157, United States.
Wayne O HemphillDepartment of Biochemistry, Center for Structural Biology, Wake Forest School of Medicine, Winston-Salem, NC 27157, United States.
Teesha HudsonDepartment of Biochemistry, Center for Structural Biology, Wake Forest School of Medicine, Winston-Salem, NC 27157, United States.
Fred W PerrinoDepartment of Biochemistry, Center for Structural Biology, Wake Forest School of Medicine, Winston-Salem, NC 27157, United States. Electronic address: fperrino@wakehealth.edu.
Wake Forest University · US

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
TRAINING PROGRAM IN IMMUNOLOGY AND PATHOGENESIST32AI007401 · NIAID · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Martha Ann Alexander-Miller · 1991 to 2026
$4.4M
The TREX1 Pathway in Autoimmune DiseaseR01AI116725 · NIAID · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI PERRINO, FRED W · 2016 to 2020
$1.9M
Structural and Computational Biophysics Training ProgramT32GM095440 · NIGMS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI HOLLIS, THOMAS J, LYLES, DOUGLAS S. · 2011 to 2020
$1.7M
NCI NIH HHS P30 CA012197NIAID NIH HHS R01 AI116725NIAID NIH HHS T32 AI007401NIGMS NIH HHS T32 GM095440
6 · The paper itself

Abstract

The cytosolic Three prime Repair EXonuclease 1 (TREX1) is a powerful DNA-degrading enzyme required for clearing cytosolic DNA to prevent aberrant inflammation and autoimmunity. In the absence of TREX1 activity, cytosolic DNA pattern recognition receptors of the innate immune system are constitutively activated by undegraded TREX1 substrates. This triggers a chronic inflammatory response in humans expressing mutant TREX1 alleles, eliciting a spectrum of rare autoimmune diseases dependent on the nature of the mutation. The precise origins of cytosolic DNA targeted by TREX1 continue to emerge, but DNA emerging from the nucleus or taken up by the cell could represent potential sources. In this Review, we explore the biochemical and immunological data supporting the role of TREX1 in suppressing cytosolic DNA sensing, and discuss the possibility that TREX1 may contribute to maintenance of genome integrity.

Indexed as

MutationAnimalsAutoimmunityCytosolDNAExodeoxyribonucleasesHumansInflammationPhosphoproteinsDNAExodeoxyribonucleasesPhosphoproteinsthree prime repair exonuclease 1AutoimmunityCytosolic DNA metabolismDNA sensingGenome stabilityTREX1

Identifiers

PMID32615442
PMCPMC7985832
OpenAlexW3034266984

What OpenQuestion 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 OpenQuestion graph.