Evidence map›Paper›PMID 28362262›Full record

ArticleeLife2017

A type I IFN-dependent DNA damage response regulates the genetic program and inflammasome activation in macrophages.

Abigail J Morales, Javier A Carrero, Putzer J Hung, Anthony T Tubbs, Jared M Andrews, Brian T Edelson, Boris Calderon, Cynthia L Innes, Richard S Paules, Jacqueline E Payton and 1 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

44 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Secrets of DNA-PKcs beyond DNA repair.NPJ precision oncology · 2024
    Review
  10. Review
  11. When DNA-damage responses meet innate and adaptive immunity.Cellular and molecular life sciences : CMLS · 2024
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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 3 institutions in 1 country.

Abigail J MoralesDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York City, United States.ORCID 0000-0001-5148-4349
Javier A CarreroDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States.
Putzer J HungDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States.
Anthony T TubbsDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States.
Jared M AndrewsDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States.
Brian T EdelsonDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States.
Boris CalderonDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States.
Cynthia L InnesEnvironmental Stress and Cancer Group, National Institute of Environmental Health Sciences, Durham, United States.
Richard S PaulesEnvironmental Stress and Cancer Group, National Institute of Environmental Health Sciences, Durham, United States.
Jacqueline E PaytonDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States.
Barry P SleckmanDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York City, United States.ORCID 0000-0001-8295-4462
Washington University in St. Louis · USCornell University · USNational Institute of Environmental Health Sciences · US

Funding

TRAINING PROGRAM IN IMMUNOLOGY AND IMMUNOGENETICST32AI007163 · NIAID · WASHINGTON UNIVERSITY · PI Kenneth M Murphy, Kodi S Ravichandran · 1985 to 2026
$14.8M
THE V(D)J RECOMBINATION REACTION AND ITS IMPACT ON LYMPHOCYTE DEVELOPMENTR01AI047829 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI SLECKMAN, BARRY P · 2000 to 2021
$7.0M
ATM FUNCTION DURING V(D)J RECOMBINATIONR01AI074953 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI SLECKMAN, BARRY P · 2009 to 2023
$5.9M
UNDERSTANDING AUTOREACTIVE T CELL PATHOGENICITYR01AI113118 · NIAID · WASHINGTON UNIVERSITY · PI EDELSON, BRIAN TODD · 2015 to 2019
$1.9M
Molecular Analysis Of Cell Cycle Control in CarcinogenesZ01ES021157 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI PAULES, RICHARD S · 1991 to 2008
$1.7M
Intramural NIH HHS Z01 ES021157NIAID NIH HHS R01 AI047829NIAID NIH HHS R01 AI074953NIAID NIH HHS R01 AI113118NIAID NIH HHS T32 AI007163
6 · The paper itself

Abstract

Macrophages produce genotoxic agents, such as reactive oxygen and nitrogen species, that kill invading pathogens. Here we show that these agents activate the DNA damage response (DDR) kinases ATM and DNA-PKcs through the generation of double stranded breaks (DSBs) in murine macrophage genomic DNA. In contrast to other cell types, initiation of this DDR depends on signaling from the type I interferon receptor. Once activated, ATM and DNA-PKcs regulate a genetic program with diverse immune functions and promote inflammasome activation and the production of IL-1β and IL-18. Indeed, following infection with

Indexed as

Gene Expression RegulationImmunity, InnateAnimalsDNA Breaks, Double-StrandedDNA DamageInflammasomesInterferon Type IListeria monocytogenesMacrophagesMiceProtein KinasesInflammasomesInterferon Type IProtein KinasesDNA damage responsesimmunologyinflammasomemacrophageType I IFN

Identifiers

PMID28362262
PMCPMC5409825
OpenAlexW2598360917

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.