Evidence map›Paper›PMID 32484234›Full record

ArticleFEBS letters2020

SON DNA-binding protein mediates macrophage autophagy and responses to intracellular infection.

David J Gregory, Glen M DeLoid, Sharon L Salmon, Dennis W Metzger, Igor Kramnik, Lester Kobzik

Open access · bronzeAbstract read
In one paragraph

Article in FEBS letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Identification of theFrontiers in cellular and infection microbiology · 2025
    Article
  5. Article
  6. Article
  7. Article
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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

6 authors at 3 institutions in 2 countries.

David J GregoryMolecular and Physiological Sciences Program, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA.ORCID 0000-0001-6534-7150
Glen M DeLoidMolecular and Physiological Sciences Program, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Sharon L SalmonDepartment of Immunology and Microbial Disease, Albany Medical College, Albany, NY, USA.
Dennis W MetzgerDepartment of Immunology and Microbial Disease, Albany Medical College, Albany, NY, USA.
Igor KramnikPulmonary Center, Department of Medicine, National Emerging Infectious Diseases Laboratories, Boston University School of Medicine, MA, USA.
Lester KobzikMolecular and Physiological Sciences Program, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Harvard University · USAlbany Medical Center Hospital · USBoston University · US

Funding

Translational Research Support CoreP30ES000002 · NIEHS · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI JAIME ELIZABETH HART · 1985 to 2026
$44.6M
Necrosis in pulmonary TB granulomas: dynamics, mechanisms, therapiesR01HL126066 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KRAMNIK, IGOR, NIEDERWEIS, MICHAEL · 2016 to 2025
$5.6M
Aberrant immune activation in the tuberculosis granuloma: a pivotal role in necrosisR01HL133190 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BISHAI, WILLIAM RAMSES, KRAMNIK, IGOR · 2016 to 2019
$3.0M
NHLBI NIH HHS R01 HL126066NHLBI NIH HHS R01 HL133190NIEHS NIH HHS P30 ES000002
6 · The paper itself

Abstract

Intracellular pathogens affect diverse host cellular defence and metabolic pathways. Here, we used infection with Francisella tularensis to identify SON DNA-binding protein as a central determinant of macrophage activities. RNAi knockdown of SON increases survival of human macrophages following F. tularensis infection or inflammasome stimulation. SON is required for macrophage autophagy, interferon response factor 3 expression, type I interferon response and inflammasome-associated readouts. SON knockdown has gene- and stimulus-specific effects on inflammatory gene expression. SON is required for accurate splicing and expression of GBF1, a key mediator of cis-Golgi structure and function. Chemical GBF1 inhibition has similar effects to SON knockdown, suggesting that SON controls macrophage functions at least in part by controlling Golgi-associated processes.

Indexed as

AutophagyCell DeathCell DifferentiationCell LineCell SurvivalDNA-Binding ProteinsFrancisella tularensisGene Expression ProfilingGene Expression RegulationGolgi ApparatusGuanine Nucleotide Exchange FactorsHost-Pathogen InteractionsHumansInflammasomesInterferon Regulatory Factor-3MacrophagesDNA-Binding ProteinsGBF1 protein, humangolgicide AGuanine Nucleotide Exchange FactorsInflammasomesInterferon Regulatory Factor-3IRF3 protein, humanMinor Histocompatibility AntigensPyridinesQuinolinesRNA, Small InterferingSON protein, humanTetradecanoylphorbol AcetateautophagyFrancisella tularensisgene expressionhost-pathogen interactionsinflammasomeinterferon response

Identifiers

PMID32484234
PMCPMC7708400
OpenAlexW3031953954

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.