Evidence map›Paper›PMID 23842753›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Irgm1 (LRG-47), a regulator of cell-autonomous immunity, does not localize to mycobacterial or listerial phagosomes in IFN-γ-induced mouse cells.

Helen M Springer, Michael Schramm, Gregory A Taylor, Jonathan C Howard

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.9field-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

30 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Macrophages From Latently Infected Mice Have Trained Immunity to HSV-1.Investigative ophthalmology & visual science · 2026
    Article
  3. Article
  4. Review
  5. Autophagy and Bacterial infections.Autophagy reports · 2025
    Review
  6. Article
  7. Article
  8. Type I IFN signaling in the absence of IRGM1 promotesbioRxiv : the preprint server for biology · 2023
    Article
  9. Article
  10. International journal of molecular sciences · 2023
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Molecular and cellular biology · 2020
    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

4 authors at 3 institutions in 3 countries.

Helen M SpringerInstitute for Genetics, University of Cologne, 50674 Cologne, Germany.
Michael Schramm
Gregory A Taylor
Jonathan C Howard
University of Cologne · DEDuke University Hospital · USInstitute of Medical Microbiology and Hygiene · DE

Funding

Regulation of IFN-g-induced Innate Immunity by LRG-47R01AI057831 · NIAID · DUKE UNIVERSITY · PI TAYLOR, GREGORY A · 2004 to 2013
$3.1M
NIAID NIH HHS AI57831NIAID NIH HHS R01 AI057831
6 · The paper itself

Abstract

The IFN-inducible protein Irgm1 (LRG-47) belongs to the family of immunity-related GTPases that function in cell-autonomous resistance against intracellular pathogens in mice. Irgm1 deficiency is associated with a severe immunodeficiency syndrome. The protein has been variously interpreted as a direct effector molecule on bacterial phagosomes or on other organelles or as an inducer of autophagy. In this study, we re-examined one of these claims, namely that Irgm1 targets mycobacterial and listerial phagosomes. We found no colocalization of endogenous Irgm1, using two immunofluorescent staining techniques, either in fibroblasts or in macrophages. We demonstrated the predicted existence of two protein isoforms of Irgm1 derived from differential splicing and described immunological reagents for their detection. Both Irgm1 isoforms localize to the Golgi apparatus and weakly to mitochondria; however, only the long Irgm1 isoforms can be detected on endolysosomal membranes. Together with the previous observation that the general immunodeficiency phenotype of Irgm1(-/-) mice is reversed in Irgm1/Irgm3 double-deficient mice, our results argue against a direct effector function of Irgm1 at the bacterial phagosome. We discuss these findings in the context of evidence that Irgm1 functions as a negative regulator of other members of the immunity-related GTPase protein family.

Indexed as

Alternative SplicingAmino Acid SequenceAnimalsAntibody SpecificityCell LineFibroblastsFluorescent Antibody Technique, DirectGolgi ApparatusGTP-Binding ProteinsGTP PhosphohydrolasesHumansImmunizationImmunologic Deficiency SyndromesInterferon-gammaListeria monocytogenesMacrophagesGTP-Binding ProteinsGTP PhosphohydrolasesIfi1 protein, mouseInterferon-gammaPeptide FragmentsProtein Isoforms

Identifiers

PMID23842753
PMCPMC3753587
OpenAlexW2161527377

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.