Evidence map›Paper›PMID 24376899›Full record

ArticlePloS one2013

Autophagy adaptor protein p62/SQSTM1 and autophagy-related gene Atg5 mediate autophagosome formation in response to Mycobacterium tuberculosis infection in dendritic cells.

Shintaro Seto, Kunio Tsujimura, Toshinobu Horii, Yukio Koide

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

45 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
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  7. Transcriptional regulatorsMicrobiology spectrum · 2024
    Article
  8. Recognition of Mycobacterium tuberculosis by macrophage Toll-like receptor and its role in autophagy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Review
  9. Negative Regulation of Autophagy during Macrophage Infection byInternational journal of molecular sciences · 2024
    Article
  10. Review
  11. Article
  12. Review
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  14. Different modalities of host cell death and their impact onAmerican journal of physiology. Cell physiology · 2022
    Review
  15. Review
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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

4 authors at 1 institution in 1 country.

Shintaro SetoDepartment of Infectious Diseases, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan.
Kunio TsujimuraDepartment of Infectious Diseases, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan.
Toshinobu HoriiDepartment of Infectious Diseases, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan.
Yukio KoideDepartment of Infectious Diseases, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan.
Hamamatsu University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mycobacterium tuberculosis is an intracellular pathogen that can survive within phagocytic cells by inhibiting phagolysosome biogenesis. However, host cells can control the intracellular M. tuberculosis burden by the induction of autophagy. The mechanism of autophagosome formation to M. tuberculosis has been well studied in macrophages, but remains unclear in dendritic cells. We therefore characterized autophagosome formation in response to M. tuberculosis infection in dendritic cells. Autophagy marker protein LC3, autophagy adaptor protein p62/SQSTM1 (p62) and ubiquitin co-localized to M. tuberculosis in dendritic cells. Mycobacterial autophagosomes fused with lysosomes during infection, and major histcompatibility complex class II molecules (MHC II) also localized to mycobacterial autophagosomes. The proteins p62 and Atg5 function in the initiation and progression of autophagosome formation to M. tuberculosis, respectively; p62 mediates ubiquitination of M. tuberculosis and Atg5 is involved in the trafficking of degradative vesicles and MHC II to mycobacterial autophagosomes. These results imply that the autophagosome formation to M. tuberculosis in dendritic cells promotes the antigen presentation of mycobacterial peptides to CD4(+) T lymphocytes via MHC II.

Indexed as

Mycobacterium tuberculosisAdaptor Proteins, Signal TransducingAnimalsAntibodies, MonoclonalAutophagyAutophagy-Related Protein 5Dendritic CellsHeat-Shock ProteinsImmunoblottingMacrophagesMiceMice, Inbred C57BLMicroscopy, ElectronMicroscopy, FluorescenceMicrotubule-Associated ProteinsPhagosomesAdaptor Proteins, Signal TransducingAntibodies, MonoclonalAtg5 protein, mouseAutophagy-Related Protein 5Heat-Shock ProteinsMap1lc3b protein, mouseMicrotubule-Associated ProteinsRNA, Small InterferingSequestosome-1 ProteinSqstm1 protein, mouse

Identifiers

PMID24376899
PMCPMC3871604
OpenAlexW2029589408

What OpenQuestion holds

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LicenceCC BY
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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.