Evidence map›Paper›PMID 30488027›Full record

ArticleFrontiers in cellular and infection microbiology2018

NLRX1 Negatively Regulates Group A

Chihiro Aikawa, Shintaro Nakajima, Miho Karimine, Takashi Nozawa, Atsuko Minowa-Nozawa, Hirotaka Toh, Shunsuke Yamada, Ichiro Nakagawa

Abstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024
    Review
  4. The NLR gene family: from discovery to present day.Nature reviews. Immunology · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Focusing on the Cell Type Specific Regulatory Actions of NLRX1.International journal of molecular sciences · 2021
    Review
  9. NLRP12 in innate immunity and inflammation.Molecular aspects of medicine · 2020
    Review
  10. Article
  11. Behind the Scenes: Nod-Like Receptor X1 Controls Inflammation and Metabolism.Frontiers in cellular and infection microbiology · 2020
    Review
  12. Article
  13. 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

8 authors.

Chihiro AikawaDepartment of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Shintaro NakajimaDepartment of Life Science Dentistry, The Nippon Dental University, Tokyo, Japan.
Miho KarimineDepartment of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Takashi NozawaDepartment of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Atsuko Minowa-NozawaDepartment of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Hirotaka TohDepartment of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Shunsuke YamadaDepartment of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Ichiro NakagawaDepartment of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Group A

Indexed as

AutophagosomesAutophagyBeclin-1CRISPR-Cas SystemsGene Knockout TechniquesHeLa CellsHost-Pathogen InteractionsHumansLysosomesMitochondrial ProteinsStreptococcal InfectionsStreptococcus pyogenesTumor Suppressor ProteinsBeclin-1Mitochondrial ProteinsNLRX1 protein, humanTumor Suppressor ProteinsUVRAG protein, humanautophagybacterial invasionBeclin 1Group A StreptococcusNLRX1UVRAG

Identifiers

PMID30488027
PMCPMC6246980

What OpenQuestion holds

Textmetadata
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.