Evidence map›Paper›PMID 28062222›Full record

ReviewClinical immunology (Orlando, Fla.)2017

Absent in Melanoma 2 proteins in SLE.

Divaker Choubey, Ravichandran Panchanathan

Abstract readReview
In one paragraph

Review in Clinical immunology (Orlando, Fla.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Article
  2. Article
  3. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. The role of inflammasomes in cutaneous pathology.Postepy dermatologii i alergologii · 2022
    Review
  8. Review
  9. Review
  10. Article
  11. Structure, Activation and Regulation of NLRP3 and AIM2 Inflammasomes.International journal of molecular sciences · 2021
    Review
  12. Complementary regulation of caspase-1 and IL-1β reveals additional mechanisms of dampened inflammation in bats.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  13. The advances in pyroptosis initiated by inflammasome in inflammatory and immune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Review
  14. Nucleic Acid Sensors and Programmed Cell Death.Journal of molecular biology · 2020
    Review
  15. Review
  16. Review
  17. Review
  18. AIM2 levels and DNA-triggered inflammasome response are increased in peripheral leukocytes of patients with abdominal aortic aneurysm.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    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

2 authors.

Divaker ChoubeyDepartment of Environmental Health, University of Cincinnati, 160 Panzeca Way, P. O. Box-670056, Cincinnati, OH 45267, United States; Research Service, ML-151, Cincinnati VA Medical Center, 3200 Vine Street, Cincinnati, OH 45220, United States. Electronic address: Divaker.choubey@uc.edu.
Ravichandran PanchanathanDepartment of Environmental Health, University of Cincinnati, 160 Panzeca Way, P. O. Box-670056, Cincinnati, OH 45267, United States; Research Service, ML-151, Cincinnati VA Medical Center, 3200 Vine Street, Cincinnati, OH 45220, United States.

Funding

Gender-Specific Role of Aim2 in Inflammation and AutoimmunityR56AI089775 · NIAID · UNIVERSITY OF CINCINNATI · PI CHOUBEY, DIVAKER · 2011 to 2011
$393k
AIM2 and IFI16 Innate Immune Sensors for Cytosolic DNA in Prostatic DiseasesI01BX001133 · VA · CINCINNATI VA MEDICAL CENTER RESEARCH · PI CHOUBEY, DIVAKER · 2012 to 2015
–
BLRD VA I01 BX001133NIAID NIH HHS R56 AI089775
6 · The paper itself

Abstract

Type I interferons (IFN-α/β)-inducible PYRIN and HIN domain-containing protein family includes Absent in Melanoma 2 (murine Aim2 and human AIM2), murine p202, and human PYRIN-only protein 3 (POP3). The generation of Aim2-deficient mice indicated that the Aim2 protein is essential for inflammasome activation, resulting in the secretion of interleukin-1β (IL-1β) and IL-18 and cell death by pyroptosis. Further, Aim2-deficiency also increased constitutive expression of the IFN-β and expression of the p202 protein. Notably, an increased expression of p202 protein in female mice associated with the development of systemic lupus erythematosus (SLE). SLE in patients is characterized by a constitutive increase in serum levels of IFN-α and an increase in the expression IFN-stimulated genes. Recent studies indicate that p202 and POP3 proteins inhibit activation of the Aim2/AIM2 inflammasome and promote IFN-β expression. Therefore, we discuss the role of Aim2/AIM2 proteins in the suppression of type I IFNs production and lupus susceptibility.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsDNA-Binding ProteinsHumansInterferon Type IInterleukin-18Interleukin-1betaLupus Erythematosus, SystemicMelanomaTumor Suppressor p53-Binding Protein 1Adaptor Proteins, Signal TransducingDNA-Binding ProteinsInterferon Type IInterleukin-18Interleukin-1betaTumor Suppressor p53-Binding Protein 1AIM2IFN-signatureInflammasomeInterferonLupus

Identifiers

PMID28062222
PMCPMC5346332

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.