Evidence map›Paper›PMID 18598717›Full record

ReviewImmunology letters2008

Interferon-inducible Ifi200-family genes in systemic lupus erythematosus.

Divaker Choubey, Ravichandran Panchanathan

Open access · greenAbstract readReview
In one paragraph

Review in Immunology letters, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

57 citing papers in PubMed, 112 citations in OpenAlex.

  1. Article
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  12. Role of inflammasomes in inflammatory autoimmune rheumatic diseases.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018
    Review
  13. Article
  14. Article
  15. Article
  16. Absent in Melanoma 2 proteins in SLE.Clinical immunology (Orlando, Fla.) · 2017
    Review
  17. Article
  18. Review
  19. Structural biology of innate immunity.Annual review of immunology · 2015
    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 at 1 institution in 1 country.

Divaker ChoubeyDepartment of Environmental Health, University of Cincinnati, 3223 Eden Avenue, P.O. Box 670056, Cincinnati, OH 45267, United States. Divaker.choubey@uc.edu
Ravichandran Panchanathan
University of Cincinnati · US

Funding

Gender-Specific Role of p202 in Lupus SusceptibilityR01AI066261 · NIAID · UNIVERSITY OF CINCINNATI · PI CHOUBEY, DIVAKER · 2005 to 2010
$1.8M
NIAID NIH HHS AI066261NIAID NIH HHS R01 AI066261
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is the prototype of complex autoimmune diseases. Studies have suggested that genetic, hormonal, and environmental factors contribute to the development of the disease. Interestingly, several recent studies involving SLE patients and mouse models of the disease have suggested a role for interferon (IFN)-stimulated genes (ISGs) in the development of SLE. One family of ISGs is the Ifi200-family, which includes mouse (Ifi202a, Ifi202b, Ifi203, Ifi204, and Ifi205) and human (IFI16, MNDA, AIM2, and IFIX) genes. The mouse genes cluster between serum amyloid P-component (Apcs) and alpha-spectrin (Spna-1) genes on chromosome 1 and the human genes cluster in syntenic region 1q23. The Ifi200-family genes encode structurally and functionally related proteins (the p200-family proteins). Increased expression of certain p200-family proteins in cells is associated with inhibition of cell proliferation, modulation of apoptosis, and cell differentiation. Our studies involving generation of B6.Nba2 congenic mice, coupled with gene expression analyses, identified the Ifi202 as a candidate lupus-susceptibility gene. Importantly, recent studies using different mouse models of SLE have suggested that increased expression of Ifi202 gene (encoding p202 protein) in immune cells contributes to lupus susceptibility. Consistent with a functional role for the p202 protein in lupus susceptibility, increased levels of IFI16 protein in human SLE patients are associated with the diseases. This review summarizes recent findings concerning the regulation and role of p200-family proteins in the development of SLE.

Indexed as

AnimalsApoptosisCell ProliferationFeedback, PhysiologicalGene Expression RegulationGenetic Predisposition to DiseaseHumansIntracellular Signaling Peptides and ProteinsLupus Erythematosus, SystemicMiceNuclear ProteinsPhosphoproteinsPolymorphism, GeneticPromoter Regions, GeneticSex FactorsTranscriptional ActivationIFI16 protein, humanIfi202b protein, mouseIntracellular Signaling Peptides and ProteinsNuclear ProteinsPhosphoproteins

Identifiers

PMID18598717
PMCPMC2585765
OpenAlexW2093658865

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.