Evidence map›Paper›PMID 18424712›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Disruption of mutually negative regulatory feedback loop between interferon-inducible p202 protein and the E2F family of transcription factors in lupus-prone mice.

Ravichandran Panchanathan, Hong Xin, Divaker Choubey

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. 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
  7. Absent in Melanoma 2 proteins in SLE.Clinical immunology (Orlando, Fla.) · 2017
    Review
  8. Absent in melanoma 2 proteins in the development of cancer.Cellular and molecular life sciences : CMLS · 2016
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Emerging roles for the interferon-inducible p200-family proteins in sex bias in systemic lupus erythematosus.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2011
    Review
  15. Interferon-inducible p200-family proteins as novel sensors of cytoplasmic DNA: role in inflammation and autoimmunity.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2010
    Review
  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

3 authors at 1 institution in 1 country.

Ravichandran PanchanathanDepartment of Environmental Health, University of Cincinnati, 3223 Eden Avenue, Cincinnati, OH 45267, USA.
Hong Xin
Divaker Choubey
Loyola University Chicago · 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 AI 066261NIAID NIH HHS R01 AI066261
6 · The paper itself

Abstract

Studies have identified IFN-inducible Ifi202 gene as a lupus susceptibility gene (encoding p202 protein) in mouse models of lupus disease. However, signaling pathways that regulate the Ifi202 expression in cells remain to be elucidated. We found that steady-state levels of Ifi202 mRNA and protein were high in mouse embryonic fibroblasts (MEFs) from E2F1 knockout (E2F1(-/-)) and E2F1 and E2F2 double knockout (E2F1(-/-)E2F2(-/-)) mice than isogenic wild-type MEFs. Moreover, overexpression of E2F1 in mouse fibroblasts decreased expression of p202. Furthermore, expression of E2F1, but not E2F4, transcription factor in mouse fibroblasts repressed the activity of 202-luc-reporter in promoter-reporter assays. Interestingly, the E2F1-mediated transcriptional repression of the 202-luc-reporter was independent of p53 and pRb expression. However, the repression was dependent on the ability of E2F1 to bind DNA. We have identified a potential E2F DNA-binding site in the 5'-regulatory region of the Ifi202 gene, and mutations in this E2F DNA-binding site reduced the E2F1-mediated transcriptional repression of 202-luc-reporter. Because p202 inhibits the E2F1-mediated transcriptional activation of genes, we compared the expression of E2F1 and its target genes in splenic cells from lupus-prone B6.Nba2 congenic mice, which express increased levels of p202, with age-matched C57BL/6 mice. We found that increased expression of Ifi202 in the congenic mice was associated with inhibition of E2F1-mediated transcription and decreased expression of E2F1 and its target genes that encode proapoptotic proteins. Our observations support the idea that increased Ifi202 expression in certain strains of mice contributes to lupus susceptibility in part by inhibiting E2F1-mediated functions.

Indexed as

AnimalsApoptosis Regulatory ProteinsDisease Models, AnimalE2F1 Transcription FactorE2F2 Transcription FactorE2F4 Transcription FactorEmbryo, MammalianFibroblastsGene Expression RegulationIntracellular Signaling Peptides and ProteinsLupus Erythematosus, SystemicMiceMice, KnockoutNIH 3T3 CellsPhosphoproteinsRetinoblastoma ProteinApoptosis Regulatory ProteinsE2f1 protein, mouseE2F1 Transcription FactorE2f2 protein, mouseE2F2 Transcription FactorE2f4 protein, mouseE2F4 Transcription FactorIfi202b protein, mouseIntracellular Signaling Peptides and ProteinsPhosphoproteinsRetinoblastoma ProteinTumor Suppressor Protein p53

Identifiers

PMID18424712
PMCPMC2810195
OpenAlexW1770930878

What OpenQuestion holds

Textmetadata
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.