Evidence map›Paper›PMID 22427641›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

The Drosophila protein mustard tailors the innate immune response activated by the immune deficiency pathway.

Zhipeng Wang, Cristin D Berkey, Paula I Watnick

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Transposon expression in theGenome research · 2020
    Article
  6. Article
  7. ZebrafishGenes · 2020
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. LysMD3 is a type II membrane protein without anThe Journal of biological chemistry · 2018
    Article
  13. TLDc proteins: new players in the oxidative stress response and neurological disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2017
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 2 institutions in 1 country.

Zhipeng WangDivision of Infectious Diseases, Children's Hospital Boston, Boston, MA 02115, USA.
Cristin D Berkey
Paula I Watnick
Boston Children's Hospital · USBoston Children's Museum · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
INFECTIOUS DISEASE AND BASIC MICROBIOLOGICAL MECHANISMST32AI007061 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI Marcia B Goldberg · 1985 to 2026
$12.1M
Progenitor Cells inHuman Skeletal MuscleP50NS040828 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI KUNKEL, LOUIS M · 2008 to 2011
$5.9M
Drosophila melanogaster as a model host for Vibrio choleraeR01AI071147 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI WATNICK, PAULA I · 2007 to 2010
$1.7M
NIAID NIH HHS AI071147NIAID NIH HHS R01 AI071147NIAID NIH HHS T32 AI007061NICHD NIH HHS P30 HD018655NICHD NIH HHS P30-HD-18655NICHD NIH HHS P30-HD18655NINDS NIH HHS P50 NS040828NINDS NIH HHS P50-NS40828
6 · The paper itself

Abstract

In this study, we describe a Drosophila melanogaster transposon insertion mutant with tolerance to Vibrio cholerae infection and markedly decreased transcription of diptericin as well as other genes regulated by the immune deficiency innate immunity signaling pathway. We present genetic evidence that this insertion affects a locus previously implicated in pupal eclosion. This genetic locus, which we have named mustard (mtd), contains a LysM domain, often involved in carbohydrate recognition, and a TLDc domain of unknown function. More than 20 Mtd isoforms containing one or both of these conserved domains are predicted. We establish that the mutant phenotype represents a gain of function and can be replicated by increased expression of a short, nuclearly localized Mtd isoform comprised almost entirely of the TLDc domain. We show that this Mtd isoform does not block Relish cleavage or translocation into the nucleus. Lastly, we present evidence suggesting that the eclosion defect previously attributed to the Mtd locus may be the result of the unopposed action of the NF-κB homolog, Relish. Mtd homologs have been implicated in resistance to oxidative stress. However, to our knowledge this is the first evidence that Mtd or its homologs alter the output of an innate immunity signaling cascade from within the nucleus.

Indexed as

Immunity, InnateAnimalsAnimals, Genetically ModifiedCell NucleusCholeraDNA Transposable ElementsDrosophila melanogasterDrosophila ProteinsGene Expression RegulationGenetic LociGenome, InsectGenotypeMaleMutagenesis, InsertionalPhenotypeSignal TransductionDNA Transposable ElementsDptA protein, DrosophilaDrosophila ProteinsRel protein, DrosophilaTranscription Factors

Identifiers

PMID22427641
PMCPMC3324637
OpenAlexW1524682659

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.