Evidence map›Paper›PMID 19654412›Full record

ArticleBlood2009

Mndal, a new interferon-inducible family member, is highly polymorphic, suppresses cell growth, and may modify plasmacytoma susceptibility.

Ke Zhang, Daniel Kagan, Wendy DuBois, Richard Robinson, Valery Bliskovsky, William C Vass, Shuling Zhang, Beverly A Mock

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. 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
0.9field-weighted citation impact, top 24% 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, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Journal of virology · 2019
    Review
  9. Review
  10. Article
  11. Article
  12. Virus-induced inflammasome activation is suppressed by prostaglandin DProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  13. Article
  14. Transgenic mouse model of IgMBlood cancer journal · 2016
    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

8 authors at 2 institutions in 1 country.

Ke ZhangLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4258, USA.
Daniel Kagan
Wendy DuBois
Richard Robinson
Valery Bliskovsky
William C Vass
Shuling Zhang
Beverly A Mock
Cancer Genetics (United States) · USCenter for Cancer Research · US

Funding

Animal Model and Genotyping Core Support FacilityZICBC011047 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DU BOIS DE VROYLANDE, WENDY · 2009 to 2025
$23.1M
Intramural NIH HHS
6 · The paper itself

Abstract

The human HIN-200 gene cluster and its mouse counterpart, the interferon inducible-200 (Ifi200) family, both on Chr 1, are associated with several diseases, including solid tumors and lupus. Our study was initiated to identify the modifier gene(s) encoded by the Pctm locus, in which mouse B-cell plasmacytomas induced by pristane are associated with heterozygosity of Chr 1 genes near the Ifi200 cluster. A screen for differentially expressed genes in granulomatous tissues induced by pristane in resistant and susceptible strains identified a new Ifi200 member whose expression was 1000-fold higher in the strain carrying the resistant allele of Pctm and was the most highly expressed Ifi200 gene. The gene, designated Mndal (for MNDA-like, myeloid nuclear differentiation antigen-like), was absent in the susceptible genome, as were genomic sequences upstream of Ifi203, the gene adjacent to Mndal. Ectopic expression of MNDAL suppressed cell growth, which, together with the disease susceptibility of heterozygotes at the Pctm locus, suggests that Mndal, perhaps with Ifi203, acts as a tumor suppressor and display(s) haploinsufficiency. Mndal is highly polymorphic among inbred mouse strains, because it is absent in 10 of 24 strains. This polymorphism may have implications for other disease modifiers mapping to the same region.

Indexed as

Polymorphism, GeneticAnimalsAntigens, Differentiation, MyelomonocyticAntineoplastic AgentsB-LymphocytesCloning, MolecularColony-Forming Units AssayDNA, ComplementaryGene Expression ProfilingHumansInterferonsMiceMice, Inbred BALB CMice, Inbred DBANIH 3T3 CellsNuclear ProteinsAntigens, Differentiation, MyelomonocyticAntineoplastic AgentsDNA, ComplementaryInterferonsMndal protein, mouseMNDA protein, humanNuclear ProteinsProteinsTranscription Factors

Identifiers

PMID19654412
PMCPMC2756205
OpenAlexW2128649909

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.