Evidence map›Paper›PMID 24489749›Full record

ArticlePloS one2014

Inducible, dose-adjustable and time-restricted reconstitution of STAT1 deficiency in vivo.

Nicole R Leitner, Caroline Lassnig, Rita Rom, Susanne Heider, Zsuzsanna Bago-Horvath, Robert Eferl, Simone Müller, Thomas Kolbe, Lukas Kenner, Thomas Rülicke and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

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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

12 authors at 4 institutions in 1 country.

Nicole R LeitnerInstitute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.
Caroline LassnigInstitute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria ; University Center Biomodels Austria (BIAT), University of Veterinary Medicine Vienna, Vienna, Austria.
Rita RomInstitute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.
Susanne HeiderClinical Institute of Pathology, Medical University of Vienna, Vienna, Austria ; Ludwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Zsuzsanna Bago-HorvathInstitute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria ; Clinical Institute of Pathology, Medical University of Vienna, Vienna, Austria ; Institute of Pharmacology and Toxicology, University of Veterinary Medicine Vienna, Vienna, Austria.
Robert EferlDepartment of Internal Medicine I, Institute for Cancer Research, Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria.
Simone MüllerInstitute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.
Thomas KolbeUniversity Center Biomodels Austria (BIAT), University of Veterinary Medicine Vienna, Vienna, Austria ; Department IFA-Tulln, Biotechnology in Animal Production, University of Natural Resources and Applied Life Sciences, Tulln, Austria.
Lukas KennerClinical Institute of Pathology, Medical University of Vienna, Vienna, Austria ; Ludwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Thomas RülickeInstitute of Laboratory Animal Science, University of Veterinary Medicine Vienna, Vienna, Austria.
Birgit StroblInstitute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.
Mathias MüllerInstitute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria ; University Center Biomodels Austria (BIAT), University of Veterinary Medicine Vienna, Vienna, Austria.
University of Veterinary Medicine Vienna · ATComprehensive Cancer Center Vienna · ATLudwig Boltzmann Institute for Cancer Research · ATMedical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signal transducer and activator of transcription (STAT) 1 is a key player in interferon (IFN) signaling, essential in mediating host defense against viruses and other pathogens. STAT1 levels are tightly regulated and loss- or gain-of-function mutations in mice and men lead to severe diseases. We have generated a doxycycline (dox) -inducible, FLAG-tagged Stat1 expression system in mice lacking endogenous STAT1 (i.e. Stat1(ind) mice). We show that STAT1 expression depends on the time and dose of dox treatment in primary cells and a variety of organs isolated from Stat1(ind) mice. In bone marrow-derived macrophages, a fraction of the amount of STAT1 present in WT cells is sufficient for full expression of IFN-induced genes. Dox-induced STAT1 established protection against virus infections in primary cells and mice. The availability of the Stat1(ind) mouse model will enable an examination of the consequences of variable amounts of STAT1. The model will also permit the study of STAT1 dose-dependent and reversible functions as well as of STAT1's contributions to the development, progression and resolution of disease.

Indexed as

AnimalsBone Marrow CellsCardiovirus InfectionsDoxycyclineEncephalomyocarditis virusFounder EffectGene Expression RegulationGenetic EngineeringInterferonsMacrophagesMaleMiceMice, TransgenicPrimary Cell CultureSignal TransductionSTAT1 Transcription FactorDoxycyclineInterferonsStat1 protein, mouseSTAT1 Transcription Factor

Identifiers

PMID24489749
PMCPMC3906053
OpenAlexW2063455820

What OpenQuestion holds

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LicenceCC BY
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.