Evidence map›Paper›PMID 19457099›Full record

ArticleJournal of neurochemistry2009

Dual transgenic reporter mice as a tool for monitoring expression of glial fibrillary acidic protein.

Woosung Cho, Tracy L Hagemann, Delinda A Johnson, Jeffrey A Johnson, Albee Messing

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  11. Bioluminescent imaging of drug efflux at the blood-brain barrier mediated by the transporter ABCG2.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  12. Review
  13. Article
  14. Article
  15. Strategies for treatment in Alexander disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2010
    Review
  16. Article
  17. 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

5 authors at 1 institution in 1 country.

Woosung ChoWaisman Center and Department of Comparative Biosciences, University of Wisconsin-Madison, Madison, Wisconsin 53705, USA. cho@waisman.wisc.edu
Tracy L Hagemann
Delinda A Johnson
Jeffrey A Johnson
Albee Messing
University of Wisconsin–Madison · US

Funding

WISCONSIN CENTER ON MENTAL RETARDATION: CORE SUPPORTP30HD003352 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI MESSING, ALBEE · 1985 to 2015
$25.2M
The impact of GFAP mutations upon filament networksP01NS042803 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI MESSING, ALBEE · 2002 to 2012
$11.1M
Mouse Models of Alexander DiseaseR01NS060120 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI MESSING, ALBEE · 2007 to 2011
$1.9M
Is a therapy for Alexander disease already FDA-approved?R03HD046599 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI MESSING, ALBEE · 2005 to 2006
$144k
NICHD NIH HHS HD03352NICHD NIH HHS HD046599NICHD NIH HHS P30 HD003352NICHD NIH HHS R03 HD046599NINDS NIH HHS NS042803NINDS NIH HHS NS060120NINDS NIH HHS P01 NS042803NINDS NIH HHS R01 NS060120
6 · The paper itself

Abstract

Glial fibrillary acidic protein (GFAP) is the major intermediate filament protein of astrocytes, and its expression changes dramatically during development and following injury. To facilitate study of the regulation of GFAP expression, we have generated dual transgenic mice expressing both firefly luciferase under the control of a 2.2 kb human GFAP promoter and Renilla luciferase under the control of a 0.5 kb human Glyceraldehyde 3 phosphate dehydrogenase (GAPDH) promoter for normalization of the GFAP signal. The GFAP-fLuc was highly expressed in brain compared to other tissues, and was limited to astrocytes, whereas the GAPDH-RLuc was more widely expressed. Normalization of the GFAP signal to the GAPDH signal reduced the inter-individual variability compared to using the GFAP signal alone. The GFAP/GAPDH ratio correctly reflected the up-regulation of GFAP that occurs following retinal degeneration in FVB/N mice because of the rd mutation. Following kainic acid-induced seizures, changes in the GFAP/GAPDH ratio precede those in total GFAP protein. In knock-in mice expressing the R236H Alexander disease mutant, GFAP promoter activity is only transiently elevated and may not entirely account for the accumulation of GFAP protein that takes place.

Indexed as

Alexander DiseaseAnimalsBiomarkersBrainDrug Evaluation, PreclinicalEpilepsyGene Expression RegulationGene Knock-In TechniquesGenes, ReporterGlial Fibrillary Acidic ProteinGlyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)HumansLuciferasesLuciferases, FireflyLuciferases, RenillaMiceBiomarkersGlial Fibrillary Acidic ProteinGlyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)LuciferasesLuciferases, FireflyLuciferases, Renilla

Identifiers

PMID19457099
PMCPMC2710392
OpenAlexW1964795521

What OpenQuestion holds

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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.