Evidence map›Paper›PMID 12000713›Full record

ArticleThe American journal of pathology2002

Ligand-dependent genetic recombination in fibroblasts : a potentially powerful technique for investigating gene function in fibrosis.

Bing Zheng, Zhaoping Zhang, Carol M Black, Benoit de Crombrugghe, Christopher P Denton

Open access · greenAbstract read
In one paragraph

Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
1.1field-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

137 citing papers in PubMed, 226 citations in OpenAlex.

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77 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Bing ZhengDepartment of Molecular Genetics, University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA.
Zhaoping Zhang
Carol M Black
Benoit de Crombrugghe
Christopher P Denton
The University of Texas MD Anderson Cancer Center · USUniversity College London · GB

Funding

Transgenic animal models for fibrotic diseaseP50AR044888 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI ARNETT, FRANK C · 1997 to 2005
$6.6M
NIAMS NIH HHS P50 AR044888NIAMS NIH HHS P50AR44888
6 · The paper itself

Abstract

Strategies for conditional induction of transgene expression in mice are likely to be valuable for testing the role of candidate genes in disease pathogenesis. We have developed a system for lineage-specific, ligand-dependent, induction of sustained transgene expression in fibroblastic cells in mice using a chimeric gene encoding the Cre-ER(T) fusion protein, under the control of a fibroblast-specific regulatory sequence from the pro alpha 2(I)collagen gene. Cre-ER(T) operates as a tamoxifen-dependent DNA recombinase to excise fragments flanked by specific LoxP consensus sequences. To test efficiency and ligand dependency of this strategy, Cre-ER(T)-expressing mice were backcrossed with heterozygous ROSA26-LacZ reporter mice, in which a floxed-STOP cassette has been introduced upstream of a bacterial beta-galactosidase (LacZ) reporter gene at a ubiquitously expressed locus. Constitutive or tamoxifen-induced LacZ expression was examined in embryonic, neonatal, and adult compound-transgenic mice. When pregnant ROSA26-LacZ females received a single dose of tamoxifen, high-level expression of LacZ in the skin was demonstrable from 24 hours after injection in double-transgenic embryos harboring both the Cre-ER(T) transgene and the target ROSA26-LacZ allele. High-level expression of LacZ was also induced postnatally by tamoxifen specifically in dermal and visceral fibroblasts. By allowing efficient embryonic or postnatal modification of alleles that have been targeted to incorporate LoxP sites, or to switch on transgenes cloned downstream of the floxed-STOP cassette, this system will allow fibroblast-specific genetic perturbations to be induced at predetermined embryonic or postnatal time points. This should greatly assist in in vivo functional studies of candidate genes in fibrotic diseases such as systemic sclerosis.

Indexed as

Recombination, GeneticAnimalsBinding SitesCrosses, GeneticEmbryo, MammalianFemaleFibroblastsFibrosisGene Expression Regulation, DevelopmentalGenetic Predisposition to DiseaseIntegrasesLac OperonLigandsMaleMiceMice, TransgenicCre recombinaseGt(ROSA)26Sor non-coding RNA, mouseIntegrasesLigandsProteinsReceptors, EstrogenRecombinant Fusion ProteinsRNA, UntranslatedTamoxifenViral Proteins

Identifiers

PMID12000713
PMCPMC1850857
OpenAlexW115384338

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.