Evidence map›Paper›PMID 33396956›Full record

ArticleInternational journal of molecular sciences2020

Phenotypic Characterization of Transgenic Mice Expressing Human IGFBP-5.

Xinh-Xinh Nguyen, Matthew Sanderson, Kristi Helke, Carol Feghali-Bostwick

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The Molecular Mechanisms of Systemic Sclerosis-Associated Lung Fibrosis.International journal of molecular sciences · 2023
    Review
  6. Review
  7. 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

4 authors at 1 institution in 1 country.

Xinh-Xinh NguyenDivision of Rheumatology & Immunology, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA.
Matthew SandersonDivision of Rheumatology & Immunology, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA.
Kristi HelkeDepartments of Comparative Medicine and Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, SC 29425, USA.
Carol Feghali-BostwickDivision of Rheumatology & Immunology, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA.ORCID 0000-0002-6750-6407
Medical University of South Carolina · US

Funding

South Carolina Clinical & Translational Research Institute (SCTR)UL1TR001450 · NCATS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T., FLUME, PATRICK A · 2015 to 2024
$41.1M
Proteomics CoreP30DK123704 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RICHARD R. DRAKE · 2020 to 2026
$8.8M
South Carolina Clinical & Translational Research Institute (SCTR)TL1TR001451 · NCATS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI FEGHALI-BOSTWICK, CAROL A. · 2015 to 2024
$4.6M
Mechanism of Action of Anti-Fibrotic PeptideR01HL121262 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI FEGHALI-BOSTWICK, CAROL A. · 2017 to 2020
$1.5M
IGF-II regulates lung fibrosis in sclerodermaR01HL153195 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI FEGHALI-BOSTWICK, CAROL A. · 2020 to 2023
$1.5M
Scleroderma Twin Study and analysis of Estrogen in patients with dcSScK24AR060297 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FEGHALI-BOSTWICK, CAROL A. · 2013 to 2025
$1.4M
NCATS NIH HHS TL1 TR001451NCATS NIH HHS UL1 TR001450NHLBI NIH HHS R01 HL121262NHLBI NIH HHS R01 HL153195NIAMS NIH HHS K24 AR060297NIDDK NIH HHS P30 DK123704
6 · The paper itself

Abstract

Pulmonary fibrosis is one of the important causes of morbidity and mortality in fibroproliferative disorders such as systemic sclerosis (SSc) and idiopathic pulmonary fibrosis (IPF). Insulin-like growth factor binding protein-5 (IGFBP-5) is a conserved member of the IGFBP family of proteins that is overexpressed in SSc and IPF lung tissues. In this study, we investigated the functional role of IGFBP-5 in the development of fibrosis in vivo using a transgenic model. We generated transgenic mice ubiquitously expressing human IGFBP-5 using CRISPR/Cas9 knock-in. Our data show that the heterozygous and homozygous mice are viable and express human IGFBP-5 (h

Indexed as

AnimalsAntibiotics, AntineoplasticBleomycinCells, CulturedExtracellular MatrixFemaleFibroblastsFibrosisHumansInsulin-Like Growth Factor Binding Protein 5LungMaleMiceMice, TransgenicPhenotypeSkinAntibiotics, AntineoplasticBleomycinIGFBP5 protein, humanInsulin-Like Growth Factor Binding Protein 5extracellular matrix (ECM), transgenic modelfibrosisinsulin-like growth factor binding protein-5 (IGFBP-5)

Identifiers

PMID33396956
PMCPMC7795366
OpenAlexW3114698554

What OpenQuestion holds

Textmetadata
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.