Evidence map›Paper›PMID 27819340›Full record

ArticleScientific reports2016

Functional screening of mammalian mechanosensitive genes using Drosophila RNAi library- Smarcd3/Bap60 is a mechanosensitive pro-inflammatory gene.

Sandeep Kumar, In-Hwan Jang, Chan Woo Kim, Dong-Won Kang, Won Jae Lee, Hanjoong Jo

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. LncRNAInternational journal of molecular sciences · 2022
    Article
  3. Article
  4. 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

6 authors at 4 institutions in 2 countries.

Sandeep KumarWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
In-Hwan JangWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Chan Woo KimWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Dong-Won KangWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Won Jae LeeNational Creative Research Initiative Center for Hologenomics, and School of Biological Sciences, Seoul National University, Seoul 151-742, South Korea.
Hanjoong JoWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Georgia Institute of Technology · USThe Wallace H. Coulter Department of Biomedical Engineering · USEmory University · USSeoul National University · KR

Funding

T cell triggering events and hypertensionP01HL095070 · NHLBI · EMORY UNIVERSITY · PI JO, HANJOONG · 2009 to 2019
$20.5M
Shear stress, endothelial miRNAs, and AV calcificationR01HL119798 · NHLBI · EMORY UNIVERSITY · PI JO, HANJOONG, YOGANATHAN, AJIT P · 2013 to 2022
$4.7M
Metabolomics of subclinical and clinical cardiovascular diseaseP20HL113451 · NHLBI · EMORY UNIVERSITY · PI JONES, DEAN PAUL · 2012 to 2016
$4.3M
Image-based analysis of miRNA deliveryR01HL124879 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI FERRARA, KATHERINE W, JO, HANJOONG · 2014 to 2017
$3.1M
NHLBI NIH HHS P01 HL095070NHLBI NIH HHS P20 HL113451NHLBI NIH HHS R01 HL119798NHLBI NIH HHS R01 HL124879
6 · The paper itself

Abstract

Disturbed blood flow (d-flow) induces atherosclerosis by altering the expression of mechanosensitive genes in the arterial endothelium. Previously, we identified >580 mechanosensitive genes in the mouse arterial endothelium, but their role in endothelial inflammation is incompletely understood. From this set, we obtained 84 Drosophila RNAi lines that silences the target gene under the control of upstream activation sequence (UAS) promoter. These lines were crossed with C564-GAL4 flies expressing GFP under the control of drosomycin promoter, an NF-κB target gene and a marker of pathogen-induced inflammation. Silencing of psmd12 or ERN1 decreased infection-induced drosomycin expression, while Bap60 silencing significantly increased the drosomycin expression. Interestingly, knockdown of Bap60 in adult flies using temperature-inducible Bap60 RNAi (C564

Indexed as

AnimalsAortaCells, CulturedChromosomal Proteins, Non-HistoneDrosophilaDrosophila ProteinsEndothelial CellsGene LibraryHumansHuman Umbilical Vein Endothelial CellsInflammationInterleukin-8MiceMice, Inbred C57BLMuscle ProteinsPromoter Regions, GeneticBap60 protein, DrosophilaChromosomal Proteins, Non-HistoneDrosophila ProteinsDRS protein, DrosophilaInterleukin-8Muscle ProteinsSmarcd3 protein, mouseTranscription FactorsVascular Cell Adhesion Molecule-1

Identifiers

PMID27819340
PMCPMC5098218
OpenAlexW2553920942

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.