Evidence map›Paper›PMID 27235449›Full record

ArticlePhysiological genomics2016

Coronary artery disease susceptibility gene ADTRP regulates cell cycle progression, proliferation, and apoptosis by global gene expression regulation.

Chunyan Luo, Fan Wang, Subo Qin, Qiuyun Chen, Qing K Wang

Open access · bronzeAbstract read
In one paragraph

Article in Physiological genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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  11. UBC9 regulates cardiac sodium channel NaJournal of molecular and cellular cardiology · 2019
    Article
  12. Long noncoding RNAThe Journal of biological chemistry · 2019
    Article
  13. Article
  14. Androgen inhibits key atherosclerotic processes by directly activating ADTRP transcription.Biochimica et biophysica acta. Molecular basis of disease · 2017
    Article
  15. Article
  16. 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

5 authors at 3 institutions in 2 countries.

Chunyan LuoThe Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, People's Republic of China;
Fan WangDepartment of Molecular Cardiology, Lerner Research Institute, Center for Cardiovascular Genetics, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio; and Department of Molecular Medicine, Department of Genetics and Genome Science, Case Western Reserve University, Cleveland, Ohio qkwang@hust.edu.cn wangq2@ccf.org.
Subo QinThe Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, People's Republic of China;
Qiuyun ChenDepartment of Molecular Cardiology, Lerner Research Institute, Center for Cardiovascular Genetics, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio; and Department of Molecular Medicine, Department of Genetics and Genome Science, Case Western Reserve University, Cleveland, Ohio.
Qing K WangThe Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, People's Republic of China; Department of Molecular Cardiology, Lerner Research Institute, Center for Cardiovascular Genetics, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio; and Department of Molecular Medicine, Department of Genetics and Genome Science, Case Western Reserve University, Cleveland, Ohio.
Case Western Reserve University · USHuazhong University of Science and Technology · CNCleveland Clinic Lerner College of Medicine · US

Funding

NGS in Large CAD Families: In-Depth Identification of Rare Risk Genomic VariantsR01HL121358 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI WANG, QING KENNETH · 2014 to 2017
$2.8M
Targeting Nav1.5 trafficking as a therapy for lethal genetic cardiac arrhythmiasR01HL126729 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI WANG, QING KENNETH · 2015 to 2018
$1.6M
NHLBI NIH HHS R01 HL121358NHLBI NIH HHS R01 HL126729
6 · The paper itself

Abstract

The ADTRP gene encodes the androgen-dependent TFPI-regulating protein and is a susceptibility gene for contrary artery disease (CAD). We performed global gene expression profiling for ADTRP knock-down using microarrays in human HepG2 cells. Follow-up real-time RT-PCR analysis demonstrated that ADTRP knock-down regulates a diverse set of genes, including upregulation of seven histone genes, downregulation of multiple cell cycle genes (CCND1, CDK4, and CDKN1A), and upregulation of apoptosis genes (CASP7 and PDCD2) in HepG2 cells and endothelial cells. Consistently, ADTRP increases the number of S phase cells during cell cycle, promotes cell proliferation, and inhibits apoptosis. Our study provides novel insights into the function of ADTRP and biological pathways involving ADTRP, which may be involved in the pathogenesis of CAD.

Indexed as

ApoptosisCell LineCell Line, TumorCell ProliferationCoronary Artery DiseaseCoronary VesselsDown-RegulationGene Expression RegulationGenes, cdcHep G2 CellsHumansHuman Umbilical Vein Endothelial CellsMembrane ProteinsSignal TransductionS PhaseUp-RegulationADTRP protein, humanMembrane ProteinsADTRPcaspase 7CDK4coronary artery disease (CAD)cyclin D1global gene expression microarrayhistonep21CIP

Identifiers

PMID27235449
PMCPMC5005456
OpenAlexW2406264304

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.