Evidence map›Paper›PMID 20371351›Full record

ArticleCell2010

A global in vivo Drosophila RNAi screen identifies NOT3 as a conserved regulator of heart function.

G Gregory Neely, Keiji Kuba, Anthony Cammarato, Kazuya Isobe, Sabine Amann, Liyong Zhang, Mitsushige Murata, Lisa Elmén, Vaijayanti Gupta, Suchir Arora and 25 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2010. 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
9.1field-weighted citation impact, top 1% 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, 223 citations in OpenAlex.

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  18. Life science alliance · 2023
    Article
  19. CRISPR screening in cardiovascular research.Frontiers in cell and developmental biology · 2023
    Review
  20. Age-related ceRNA networks in adultFrontiers in genetics · 2023
    Article

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

35 authors at 12 institutions in 7 countries.

G Gregory NeelyInstitute of Molecular Biotechnology of Austrian Academy of Sciences, Dr. Bohr Gasse 3-5, A-1030 Vienna, Austria.
Keiji Kuba
Anthony Cammarato
Kazuya Isobe
Sabine Amann
Liyong Zhang
Mitsushige Murata
Lisa Elmén
Vaijayanti Gupta
Suchir Arora
Rinku Sarangi
Debasis Dan
Susumu Fujisawa
Takako Usami
Cui-ping Xia
Alex C Keene
Nakissa N Alayari
Hiroyuki Yamakawa
Ulrich Elling
Christian Berger
Maria Novatchkova
Rubina Koglgruber
Keiichi Fukuda
Hiroshi Nishina
Mitsuaki Isobe
J Andrew Pospisilik
Yumiko Imai
Arne Pfeufer
Andrew A Hicks
Peter P Pramstaller
Sai Subramaniam
Akinori Kimura
Karen Ocorr
Rolf Bodmer
Josef M Penninger
Institute of Molecular Biotechnology · ATSanford Burnham Prebys Medical Discovery Institute · USStrand Life Sciences (India) · INAkita University · JPAustrian Academy of Sciences · ATTokyo Medical and Dental University · JPKeio University · JPEurac Research · ITNew York University · USOspedale di Bolzano · ITTechnical University of Munich · DEUniversity of Toronto · CA

Funding

HEART DEVELOPMENT IN DROSOPHILAR01HL054732 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BODMER, ROLF · 1995 to 2024
$11.3M
Regulation of Lateral Neuron function in Drosophila larvaeF32GM086207 · NIGMS · NEW YORK UNIVERSITY · PI KEENE, ALEX C · 2008 to 2010
$155k
NHLBI NIH HHS R01 HL054732NIGMS NIH HHS F32 GM086207
6 · The paper itself

Abstract

Heart diseases are the most common causes of morbidity and death in humans. Using cardiac-specific RNAi-silencing in Drosophila, we knocked down 7061 evolutionarily conserved genes under conditions of stress. We present a first global roadmap of pathways potentially playing conserved roles in the cardiovascular system. One critical pathway identified was the CCR4-Not complex implicated in transcriptional and posttranscriptional regulatory mechanisms. Silencing of CCR4-Not components in adult Drosophila resulted in myofibrillar disarray and dilated cardiomyopathy. Heterozygous not3 knockout mice showed spontaneous impairment of cardiac contractility and increased susceptibility to heart failure. These heart defects were reversed via inhibition of HDACs, suggesting a mechanistic link to epigenetic chromatin remodeling. In humans, we show that a common NOT3 SNP correlates with altered cardiac QT intervals, a known cause of potentially lethal ventricular tachyarrhythmias. Thus, our functional genome-wide screen in Drosophila can identify candidates that directly translate into conserved mammalian genes involved in heart function.

Indexed as

Models, AnimalAnimalsCardiomyopathiesDrosophila melanogasterFemaleGenome-Wide Association StudyHeartHumansMaleMiceMice, KnockoutPromoter Regions, GeneticRNA Interference

Identifiers

PMID20371351
PMCPMC2855221
OpenAlexW2091998897

What OpenQuestion holds

Textmetadata
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.