Evidence map›Paper›PMID 31006653›Full record

ArticleThe Journal of biological chemistry2019

Disruption of valosin-containing protein activity causes cardiomyopathy and reveals pleiotropic functions in cardiac homeostasis.

Matthew J Brody, Davy Vanhoutte, Chinmay V Bakshi, Ruije Liu, Robert N Correll, Michelle A Sargent, Jeffery D Molkentin

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

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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

7 authors at 4 institutions in 1 country.

Matthew J BrodyFrom the Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio 45229-3039.
Davy VanhoutteFrom the Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio 45229-3039.
Chinmay V BakshiFrom the Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio 45229-3039.
Ruije LiuFrom the Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio 45229-3039.
Robert N CorrellFrom the Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio 45229-3039.
Michelle A SargentFrom the Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio 45229-3039.
Jeffery D MolkentinFrom the Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio 45229-3039, Jeff.Molkentin@cchmc.org.
Cincinnati Children's Hospital Medical Center · USHoward Hughes Medical Institute · USUniversity of Alabama · USUniversity of Cincinnati · US

Funding

Thrombospondin 4 regulates adaptive ER stress responseRenewal - Resubmission - 1R01HL105924 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI Jeffery D Molkentin · 2011 to 2026
$7.3M
MOLECULAR PATHWAYS CONTROLLING CARDIAC GENE EXPRESSIONR01HL060562 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI MOLKENTIN, JEFFERY D · 1998 to 2021
$4.1M
The role of palmitoylation in cardiac signal transduction and disease pathogenesisK99HL136695 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI BRODY, MATTHEW JACOB · 2018 to 2019
$258k
The role of thrombospondin-4 in the secretory pathway, extracellular matrix produF32HL124698 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI BRODY, MATTHEW JACOB · 2014 to 2017
$159k
Howard Hughes Medical InstituteNHLBI NIH HHS F32 HL124698NHLBI NIH HHS K99 HL136695NHLBI NIH HHS R01 HL060562NHLBI NIH HHS R01 HL105924
6 · The paper itself

Abstract

Valosin-containing protein (VCP), also known as p97, is an ATPase with diverse cellular functions, although the most highly characterized is targeting of misfolded or aggregated proteins to degradation pathways, including the endoplasmic reticulum-associated degradation (ERAD) pathway. However, how VCP functions in the heart has not been carefully examined despite the fact that human mutations in VCP cause Paget disease of bone and frontotemporal dementia, an autosomal dominant multisystem proteinopathy that includes disease in the heart, skeletal muscle, brain, and bone. Here we generated heart-specific transgenic mice overexpressing WT VCP or a VCP

Indexed as

AnimalsCardiomyopathiesCells, CulturedEndoplasmic Reticulum-Associated DegradationHeartLaminsMiceMice, TransgenicMutagenesis, Site-DirectedMyocardiumMyocytes, CardiacNuclear ProteinsProtein SubunitsRatsRibosomal ProteinsRNA-Binding ProteinsLaminsNuclear ProteinsProtein SubunitsRibosomal ProteinsRNA-Binding ProteinsValosin Containing Proteincardiac hypertrophycardiomyocytecardiomyopathyendoplasmic reticulum–associated protein degradation (ERAD)protein aggregationRNA turnover

Identifiers

PMID31006653
PMCPMC6552413
OpenAlexW2940379717

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.