Pathologic gene network rewiring implicates PPP1R3A as a central regulator in pressure overload heart failure

The genetic and pathogenetic basis of heart failure is incompletely understood. Here, the authors present a high-fidelity tissue collection from rapidly preserved failing and non-failing control hearts which are used for eQTL mapping and network analysis, resulting in the prioritization of PPP1R3A a...

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Main Authors: Pablo Cordero, Victoria N. Parikh, Elizabeth T. Chin, Ayca Erbilgin, Michael J. Gloudemans, Ching Shang, Yong Huang, Alex C. Chang, Kevin S. Smith, Frederick Dewey, Kathia Zaleta, Michael Morley, Jeff Brandimarto, Nicole Glazer, Daryl Waggott, Aleksandra Pavlovic, Mingming Zhao, Christine S. Moravec, W. H. Wilson Tang, Jamie Skreen, Christine Malloy, Sridhar Hannenhalli, Hongzhe Li, Scott Ritter, Mingyao Li, Daniel Bernstein, Andrew Connolly, Hakon Hakonarson, Aldons J. Lusis, Kenneth B. Margulies, Anna A. Depaoli-Roach, Stephen B. Montgomery, Matthew T. Wheeler, Thomas Cappola, Euan A. Ashley
Format: Article
Language:English
Published: Nature Publishing Group 2019-06-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-019-10591-5
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spelling doaj-2ca5a8edf42d48a4acecfce1aa70adac2021-05-11T11:57:15ZengNature Publishing GroupNature Communications2041-17232019-06-0110111410.1038/s41467-019-10591-5Pathologic gene network rewiring implicates PPP1R3A as a central regulator in pressure overload heart failurePablo Cordero0Victoria N. Parikh1Elizabeth T. Chin2Ayca Erbilgin3Michael J. Gloudemans4Ching Shang5Yong Huang6Alex C. Chang7Kevin S. Smith8Frederick Dewey9Kathia Zaleta10Michael Morley11Jeff Brandimarto12Nicole Glazer13Daryl Waggott14Aleksandra Pavlovic15Mingming Zhao16Christine S. Moravec17W. H. Wilson Tang18Jamie Skreen19Christine Malloy20Sridhar Hannenhalli21Hongzhe Li22Scott Ritter23Mingyao Li24Daniel Bernstein25Andrew Connolly26Hakon Hakonarson27Aldons J. Lusis28Kenneth B. Margulies29Anna A. Depaoli-Roach30Stephen B. Montgomery31Matthew T. Wheeler32Thomas Cappola33Euan A. Ashley34Division of Cardiovascular Medicine, Stanford UniversityDivision of Cardiovascular Medicine, Stanford UniversityDivision of Cardiovascular Medicine, Stanford UniversityDivision of Cardiovascular Medicine, Stanford UniversityBiomedical Informatics Program, Stanford UniversityDivision of Cardiovascular Medicine, Stanford UniversityDivision of Cardiovascular Medicine, Stanford UniversityDivision of Cardiovascular Medicine, Stanford UniversityDepartment of Pathology, Stanford UniversityDivision of Cardiovascular Medicine, Stanford UniversityDivision of Cardiovascular Medicine, Stanford UniversityDivision of Cardiology, University of PennsylvaniaDepartment of Medicine, University of PennsylvaniaDepartment of Medicine, Boston University School of MedicineDivision of Cardiovascular Medicine, Stanford UniversityDivision of Cardiovascular Medicine, Stanford UniversityDepartment of Pediatrics, Stanford UniversityDepartment of Cardiovascular and Metabolic Sciences, Lerner Research InstituteDepartment of Cardiovascular and Metabolic Sciences, Lerner Research InstituteProvidence Medical Group—MilwaukieCenter for Bioinformatics and Computational Biology, University of MarylandCenter for Bioinformatics and Computational Biology, University of MarylandBiostatistics and Epidemiology, University of PennsylvaniaDivision of Cardiology, University of PennsylvaniaBiostatistics and Epidemiology, University of PennsylvaniaDepartment of Pediatrics, Stanford UniversityDepartment of Pathology, University of California San FranciscoDepartment of Pediatrics, The Children’s Hospital of PhiladelphiaDepartments of Medicine, University of California Los AngelesDivision of Cardiology, University of PennsylvaniaSchool of Medicine, Indiana UniversityDepartment of Pathology, Stanford UniversityDivision of Cardiovascular Medicine, Stanford UniversityDivision of Cardiology, University of PennsylvaniaDivision of Cardiovascular Medicine, Stanford UniversityThe genetic and pathogenetic basis of heart failure is incompletely understood. Here, the authors present a high-fidelity tissue collection from rapidly preserved failing and non-failing control hearts which are used for eQTL mapping and network analysis, resulting in the prioritization of PPP1R3A as a heart failure gene.https://doi.org/10.1038/s41467-019-10591-5
collection DOAJ
language English
format Article
sources DOAJ
author Pablo Cordero
Victoria N. Parikh
Elizabeth T. Chin
Ayca Erbilgin
Michael J. Gloudemans
Ching Shang
Yong Huang
Alex C. Chang
Kevin S. Smith
Frederick Dewey
Kathia Zaleta
Michael Morley
Jeff Brandimarto
Nicole Glazer
Daryl Waggott
Aleksandra Pavlovic
Mingming Zhao
Christine S. Moravec
W. H. Wilson Tang
Jamie Skreen
Christine Malloy
Sridhar Hannenhalli
Hongzhe Li
Scott Ritter
Mingyao Li
Daniel Bernstein
Andrew Connolly
Hakon Hakonarson
Aldons J. Lusis
Kenneth B. Margulies
Anna A. Depaoli-Roach
Stephen B. Montgomery
Matthew T. Wheeler
Thomas Cappola
Euan A. Ashley
spellingShingle Pablo Cordero
Victoria N. Parikh
Elizabeth T. Chin
Ayca Erbilgin
Michael J. Gloudemans
Ching Shang
Yong Huang
Alex C. Chang
Kevin S. Smith
Frederick Dewey
Kathia Zaleta
Michael Morley
Jeff Brandimarto
Nicole Glazer
Daryl Waggott
Aleksandra Pavlovic
Mingming Zhao
Christine S. Moravec
W. H. Wilson Tang
Jamie Skreen
Christine Malloy
Sridhar Hannenhalli
Hongzhe Li
Scott Ritter
Mingyao Li
Daniel Bernstein
Andrew Connolly
Hakon Hakonarson
Aldons J. Lusis
Kenneth B. Margulies
Anna A. Depaoli-Roach
Stephen B. Montgomery
Matthew T. Wheeler
Thomas Cappola
Euan A. Ashley
Pathologic gene network rewiring implicates PPP1R3A as a central regulator in pressure overload heart failure
Nature Communications
author_facet Pablo Cordero
Victoria N. Parikh
Elizabeth T. Chin
Ayca Erbilgin
Michael J. Gloudemans
Ching Shang
Yong Huang
Alex C. Chang
Kevin S. Smith
Frederick Dewey
Kathia Zaleta
Michael Morley
Jeff Brandimarto
Nicole Glazer
Daryl Waggott
Aleksandra Pavlovic
Mingming Zhao
Christine S. Moravec
W. H. Wilson Tang
Jamie Skreen
Christine Malloy
Sridhar Hannenhalli
Hongzhe Li
Scott Ritter
Mingyao Li
Daniel Bernstein
Andrew Connolly
Hakon Hakonarson
Aldons J. Lusis
Kenneth B. Margulies
Anna A. Depaoli-Roach
Stephen B. Montgomery
Matthew T. Wheeler
Thomas Cappola
Euan A. Ashley
author_sort Pablo Cordero
title Pathologic gene network rewiring implicates PPP1R3A as a central regulator in pressure overload heart failure
title_short Pathologic gene network rewiring implicates PPP1R3A as a central regulator in pressure overload heart failure
title_full Pathologic gene network rewiring implicates PPP1R3A as a central regulator in pressure overload heart failure
title_fullStr Pathologic gene network rewiring implicates PPP1R3A as a central regulator in pressure overload heart failure
title_full_unstemmed Pathologic gene network rewiring implicates PPP1R3A as a central regulator in pressure overload heart failure
title_sort pathologic gene network rewiring implicates ppp1r3a as a central regulator in pressure overload heart failure
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2019-06-01
description The genetic and pathogenetic basis of heart failure is incompletely understood. Here, the authors present a high-fidelity tissue collection from rapidly preserved failing and non-failing control hearts which are used for eQTL mapping and network analysis, resulting in the prioritization of PPP1R3A as a heart failure gene.
url https://doi.org/10.1038/s41467-019-10591-5
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