REEP5 depletion causes sarco-endoplasmic reticulum vacuolization and cardiac functional defects

The sarcoplasmic (SR) and endoplasmic reticulum (ER) are involved in heart development but how this arises is unclear. Here, the authors show that loss of a SR/ER protein REEP5 causes membrane destabilization and decreased cardiac myocyte contractility, with cardiac dysfunction in mutant mouse and z...

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Autores principales: Shin-Haw Lee, Sina Hadipour-Lakmehsari, Harsha R. Murthy, Natalie Gibb, Tetsuaki Miyake, Allen C. T. Teng, Jake Cosme, Jessica C. Yu, Mark Moon, SangHyun Lim, Victoria Wong, Peter Liu, Filio Billia, Rodrigo Fernandez-Gonzalez, Igor Stagljar, Parveen Sharma, Thomas Kislinger, Ian C. Scott, Anthony O. Gramolini
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Lenguaje:EN
Publicado: Nature Portfolio 2020
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Acceso en línea:https://doaj.org/article/9f62361bf8a34f7da79df62e9762126b
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spelling oai:doaj.org-article:9f62361bf8a34f7da79df62e9762126b2021-12-02T14:40:50ZREEP5 depletion causes sarco-endoplasmic reticulum vacuolization and cardiac functional defects10.1038/s41467-019-14143-92041-1723https://doaj.org/article/9f62361bf8a34f7da79df62e9762126b2020-02-01T00:00:00Zhttps://doi.org/10.1038/s41467-019-14143-9https://doaj.org/toc/2041-1723The sarcoplasmic (SR) and endoplasmic reticulum (ER) are involved in heart development but how this arises is unclear. Here, the authors show that loss of a SR/ER protein REEP5 causes membrane destabilization and decreased cardiac myocyte contractility, with cardiac dysfunction in mutant mouse and zebrafish models.Shin-Haw LeeSina Hadipour-LakmehsariHarsha R. MurthyNatalie GibbTetsuaki MiyakeAllen C. T. TengJake CosmeJessica C. YuMark MoonSangHyun LimVictoria WongPeter LiuFilio BilliaRodrigo Fernandez-GonzalezIgor StagljarParveen SharmaThomas KislingerIan C. ScottAnthony O. GramoliniNature PortfolioarticleScienceQENNature Communications, Vol 11, Iss 1, Pp 1-20 (2020)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Shin-Haw Lee
Sina Hadipour-Lakmehsari
Harsha R. Murthy
Natalie Gibb
Tetsuaki Miyake
Allen C. T. Teng
Jake Cosme
Jessica C. Yu
Mark Moon
SangHyun Lim
Victoria Wong
Peter Liu
Filio Billia
Rodrigo Fernandez-Gonzalez
Igor Stagljar
Parveen Sharma
Thomas Kislinger
Ian C. Scott
Anthony O. Gramolini
REEP5 depletion causes sarco-endoplasmic reticulum vacuolization and cardiac functional defects
description The sarcoplasmic (SR) and endoplasmic reticulum (ER) are involved in heart development but how this arises is unclear. Here, the authors show that loss of a SR/ER protein REEP5 causes membrane destabilization and decreased cardiac myocyte contractility, with cardiac dysfunction in mutant mouse and zebrafish models.
format article
author Shin-Haw Lee
Sina Hadipour-Lakmehsari
Harsha R. Murthy
Natalie Gibb
Tetsuaki Miyake
Allen C. T. Teng
Jake Cosme
Jessica C. Yu
Mark Moon
SangHyun Lim
Victoria Wong
Peter Liu
Filio Billia
Rodrigo Fernandez-Gonzalez
Igor Stagljar
Parveen Sharma
Thomas Kislinger
Ian C. Scott
Anthony O. Gramolini
author_facet Shin-Haw Lee
Sina Hadipour-Lakmehsari
Harsha R. Murthy
Natalie Gibb
Tetsuaki Miyake
Allen C. T. Teng
Jake Cosme
Jessica C. Yu
Mark Moon
SangHyun Lim
Victoria Wong
Peter Liu
Filio Billia
Rodrigo Fernandez-Gonzalez
Igor Stagljar
Parveen Sharma
Thomas Kislinger
Ian C. Scott
Anthony O. Gramolini
author_sort Shin-Haw Lee
title REEP5 depletion causes sarco-endoplasmic reticulum vacuolization and cardiac functional defects
title_short REEP5 depletion causes sarco-endoplasmic reticulum vacuolization and cardiac functional defects
title_full REEP5 depletion causes sarco-endoplasmic reticulum vacuolization and cardiac functional defects
title_fullStr REEP5 depletion causes sarco-endoplasmic reticulum vacuolization and cardiac functional defects
title_full_unstemmed REEP5 depletion causes sarco-endoplasmic reticulum vacuolization and cardiac functional defects
title_sort reep5 depletion causes sarco-endoplasmic reticulum vacuolization and cardiac functional defects
publisher Nature Portfolio
publishDate 2020
url https://doaj.org/article/9f62361bf8a34f7da79df62e9762126b
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