CHIP phosphorylation by protein kinase G enhances protein quality control and attenuates cardiac ischemic injury

Carboxyl terminus of Hsc70-interacting protein (CHIP) is proteostasis regulator. Here the authors show that CHIP-mediated protein turnover is enhanced by PKG-mediated phosphorylation, which results in attenuated cardiac ischemic proteotoxicity.

Bibliographic Details
Main Authors: Mark J. Ranek, Christian Oeing, Rebekah Sanchez-Hodge, Kristen M. Kokkonen-Simon, Danielle Dillard, M. Imran Aslam, Peter P. Rainer, Sumita Mishra, Brittany Dunkerly-Eyring, Ronald J. Holewinski, Cornelia Virus, Huaqun Zhang, Matthew M. Mannion, Vineet Agrawal, Virginia Hahn, Dong I. Lee, Masayuki Sasaki, Jennifer E. Van Eyk, Monte S. Willis, Richard C. Page, Jonathan C. Schisler, David A. Kass
Format: Article
Language:English
Published: Nature Publishing Group 2020-10-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-020-18980-x
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spelling doaj-7e6f8490744a4cef9d24e2c03e23c4992021-05-11T09:18:15ZengNature Publishing GroupNature Communications2041-17232020-10-0111111210.1038/s41467-020-18980-xCHIP phosphorylation by protein kinase G enhances protein quality control and attenuates cardiac ischemic injuryMark J. Ranek0Christian Oeing1Rebekah Sanchez-Hodge2Kristen M. Kokkonen-Simon3Danielle Dillard4M. Imran Aslam5Peter P. Rainer6Sumita Mishra7Brittany Dunkerly-Eyring8Ronald J. Holewinski9Cornelia Virus10Huaqun Zhang11Matthew M. Mannion12Vineet Agrawal13Virginia Hahn14Dong I. Lee15Masayuki Sasaki16Jennifer E. Van Eyk17Monte S. Willis18Richard C. Page19Jonathan C. Schisler20David A. Kass21Division of Cardiology, Department of Medicine, Johns Hopkins Medical InstitutionsDivision of Cardiology, Department of Medicine, Johns Hopkins Medical InstitutionsDivision of Cardiology, McAllister Heart Institute, The University of North Carolina at Chapel HillDivision of Cardiology, Department of Medicine, Johns Hopkins Medical InstitutionsDivision of Cardiology, Department of Medicine, Johns Hopkins Medical InstitutionsDivision of Cardiology, Department of Medicine, Johns Hopkins Medical InstitutionsDivision of Cardiology, Department of Medicine, Johns Hopkins Medical InstitutionsDivision of Cardiology, Department of Medicine, Johns Hopkins Medical InstitutionsDivision of Cardiology, Department of Medicine, Johns Hopkins Medical InstitutionsCedar Sinai Medical Center, Advanced Clinical Biosystems Research Institute, The Smidt Heart InstituteDivision of Cardiology, McAllister Heart Institute, The University of North Carolina at Chapel HillDepartment of Chemistry and Biochemistry, Miami UniversityDepartment of Chemistry and Biochemistry, Miami UniversityDivision of Cardiology, Department of Medicine, Johns Hopkins Medical InstitutionsDivision of Cardiology, Department of Medicine, Johns Hopkins Medical InstitutionsDivision of Cardiology, Department of Medicine, Johns Hopkins Medical InstitutionsDivision of Cardiology, Department of Medicine, Johns Hopkins Medical InstitutionsCedar Sinai Medical Center, Advanced Clinical Biosystems Research Institute, The Smidt Heart InstituteDivision of Cardiology, McAllister Heart Institute, The University of North Carolina at Chapel HillDepartment of Chemistry and Biochemistry, Miami UniversityDivision of Cardiology, McAllister Heart Institute, The University of North Carolina at Chapel HillDivision of Cardiology, Department of Medicine, Johns Hopkins Medical InstitutionsCarboxyl terminus of Hsc70-interacting protein (CHIP) is proteostasis regulator. Here the authors show that CHIP-mediated protein turnover is enhanced by PKG-mediated phosphorylation, which results in attenuated cardiac ischemic proteotoxicity.https://doi.org/10.1038/s41467-020-18980-x
collection DOAJ
language English
format Article
sources DOAJ
author Mark J. Ranek
Christian Oeing
Rebekah Sanchez-Hodge
Kristen M. Kokkonen-Simon
Danielle Dillard
M. Imran Aslam
Peter P. Rainer
Sumita Mishra
Brittany Dunkerly-Eyring
Ronald J. Holewinski
Cornelia Virus
Huaqun Zhang
Matthew M. Mannion
Vineet Agrawal
Virginia Hahn
Dong I. Lee
Masayuki Sasaki
Jennifer E. Van Eyk
Monte S. Willis
Richard C. Page
Jonathan C. Schisler
David A. Kass
spellingShingle Mark J. Ranek
Christian Oeing
Rebekah Sanchez-Hodge
Kristen M. Kokkonen-Simon
Danielle Dillard
M. Imran Aslam
Peter P. Rainer
Sumita Mishra
Brittany Dunkerly-Eyring
Ronald J. Holewinski
Cornelia Virus
Huaqun Zhang
Matthew M. Mannion
Vineet Agrawal
Virginia Hahn
Dong I. Lee
Masayuki Sasaki
Jennifer E. Van Eyk
Monte S. Willis
Richard C. Page
Jonathan C. Schisler
David A. Kass
CHIP phosphorylation by protein kinase G enhances protein quality control and attenuates cardiac ischemic injury
Nature Communications
author_facet Mark J. Ranek
Christian Oeing
Rebekah Sanchez-Hodge
Kristen M. Kokkonen-Simon
Danielle Dillard
M. Imran Aslam
Peter P. Rainer
Sumita Mishra
Brittany Dunkerly-Eyring
Ronald J. Holewinski
Cornelia Virus
Huaqun Zhang
Matthew M. Mannion
Vineet Agrawal
Virginia Hahn
Dong I. Lee
Masayuki Sasaki
Jennifer E. Van Eyk
Monte S. Willis
Richard C. Page
Jonathan C. Schisler
David A. Kass
author_sort Mark J. Ranek
title CHIP phosphorylation by protein kinase G enhances protein quality control and attenuates cardiac ischemic injury
title_short CHIP phosphorylation by protein kinase G enhances protein quality control and attenuates cardiac ischemic injury
title_full CHIP phosphorylation by protein kinase G enhances protein quality control and attenuates cardiac ischemic injury
title_fullStr CHIP phosphorylation by protein kinase G enhances protein quality control and attenuates cardiac ischemic injury
title_full_unstemmed CHIP phosphorylation by protein kinase G enhances protein quality control and attenuates cardiac ischemic injury
title_sort chip phosphorylation by protein kinase g enhances protein quality control and attenuates cardiac ischemic injury
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2020-10-01
description Carboxyl terminus of Hsc70-interacting protein (CHIP) is proteostasis regulator. Here the authors show that CHIP-mediated protein turnover is enhanced by PKG-mediated phosphorylation, which results in attenuated cardiac ischemic proteotoxicity.
url https://doi.org/10.1038/s41467-020-18980-x
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