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.
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2020-10-01
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Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/s41467-020-18980-x |
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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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