{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Blackwood EA"],"funding":["NHLBI NIH HHS"],"pagination":["66-82"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9797446"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["147(1)"],"pubmed_abstract":["Background
Cardiac hypertrophy increases demands on protein folding, which causes an accumulation of misfolded proteins in the endoplasmic reticulum (ER). These misfolded proteins can be removed by the adaptive retrotranslocation, polyubiquitylation, and a proteasome-mediated degradation process, ER-associated degradation (ERAD), which, as a biological process and rate, has not been studied in vivo. To investigate a role for ERAD in a pathophysiological model, we examined the function of the functional initiator of ERAD, valosin-containing protein-interacting membrane protein (VIMP), positing that VIMP would be adaptive in pathological cardiac hypertrophy in mice.Methods
We developed a new method involving cardiac myocyte-specific adeno-associated virus serovar 9-mediated e"],"journal":["Circulation"],"pubmed_title":["Noncanonical Form of ERAD Regulates Cardiac Hypertrophy."],"pmcid":["PMC9797446"],"funding_grant_id":["R01 HL105993","R01 HL141463","R01 HL149891","R56 HL121539","R01 HL157027","F31 HL140850","R01 HL135893","R01 HL149931"],"pubmed_authors":["Murray VB","Bedi KC","Thuerauf DJ","Glembotski CC","Blackwood EA","MacDonnell LF","Bilal AS","Margulies KB"],"additional_accession":[]},"is_claimable":false,"name":"Noncanonical Form of ERAD Regulates Cardiac Hypertrophy.","description":"Background
Cardiac hypertrophy increases demands on protein folding, which causes an accumulation of misfolded proteins in the endoplasmic reticulum (ER). These misfolded proteins can be removed by the adaptive retrotranslocation, polyubiquitylation, and a proteasome-mediated degradation process, ER-associated degradation (ERAD), which, as a biological process and rate, has not been studied in vivo. To investigate a role for ERAD in a pathophysiological model, we examined the function of the functional initiator of ERAD, valosin-containing protein-interacting membrane protein (VIMP), positing that VIMP would be adaptive in pathological cardiac hypertrophy in mice.Methods
We developed a new method involving cardiac myocyte-specific adeno-associated virus serovar 9-mediated e","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2025-04-05T15:52:52.703Z","creation":"2025-04-05T15:52:52.703Z"},"accession":"S-EPMC9797446","cross_references":{"pubmed":["36317534"],"doi":["10.1161/CIRCULATIONAHA.122.061557","10.1161/circulationaha.122.061557"]}}