{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Basak M"],"funding":["Indian Council of Medical Research","Defence Research and Development Organisation","Department of Biotechnology, Ministry of Science and Technology, India"],"pagination":["e2213537120"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9910480"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["120(1)"],"pubmed_abstract":["Dose-limiting cardiotoxicity remains a major limitation in the clinical use of cancer chemotherapeutics. Here, we describe a role for Regulator of G protein Signaling 7 (RGS7) in chemotherapy-dependent heart damage, the demonstration for a functional role of RGS7 outside of the nervous system and retina. Though expressed at low levels basally, we observed robust up-regulation of RGS7 in the human and murine myocardium following chemotherapy exposure. In ventricular cardiomyocytes (VCM), RGS7 forms a complex with Ca<sup>2+</sup>/calmodulin-dependent protein kinase (CaMKII) supported by key residues (K412 and P391) in the RGS domain of RGS7. In VCM treated with chemotherapeutic drugs, RGS7 facilitates CaMKII oxidation and phosphorylation and CaMKII-dependent oxidative stress, mitochondrial d"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["A RGS7-CaMKII complex drives myocyte-intrinsic and myocyte-extrinsic mechanisms of chemotherapy-induced cardiotoxicity."],"pmcid":["PMC9910480"],"funding_grant_id":["5/4/1-26/2020-NCD-I","BT/PR28635/MED/30/2145/2019","DG-(TM)/81/48222/LSRB- 307/SH&amp;DD&amp;BD/2017"],"pubmed_authors":["Kumar D","Mahata T","Biswas S","Sarkar S","Sengar AS","Basak M","Maity B","Kumar M","Das P","Stewart A","Kumar P","Das K"],"additional_accession":[]},"is_claimable":false,"name":"A RGS7-CaMKII complex drives myocyte-intrinsic and myocyte-extrinsic mechanisms of chemotherapy-induced cardiotoxicity.","description":"Dose-limiting cardiotoxicity remains a major limitation in the clinical use of cancer chemotherapeutics. Here, we describe a role for Regulator of G protein Signaling 7 (RGS7) in chemotherapy-dependent heart damage, the demonstration for a functional role of RGS7 outside of the nervous system and retina. Though expressed at low levels basally, we observed robust up-regulation of RGS7 in the human and murine myocardium following chemotherapy exposure. In ventricular cardiomyocytes (VCM), RGS7 forms a complex with Ca<sup>2+</sup>/calmodulin-dependent protein kinase (CaMKII) supported by key residues (K412 and P391) in the RGS domain of RGS7. In VCM treated with chemotherapeutic drugs, RGS7 facilitates CaMKII oxidation and phosphorylation and CaMKII-dependent oxidative stress, mitochondrial d","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2025-05-31T23:46:32.886Z","creation":"2025-05-31T23:46:32.886Z"},"accession":"S-EPMC9910480","cross_references":{"pubmed":["36574707"],"doi":["10.1073/pnas.2213537120"]}}