{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Huang L"],"funding":["BLRD VA","NIDDK NIH HHS","NCI NIH HHS"],"pagination":["2303-15"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4178431"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["25(10)"],"pubmed_abstract":["Stanniocalcin-1 is an intracrine protein; it binds to the cell surface, is internalized to the mitochondria, and diminishes superoxide generation through induction of uncoupling proteins. In vitro, stanniocalcin-1 inhibits macrophages and preserves endothelial barrier function, and transgenic overexpression of stanniocalcin-1 in mice protects against ischemia-reperfusion kidney injury. We sought to determine the kidney phenotype after kidney endothelium-specific expression of stanniocalcin-1 small hairpin RNA (shRNA). We generated transgenic mice that express stanniocalcin-1 shRNA or scrambled shRNA upon removal of a floxed reporter (phosphoglycerate kinase-driven enhanced green fluorescent protein) and used ultrasound microbubbles to deliver tyrosine kinase receptor-2 promoter-driven Cre "],"journal":["Journal of the American Society of Nephrology : JASN"],"pubmed_title":["AKI after conditional and kidney-specific knockdown of stanniocalcin-1."],"pmcid":["PMC4178431"],"funding_grant_id":["R01 CA116097","R01-DK080306","P30-CA125123","T32-DK062706","T32 DK062706","R01 DK080306","I01 BX002006","P30 CA125123","R01 CA122623"],"pubmed_authors":["Belousova T","Ju H","Pan JS","Lu L","Nuotio-Antar A","Huang L","Du J","Sheikh-Hamad D","Truong LD","Zhang P"],"additional_accession":[]},"is_claimable":false,"name":"AKI after conditional and kidney-specific knockdown of stanniocalcin-1.","description":"Stanniocalcin-1 is an intracrine protein; it binds to the cell surface, is internalized to the mitochondria, and diminishes superoxide generation through induction of uncoupling proteins. In vitro, stanniocalcin-1 inhibits macrophages and preserves endothelial barrier function, and transgenic overexpression of stanniocalcin-1 in mice protects against ischemia-reperfusion kidney injury. We sought to determine the kidney phenotype after kidney endothelium-specific expression of stanniocalcin-1 small hairpin RNA (shRNA). We generated transgenic mice that express stanniocalcin-1 shRNA or scrambled shRNA upon removal of a floxed reporter (phosphoglycerate kinase-driven enhanced green fluorescent protein) and used ultrasound microbubbles to deliver tyrosine kinase receptor-2 promoter-driven Cre ","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Oct","modification":"2026-05-02T00:16:04.947Z","creation":"2019-03-27T01:36:40Z"},"accession":"S-EPMC4178431","cross_references":{"pubmed":["24700878"],"doi":["10.1681/ASN.2013070690","10.1681/asn.2013070690"]}}