RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/36117313http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/36117313http://www.w3.org/2000/01/rdf-schema#comment"Proteinuria is a major manifestation of kidney disease, reflecting injuries of glomerular podocytes. Actin cytoskeleton plays a pivotal role in stabilizing the foot processes of podocytes against the hydrostatic pressure of filtration. Calponin is an actin associated protein that regulates mechanical tension-related cytoskeleton functions and its role in podocytes has not been established. Here we studied the kidney phenotypes of calponin isoform 2 knockout (KO) mice. Urine samples were examined to quantify the ratio of albumin and creatinine. Kidney tissue samples were collected for histology and ultrastructural studies. A mouse podocyte cell line (E11) was used to study the expression and cellular localization of calponin 2. In comparison with wild-type (WT) controls, calponin 2 KO mice showed age-progressive high proteinuria and degeneration of renal glomeruli. High levels of calponin 2 are expressed in E11 podocytes and colocalized with actin stress fibers, tropomyosin and myosin IIA. Electron microscopy showed that aging calponin 2 KO mice had effacement of the podocyte foot processes and increased thickness of the glomerular basement membrane as compared to that of WT control. The findings demonstrate that deletion of calponin 2 aggravates age-progressive degeneration of the glomerular structure and function as filtration barrier. The critical role of calponin 2 in podocytes suggests a molecular target for understanding the pathogenesis of proteinuria and therapeutic development."xsd:string
http://purl.uniprot.org/citations/36117313http://purl.org/dc/terms/identifier"doi:10.14814/phy2.15370"xsd:string
http://purl.uniprot.org/citations/36117313http://purl.uniprot.org/core/author"Jin J.P."xsd:string
http://purl.uniprot.org/citations/36117313http://purl.uniprot.org/core/author"Hsieh T.B."xsd:string
http://purl.uniprot.org/citations/36117313http://purl.uniprot.org/core/date"2022"xsd:gYear
http://purl.uniprot.org/citations/36117313http://purl.uniprot.org/core/name"Physiol Rep"xsd:string
http://purl.uniprot.org/citations/36117313http://purl.uniprot.org/core/pages"e15370"xsd:string
http://purl.uniprot.org/citations/36117313http://purl.uniprot.org/core/title"Loss of Calponin 2 causes age-progressive proteinuria in mice."xsd:string
http://purl.uniprot.org/citations/36117313http://purl.uniprot.org/core/volume"10"xsd:string
http://purl.uniprot.org/citations/36117313http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/36117313
http://purl.uniprot.org/citations/36117313http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/36117313
http://purl.uniprot.org/uniprot/#_D3Z7R6-mappedCitation-36117313http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/36117313
http://purl.uniprot.org/uniprot/#_Q08093-mappedCitation-36117313http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/36117313
http://purl.uniprot.org/uniprot/#_Q922F8-mappedCitation-36117313http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/36117313
http://purl.uniprot.org/uniprot/#_Q543F3-mappedCitation-36117313http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/36117313
http://purl.uniprot.org/uniprot/Q922F8http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/36117313
http://purl.uniprot.org/uniprot/Q08093http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/36117313
http://purl.uniprot.org/uniprot/Q543F3http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/36117313
http://purl.uniprot.org/uniprot/D3Z7R6http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/36117313