Isbn: 9783659751509 - genetic and cellular studies of the podocyte in fsgs: fsgs is an abbreviation for a kidney disease named focal segmental glomerulosclersis (8 resultados)

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Taschenbuch. Condición: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -The podocyte forms the outer layer of the filtration barrier to prevent albumin leakage. Podocyte damage leads to focal segmental glomerulosclerosis (FSGS), a leading cause of chronic kidney disease. I performed a genetic analysis of both familial and sporadic FSGS patients, and I investigated the role of the actin cytoskeleton in podocytes. We identified a new FSGS susceptibility gene, ARHGAP24, and showed that it was mutated in a family with FSGS. My work suggested that this balance between Rac and Rho might be important in FSGS. Using an inducible transgenic mouse model and multi-photon intravital microscopy, we validated that high activity of Rac1, is responsible for podocyte foot process effacement, increased membrane dynamics, and podocyte shedding into the urine, which could lead to proteinuria and FSGS. By sequencing a large cohort of sporadic FSGS patients, and using a novel podocyte-specific indicible RNAi mouse model that I developed, we validated four novel genes that could contribute to FSGS. Some of these genes function as regulators of the actin cytoskeleton. Our genetic study reinforces the role of actin cytoskeletal regulation in the pathogenesis of FSGS. 148 pp. Englisch.…

Condición: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Autor/Autorin: Yu HaiyangHaiyang Yu,A postdoctoral researcher mentored by Dr. Don W. Cleveland in Ludwig Institute for Cancer Research (San Diego Branch)when this work is published. He earned a bachelor s degree from Nankai Univeristy, in Tianjin, .…

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Taschenbuch. Condición: Neu. This item is printed on demand - Print on Demand Titel. Neuware -The podocyte forms the outer layer of the filtration barrier to prevent albumin leakage. Podocyte damage leads to focal segmental glomerulosclerosis (FSGS), a leading cause of chronic kidney disease. I performed a genetic analysis of both familial and sporadic FSGS patients, and I investigated the role of the actin cytoskeleton in podocytes. We identified a new FSGS susceptibility gene, ARHGAP24, and showed that it was mutated in a family with FSGS. My work suggested that this balance between Rac and Rho might be important in FSGS. Using an inducible transgenic mouse model and multi-photon intravital microscopy, we validated that high activity of Rac1, is responsible for podocyte foot process effacement, increased membrane dynamics, and podocyte shedding into the urine, which could lead to proteinuria and FSGS. By sequencing a large cohort of sporadic FSGS patients, and using a novel podocyte-specific indicible RNAi mouse model that I developed, we validated four novel genes that could contribute to FSGS. Some of these genes function as regulators of the actin cytoskeleton. Our genetic study reinforces the role of actin cytoskeletal regulation in the pathogenesis of FSGS.VDM Verlag, Dudweiler Landstraße 99, 66123 Saarbrücken 148 pp. Englisch.…

Taschenbuch. Condición: Neu. nach der Bestellung gedruckt Neuware - Printed after ordering - The podocyte forms the outer layer of the filtration barrier to prevent albumin leakage. Podocyte damage leads to focal segmental glomerulosclerosis (FSGS), a leading cause of chronic kidney disease. I performed a genetic analysis of both familial and sporadic FSGS patients, and I investigated the role of the actin cytoskeleton in podocytes. We identified a new FSGS susceptibility gene, ARHGAP24, and showed that it was mutated in a family with FSGS. My work suggested that this balance between Rac and Rho might be important in FSGS. Using an inducible transgenic mouse model and multi-photon intravital microscopy, we validated that high activity of Rac1, is responsible for podocyte foot process effacement, increased membrane dynamics, and podocyte shedding into the urine, which could lead to proteinuria and FSGS. By sequencing a large cohort of sporadic FSGS patients, and using a novel podocyte-specific indicible RNAi mouse model that I developed, we validated four novel genes that could contribute to FSGS. Some of these genes function as regulators of the actin cytoskeleton. Our genetic study reinforces the role of actin cytoskeletal regulation in the pathogenesis of FSGS.…