Items related to Genetic and Cellular Studies of the podocyte in FSGS
Synopsis
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.
"synopsis" may belong to another edition of this title.
Buy New
View this item
US$ 66.75
US$ 26.66 shipping from Germany to U.S.A.
Destination, rates & speedsSearch results for Genetic and Cellular Studies of the podocyte in FSGS
Seller Image
Genetic and Cellular Studies of the podocyte in FSGS
Published by
LAP LAMBERT Academic Publishing Jul 2015, 2015
ISBN 10: 3659751502
ISBN 13: 9783659751509
New
Taschenbuch
Seller: BuchWeltWeit Ludwig Meier e.K., Bergisch Gladbach, Germany
Seller rating 5 out of 5 stars
Taschenbuch. Condition: 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. Seller Inventory # 9783659751509
Quantity: 2 available
Seller Image
Genetic and Cellular Studies of the podocyte in FSGS : FSGS is an abbreviation for a kidney disease named focal segmental glomerulosclersis
Published by
LAP LAMBERT Academic Publishing, 2015
ISBN 10: 3659751502
ISBN 13: 9783659751509
New
Taschenbuch
Seller: AHA-BUCH GmbH, Einbeck, Germany
Seller rating 5 out of 5 stars
Taschenbuch. Condition: 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. Seller Inventory # 9783659751509
Quantity: 1 available
Seller Image
Genetic and Cellular Studies of the podocyte in FSGS
Published by
LAP LAMBERT Academic Publishing, 2015
ISBN 10: 3659751502
ISBN 13: 9783659751509
New
Softcover
Seller: moluna, Greven, Germany
Seller rating 5 out of 5 stars
Condition: 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, . Seller Inventory # 158962127
Quantity: Over 20 available
Seller Image
Genetic and Cellular Studies of the podocyte in FSGS
Published by
LAP LAMBERT Academic Publishing Jul 2015, 2015
ISBN 10: 3659751502
ISBN 13: 9783659751509
New
Taschenbuch
Seller: buchversandmimpf2000, Emtmannsberg, BAYE, Germany
Seller rating 5 out of 5 stars
Taschenbuch. Condition: 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.Books on Demand GmbH, Überseering 33, 22297 Hamburg 148 pp. Englisch. Seller Inventory # 9783659751509
Quantity: 1 available
Stock Image
Genetic and Cellular Studies of the podocyte in FSGS
Published by
LAP Lambert Academic Publishing, 2015
ISBN 10: 3659751502
ISBN 13: 9783659751509
Used
paperback
Seller: Mispah books, Redhill, SURRE, United Kingdom
Seller rating 4 out of 5 stars
paperback. Condition: Like New. Like New. book. Seller Inventory # ERICA80036597515026
Quantity: 1 available