Nuclear exclusion of YAP exacerbates podocyte apoptosis and disease progression in Adriamycin-induced focal segmental glomerulosclerosis
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
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1530-0307
- Extent
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Online-Ressource
- Language
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Englisch
- Notes
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online resource.
- Bibliographic citation
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Nuclear exclusion of YAP exacerbates podocyte apoptosis and disease progression in Adriamycin-induced focal segmental glomerulosclerosis ; day:17 ; month:11 ; year:2020 ; pages:1-13
Laboratory investigation ; (17.11.2020), 1-13
- Creator
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Zhuang, Qiyuan
Li, Fang
Liu, Jun
Wang, Hongyu
Tian, Yuchen
Zhang, Zhigang
Wang, Feng
Zhao, Zhonghua
Chen, Jianchun
Wu, Huijuan
- Contributor
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SpringerLink (Online service)
- DOI
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10.1038/s41374-020-00503-3
- URN
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urn:nbn:de:101:1-2020122820451620780561
- Rights
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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15.08.2025, 7:38 AM CEST
Data provider
This object is provided by:
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Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Zhuang, Qiyuan
- Li, Fang
- Liu, Jun
- Wang, Hongyu
- Tian, Yuchen
- Zhang, Zhigang
- Wang, Feng
- Zhao, Zhonghua
- Chen, Jianchun
- Wu, Huijuan
- SpringerLink (Online service)
Other Objects (12)
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Therapeutic Potential Targeting Podocyte Mitochondrial Dysfunction in Focal Segmental Glomerulosclerosis
Btg2 Promotes Focal Segmental Glomerulosclerosis via Smad3‐Dependent Podocyte‐Mesenchymal Transition
RhoA deficiency disrupts podocyte cytoskeleton and induces podocyte apoptosis by inhibiting YAP/dendrin signal
Nuclear YAP localization as a key regulator of podocyte function
Cyclosporine A Protects Podocytes by Regulating Transgelin in Adriamycin-Induced Podocyte Injury
Pharmacogenetic podocyte depletion in zebrafish larvae as a model for focal segmental glomerulosclerosis
AF1q Contributes to Adriamycin-Induced Podocyte Injury by Activating Wnt/β-Catenin Signaling
Acatalasemic mice are mildly susceptible to adriamycin nephropathy and exhibit increased albuminuria and glomerulosclerosis
Minnelide Markedly Reduces Proteinuria in Mice with Adriamycin Nephropathy by Protecting Against Podocyte Injury
B7-1 mediates podocyte injury and glomerulosclerosis through communication with Hsp90ab1-LRP5-β-catenin pathway
Assessment of podocyte detachment as a pivotal step in the development of focal segmental glomerulosclerosis
Angiopoietin-like-3 knockout protects against glomerulosclerosis in murine adriamycin-induced nephropathy by attenuating podocyte loss
Therapeutic Potential Targeting Podocyte Mitochondrial Dysfunction in Focal Segmental Glomerulosclerosis
Btg2 Promotes Focal Segmental Glomerulosclerosis via Smad3‐Dependent Podocyte‐Mesenchymal Transition
RhoA deficiency disrupts podocyte cytoskeleton and induces podocyte apoptosis by inhibiting YAP/dendrin signal
Nuclear YAP localization as a key regulator of podocyte function
Cyclosporine A Protects Podocytes by Regulating Transgelin in Adriamycin-Induced Podocyte Injury
Pharmacogenetic podocyte depletion in zebrafish larvae as a model for focal segmental glomerulosclerosis
AF1q Contributes to Adriamycin-Induced Podocyte Injury by Activating Wnt/β-Catenin Signaling
Acatalasemic mice are mildly susceptible to adriamycin nephropathy and exhibit increased albuminuria and glomerulosclerosis
Minnelide Markedly Reduces Proteinuria in Mice with Adriamycin Nephropathy by Protecting Against Podocyte Injury
B7-1 mediates podocyte injury and glomerulosclerosis through communication with Hsp90ab1-LRP5-β-catenin pathway
Assessment of podocyte detachment as a pivotal step in the development of focal segmental glomerulosclerosis
Angiopoietin-like-3 knockout protects against glomerulosclerosis in murine adriamycin-induced nephropathy by attenuating podocyte loss
Therapeutic Potential Targeting Podocyte Mitochondrial Dysfunction in Focal Segmental Glomerulosclerosis
Btg2 Promotes Focal Segmental Glomerulosclerosis via Smad3‐Dependent Podocyte‐Mesenchymal Transition
RhoA deficiency disrupts podocyte cytoskeleton and induces podocyte apoptosis by inhibiting YAP/dendrin signal
Nuclear YAP localization as a key regulator of podocyte function
Cyclosporine A Protects Podocytes by Regulating Transgelin in Adriamycin-Induced Podocyte Injury
Pharmacogenetic podocyte depletion in zebrafish larvae as a model for focal segmental glomerulosclerosis
AF1q Contributes to Adriamycin-Induced Podocyte Injury by Activating Wnt/β-Catenin Signaling
Acatalasemic mice are mildly susceptible to adriamycin nephropathy and exhibit increased albuminuria and glomerulosclerosis
Minnelide Markedly Reduces Proteinuria in Mice with Adriamycin Nephropathy by Protecting Against Podocyte Injury
B7-1 mediates podocyte injury and glomerulosclerosis through communication with Hsp90ab1-LRP5-β-catenin pathway