Journal

Journal of the American Society of Nephrology : JASN
ISSN: 1533-3450
Titre abrégé: J Am Soc Nephrol
Pays: United States
ID NLM: 9013836

Informations de publication

Date de publication:
10 2020
Historique:
received: 30 03 2020
accepted: 15 06 2020
pubmed: 5 8 2020
medline: 6 3 2021
entrez: 5 8 2020
Statut: ppublish

Résumé

Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease leading to renal failure, wherein multiple cysts form in renal tubules and collecting ducts derived from distinct precursors: the nephron progenitor and ureteric bud (UB), respectively. Recent progress in induced pluripotent stem cell (iPSC) biology has enabled cyst formation in nephron progenitor-derived human kidney organoids in which CRISPR-Cas9 technology deleted Cysts formed in UB organoids with homozygous Cysts form in

Sections du résumé

BACKGROUND
Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease leading to renal failure, wherein multiple cysts form in renal tubules and collecting ducts derived from distinct precursors: the nephron progenitor and ureteric bud (UB), respectively. Recent progress in induced pluripotent stem cell (iPSC) biology has enabled cyst formation in nephron progenitor-derived human kidney organoids in which
METHODS
CRISPR-Cas9 technology deleted
RESULTS
Cysts formed in UB organoids with homozygous
CONCLUSIONS
Cysts form in

Identifiants

pubmed: 32747355
pii: ASN.2020030378
doi: 10.1681/ASN.2020030378
pmc: PMC7609014
doi:

Substances chimiques

TRPP Cation Channels 0
polycystic kidney disease 1 protein 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2355-2371

Informations de copyright

Copyright © 2020 by the American Society of Nephrology.

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Auteurs

Shohei Kuraoka (S)

Department of Kidney Development, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.
Department of Pediatrics, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.

Shunsuke Tanigawa (S)

Department of Kidney Development, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.

Atsuhiro Taguchi (A)

Department of Kidney Development, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.

Akitsu Hotta (A)

Department of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, Japan.

Hitoshi Nakazato (H)

Department of Pediatrics, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.

Kenji Osafune (K)

Department of Cell Growth and Differentiation, Center for iPS Cell Research and Application, Kyoto University, Kyoto, Japan.

Akio Kobayashi (A)

Department of Kidney Development, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.

Ryuichi Nishinakamura (R)

Department of Kidney Development, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan ryuichi@kumamoto-u.ac.jp.

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