Ciliary exclusion of Polycystin-2 promotes kidney cystogenesis in an autosomal dominant polycystic kidney disease model

The molecular role of ciliary Polycystin-2 (PC2) in cyst formation and polycystic kidney disease (ADKPD) is unclear. Here, the authors identify a PC2 mutant lacking ciliary localisation but with active Ca2+ channel function in mice, that is sufficient to generate an ADPKD phenotype.

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Autores principales:	Rebecca V. Walker, Jennifer L. Keynton, Daniel T. Grimes, Vrinda Sreekumar, Debbie J. Williams, Chris Esapa, Dongsheng Wu, Martin M. Knight, Dominic P. Norris
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2019
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/547e1a8754cb4905b8faf5dab5e28885
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spelling	oai:doaj.org-article:547e1a8754cb4905b8faf5dab5e288852021-12-02T15:35:09ZCiliary exclusion of Polycystin-2 promotes kidney cystogenesis in an autosomal dominant polycystic kidney disease model10.1038/s41467-019-12067-y2041-1723https://doaj.org/article/547e1a8754cb4905b8faf5dab5e288852019-09-01T00:00:00Zhttps://doi.org/10.1038/s41467-019-12067-yhttps://doaj.org/toc/2041-1723The molecular role of ciliary Polycystin-2 (PC2) in cyst formation and polycystic kidney disease (ADKPD) is unclear. Here, the authors identify a PC2 mutant lacking ciliary localisation but with active Ca2+ channel function in mice, that is sufficient to generate an ADPKD phenotype.Rebecca V. WalkerJennifer L. KeyntonDaniel T. GrimesVrinda SreekumarDebbie J. WilliamsChris EsapaDongsheng WuMartin M. KnightDominic P. NorrisNature PortfolioarticleScienceQENNature Communications, Vol 10, Iss 1, Pp 1-11 (2019)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Rebecca V. Walker Jennifer L. Keynton Daniel T. Grimes Vrinda Sreekumar Debbie J. Williams Chris Esapa Dongsheng Wu Martin M. Knight Dominic P. Norris Ciliary exclusion of Polycystin-2 promotes kidney cystogenesis in an autosomal dominant polycystic kidney disease model
description	The molecular role of ciliary Polycystin-2 (PC2) in cyst formation and polycystic kidney disease (ADKPD) is unclear. Here, the authors identify a PC2 mutant lacking ciliary localisation but with active Ca2+ channel function in mice, that is sufficient to generate an ADPKD phenotype.
format	article
author	Rebecca V. Walker Jennifer L. Keynton Daniel T. Grimes Vrinda Sreekumar Debbie J. Williams Chris Esapa Dongsheng Wu Martin M. Knight Dominic P. Norris
author_facet	Rebecca V. Walker Jennifer L. Keynton Daniel T. Grimes Vrinda Sreekumar Debbie J. Williams Chris Esapa Dongsheng Wu Martin M. Knight Dominic P. Norris
author_sort	Rebecca V. Walker
title	Ciliary exclusion of Polycystin-2 promotes kidney cystogenesis in an autosomal dominant polycystic kidney disease model
title_short	Ciliary exclusion of Polycystin-2 promotes kidney cystogenesis in an autosomal dominant polycystic kidney disease model
title_full	Ciliary exclusion of Polycystin-2 promotes kidney cystogenesis in an autosomal dominant polycystic kidney disease model
title_fullStr	Ciliary exclusion of Polycystin-2 promotes kidney cystogenesis in an autosomal dominant polycystic kidney disease model
title_full_unstemmed	Ciliary exclusion of Polycystin-2 promotes kidney cystogenesis in an autosomal dominant polycystic kidney disease model
title_sort	ciliary exclusion of polycystin-2 promotes kidney cystogenesis in an autosomal dominant polycystic kidney disease model
publisher	Nature Portfolio
publishDate	2019
url	https://doaj.org/article/547e1a8754cb4905b8faf5dab5e28885
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Ciliary exclusion of Polycystin-2 promotes kidney cystogenesis in an autosomal dominant polycystic kidney disease model

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