AKAPs-PKA disruptors increase AQP2 activity independently of vasopressin in a model of nephrogenic diabetes insipidus

Patients suffering from congenital nephrogenic diabetes insipidus (NDI) fail to concentrate urine due to mutations in vasopressin type 2 receptor (V2R). Here Ando et al. show that agents disrupting the interaction between PKA and AKAPs restore aquaporin-2 activity downstream of V2R, offering a thera...

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Autores principales:	Fumiaki Ando, Shuichi Mori, Naofumi Yui, Tetsuji Morimoto, Naohiro Nomura, Eisei Sohara, Tatemitsu Rai, Sei Sasaki, Yoshiaki Kondo, Hiroyuki Kagechika, Shinichi Uchida
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/8c60b14a92e94b27bd57f69fed3d984d
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spelling	oai:doaj.org-article:8c60b14a92e94b27bd57f69fed3d984d2021-12-02T16:56:54ZAKAPs-PKA disruptors increase AQP2 activity independently of vasopressin in a model of nephrogenic diabetes insipidus10.1038/s41467-018-03771-22041-1723https://doaj.org/article/8c60b14a92e94b27bd57f69fed3d984d2018-04-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-03771-2https://doaj.org/toc/2041-1723Patients suffering from congenital nephrogenic diabetes insipidus (NDI) fail to concentrate urine due to mutations in vasopressin type 2 receptor (V2R). Here Ando et al. show that agents disrupting the interaction between PKA and AKAPs restore aquaporin-2 activity downstream of V2R, offering a therapeutic approach for the treatment of NDI.Fumiaki AndoShuichi MoriNaofumi YuiTetsuji MorimotoNaohiro NomuraEisei SoharaTatemitsu RaiSei SasakiYoshiaki KondoHiroyuki KagechikaShinichi UchidaNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-11 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Fumiaki Ando Shuichi Mori Naofumi Yui Tetsuji Morimoto Naohiro Nomura Eisei Sohara Tatemitsu Rai Sei Sasaki Yoshiaki Kondo Hiroyuki Kagechika Shinichi Uchida AKAPs-PKA disruptors increase AQP2 activity independently of vasopressin in a model of nephrogenic diabetes insipidus
description	Patients suffering from congenital nephrogenic diabetes insipidus (NDI) fail to concentrate urine due to mutations in vasopressin type 2 receptor (V2R). Here Ando et al. show that agents disrupting the interaction between PKA and AKAPs restore aquaporin-2 activity downstream of V2R, offering a therapeutic approach for the treatment of NDI.
format	article
author	Fumiaki Ando Shuichi Mori Naofumi Yui Tetsuji Morimoto Naohiro Nomura Eisei Sohara Tatemitsu Rai Sei Sasaki Yoshiaki Kondo Hiroyuki Kagechika Shinichi Uchida
author_facet	Fumiaki Ando Shuichi Mori Naofumi Yui Tetsuji Morimoto Naohiro Nomura Eisei Sohara Tatemitsu Rai Sei Sasaki Yoshiaki Kondo Hiroyuki Kagechika Shinichi Uchida
author_sort	Fumiaki Ando
title	AKAPs-PKA disruptors increase AQP2 activity independently of vasopressin in a model of nephrogenic diabetes insipidus
title_short	AKAPs-PKA disruptors increase AQP2 activity independently of vasopressin in a model of nephrogenic diabetes insipidus
title_full	AKAPs-PKA disruptors increase AQP2 activity independently of vasopressin in a model of nephrogenic diabetes insipidus
title_fullStr	AKAPs-PKA disruptors increase AQP2 activity independently of vasopressin in a model of nephrogenic diabetes insipidus
title_full_unstemmed	AKAPs-PKA disruptors increase AQP2 activity independently of vasopressin in a model of nephrogenic diabetes insipidus
title_sort	akaps-pka disruptors increase aqp2 activity independently of vasopressin in a model of nephrogenic diabetes insipidus
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/8c60b14a92e94b27bd57f69fed3d984d
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AKAPs-PKA disruptors increase AQP2 activity independently of vasopressin in a model of nephrogenic diabetes insipidus

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