Nature Communications (Apr 2018)

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

  • Fumiaki Ando,
  • Shuichi Mori,
  • Naofumi Yui,
  • Tetsuji Morimoto,
  • Naohiro Nomura,
  • Eisei Sohara,
  • Tatemitsu Rai,
  • Sei Sasaki,
  • Yoshiaki Kondo,
  • Hiroyuki Kagechika,
  • Shinichi Uchida

DOI
https://doi.org/10.1038/s41467-018-03771-2
Journal volume & issue
Vol. 9, no. 1
pp. 1 – 11

Abstract

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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.