論文

査読有り
2018年3月

Glycogen synthase kinase 3ß functions as a positive effector in the WNK signaling pathway.

PLoS One
  • Sato, A
  • ,
  • Shibuya, H

13
開始ページ
e0193204
終了ページ
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1371/journal.

The with no lysine (WNK) protein kinase family is conserved among many species. Some<br />
mutations in human WNK gene are associated with pseudohypoaldosteronism type II, a<br />
form of hypertension, and hereditary sensory and autonomic neuropathy type 2A. In kidney,<br />
WNK regulates the activity of STE20/SPS1-related, proline alanine-rich kinase and/or oxidative-<br />
stress responsive 1, which in turn regulate ion co-transporters. The misregulation of this<br />
pathway is involved in the pathogenesis of pseudohypoaldosteronism type II. In the neural<br />
system, WNK is involved in the specification of the cholinergic neuron, but the pathogenesis<br />
of hereditary sensory and autonomic neuropathy type 2A is still unknown. To better understand<br />
the WNK pathway, we isolated WNK-associated genes using Drosophila. We identified<br />
Glycogen synthase kinase 3ß (GSK3ß)/Shaggy (Sgg) as a candidate gene that was<br />
shown to interact with the WNK signaling pathway in both Drosophila and mammalian cells.<br />
Furthermore, GSK3ß was involved in neural specification downstream of WNK. These<br />
results suggest that GSK3ß/Sgg functions as a positive effector in the WNK signaling<br />
pathway.

リンク情報
DOI
https://doi.org/10.1371/journal.

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