| First Author | Lee BH | Year | 2007 |
| Journal | J Biol Chem | Volume | 282 |
| Issue | 25 | Pages | 17985-96 |
| PubMed ID | 17392271 | Mgi Jnum | J:123388 |
| Mgi Id | MGI:3718181 | Doi | 10.1074/jbc.M702664200 |
| Citation | Lee BH, et al. (2007) Biological cross-talk between WNK1 and the transforming growth factor beta-Smad signaling pathway. J Biol Chem 282(25):17985-96 |
| abstractText | WNKs (with no lysine (K)), unique serine/threonine protein kinases, have been best studied in the context of cell volume regulation and ion homeostasis. Here we describe a biological link between WNKs and transforming growth factor (TGF) beta-Smad signaling. Both WNK1 and WNK4 directly bind to and phosphorylate Smad2. Knockdown of WNK1 in HeLa cells using small interfering RNA reduces Smad2 protein expression; this decrease is at least partially due to down-regulation of Smad2 transcription. In contrast, phosphorylated Smad2 significantly accumulated in the nucleus as a consequence of depletion of WNK1, resulting in Smad-mediated transcriptional responses. In addition, TGFbeta-induced target gene transcripts were increased in WNK1 small interfering RNA cells. These findings suggest WNK1 as a dual modulator of TGFbeta-Smad signaling pathways. |
