Zipper-interacting protein kinase (ZIPK) modulates canonical Wnt/beta-catenin signaling through interaction with Nemo-like kinase and T-cell factor 4 (NLK/TCF4).
Article Details
- CitationCopy to clipboard
Togi S, Ikeda O, Kamitani S, Nakasuji M, Sekine Y, Muromoto R, Nanbo A, Oritani K, Kawai T, Akira S, Matsuda T
Zipper-interacting protein kinase (ZIPK) modulates canonical Wnt/beta-catenin signaling through interaction with Nemo-like kinase and T-cell factor 4 (NLK/TCF4).
J Biol Chem. 2011 May 27;286(21):19170-7. doi: 10.1074/jbc.M110.189829. Epub 2011 Mar 30.
- PubMed ID
- 21454679 [ View in PubMed]
- Abstract
Zipper-interacting protein kinase (ZIPK) is a widely expressed serine/threonine kinase that has been implicated in apoptosis and transcriptional regulation. Here, we identified Nemo-like kinase (NLK) as a novel ZIPK-binding partner and found that ZIPK regulates NLK-mediated repression of canonical Wnt/beta-catenin signaling. Indeed, siRNA-mediated reduction of endogenous ZIPK expression reduced Wnt/beta-catenin signaling. Furthermore, ZIPK affected the formation of NLK-T-cell factor 4 (TCF4) complex. Importantly, ZIPK siRNA treatment in human colon carcinoma cells resulted in a reduction of beta-catenin/TCF-mediated gene expression and cell growth. These results indicate that ZIPK may serve as a transcriptional regulator of canonical Wnt/beta-catenin signaling through interaction with NLK/TCF4.