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Publication : Nek1 and TAZ interact to maintain normal levels of polycystin 2.

First Author  Yim H Year  2011
Journal  J Am Soc Nephrol Volume  22
Issue  5 Pages  832-7
PubMed ID  21474562 Mgi Jnum  J:219077
Mgi Id  MGI:5619460 Doi  10.1681/ASN.2010090992
Citation  Yim H, et al. (2011) Nek1 and TAZ interact to maintain normal levels of polycystin 2. J Am Soc Nephrol 22(5):832-7
abstractText  Polycystic kidney disease (PKD) in mice can arise from defects in Nek kinases, which participate in ciliogenesis. PKD can also arise from loss of the protein TAZ, an adaptor protein in the E3 ubiquitin ligase complex that targets the ciliary protein polycystin 2 (PC2) for degradation, but whether Nek and TAZ contribute to the same biochemical pathway is unknown. Here, we report that the nimA-related protein kinase Nek1 phosphorylates TAZ at a site essential for the ubiquitination and proteasomal degradation of PC2. Loss of Nek1 leads to underphosphorylation of TAZ, thereby promoting the abnormal accumulation of PC2. Furthermore, TAZ targets Nek1 for degradation. These data suggest that TAZ and Nek1 constitute a negative feedback loop linked through phosphorylation and ubiquitination and that the interaction of Nek1 and TAZ maintain PC2 at the level needed for proper ciliogenesis.
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