PMID:17636028

Citation	Tian, Y, Kolb, R, Hong, JH, Carroll, J, Li, D, You, J, Bronson, R, Yaffe, MB, Zhou, J and Benjamin, T (2007) TAZ promotes PC2 degradation through a SCFbeta-Trcp E3 ligase complex. Mol. Cell. Biol. 27:6383-95
Abstract	Studies of a TAZ knockout mouse reveal a novel function of the transcriptional regulator TAZ, that is, as a binding partner of the F-box protein beta-Trcp. TAZ-/- mice develop polycystic kidney disease (PKD) and emphysema. The calcium-permeable cation channel protein polycystin 2 (PC2) is overexpressed in kidneys of TAZ-/- mice as a result of decreased degradation via an SCF(beta-Trcp) E3 ubiquitin ligase pathway. Replacements of serines in a phosphodegron motif in TAZ prevent beta-Trcp binding and PC2 degradation. Coexpression of a cytoplasmic fragment of polycystin 1 blocks the PC2-TAZ interaction and prevents TAZ-mediated degradation of PC2. Depletion of TAZ in zebrafish also results in a cystic kidney accompanied by overexpression of PC2. These results establish a common role of TAZ across vertebrate species in a protein degradation pathway regulated by phosphorylation and implicate deficiencies in this pathway in the development of PKD.
Links	PubMed PMC2099608 Online version:10.1128/MCB.00254-07
Keywords	Animals; Cell Line; Cullin Proteins/metabolism; F-Box Proteins/metabolism; Fluorescent Antibody Technique, Indirect; Glutathione Transferase/metabolism; Humans; Immunohistochemistry; Kidney/cytology; Mice; Mice, Knockout; Models, Biological; Precipitin Tests; Proteins/genetics; Proteins/metabolism; Recombinant Proteins/metabolism; SKP Cullin F-Box Protein Ligases/genetics; SKP Cullin F-Box Protein Ligases/metabolism; TRPP Cation Channels/metabolism; Transcription Factors/genetics; Transcription Factors/metabolism; Ubiquitins/metabolism
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