Taz Promotes Pc2 Degradation Through a Scfbeta-trcp E3 Ligase Complex.
From: Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.
Molecular and cellular biology
- Publish Date: Sep 2007
- ISSN: 0270-7306
- Volume: 27
- Issue: 18
- Pages: 6383-95
- Medium: Print
- Language: English
- Citation (JAMA): Tian Yu, Kolb Robert, Hong Jeong-Ho, et al. Taz Promotes Pc2 Degradation Through a Scfbeta-trcp E3 Ligase Complex.. Mol. Cell. Biol. Sep 2007;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.
Mesh Headings (Keywords): Animals, Cell Line, Cullin Proteins, F-Box Proteins, Fluorescent Antibody Technique, Indirect, Glutathione Transferase, Humans, Immunohistochemistry, Kidney, Mice, Mice, Knockout, Models, Biological, Precipitin Tests, Proteins, Recombinant Proteins, SKP Cullin F-Box Protein Ligases, TRPP Cation Channels, Transcription Factors, Ubiquitins
Check for Full Text / PubMed Unique Identifier (PMID): 17636028
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