Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 27, Issue 18, Pages 6383-6395Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.00254-07
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Funding
- National Research Foundation of Korea [과C6A2204] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- NCI NIH HHS [CA 90992, R01 CA090992, R01 CA092520, R01 CA92520] Funding Source: Medline
- NIDDK NIH HHS [R01DK40703, R01 DK053357, R01DK53357, R01 DK040703, R01 DK051050, R01DK51050] Funding Source: Medline
- NIGMS NIH HHS [GM60594, R01 GM060594] Funding Source: Medline
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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.
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