ArticleThe Journal of biological chemistry2010
Polycystin-2 activity is controlled by transcriptional coactivator with PDZ binding motif and PALS1-associated tight junction protein.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- DLG1 functions upstream of SDCCAG3 and IFT20 to control ciliary targeting of polycystin-2.EMBO reports · 2024Article
- DLG1 functions upstream of SDCCAG3 and IFT20 to control ciliary targeting of polycystin-2.bioRxiv : the preprint server for biology · 2024Article
- PATJ inhibits histone deacetylase 7 to control tight junction formation and cell polarity.Cellular and molecular life sciences : CMLS · 2023Article
- Yap controls notochord formation and neural tube patterning by integrating mechanotransduction withScience advances · 2023Article
- Research Progress on PATJ and Underlying Mechanisms Associated with Functional Outcomes After Stroke.Neuropsychiatric disease and treatment · 2021Review
- Cell Polarity Protein Pals1-Associated Tight Junction Expression Is a Favorable Prognostic Marker in Clear Cell Renal Cell Carcinoma.Frontiers in genetics · 2020Article
- Intracellular APOL1 Risk Variants Cause Cytotoxicity Accompanied by Energy Depletion.Journal of the American Society of Nephrology : JASN · 2017Article
- The Vac14-interaction network is linked to regulators of the endolysosomal and autophagic pathway.Molecular & cellular proteomics : MCP · 2014Article
- Regulation of the Hippo pathway and implications for anticancer drug development.Trends in pharmacological sciences · 2013Review
- TAZ suppresses NFAT5 activity through tyrosine phosphorylation.Molecular and cellular biology · 2012Article
- Integrating developmental signals: a Hippo in the (path)way.Oncogene · 2012Review
- The transcriptional coactivator TAZ regulates mesenchymal differentiation in malignant glioma.Genes & development · 2011Article
- Regulation and function of the TAZ transcription co-activator.International journal of biochemistry and molecular biology · 2011Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is the most frequent monogenic cause of kidney failure, characterized by the development of renal cysts. ADPKD is caused by mutations of the polycystin-1 (PC1) or polycystin-2 (PC2) genes. PC2 encodes a Ca(2+)-permeable cation channel, and its dysfunction has been implicated in cyst development. The transcriptional coactivator with PDZ binding motif (TAZ) is required for the integrity of renal cilia. Its absence results in the development of renal cysts in a knock-out mouse model. TAZ directly interacts with PC2, and it has been suggested that another yet unidentified PDZ domain protein may be involved in the TAZ/PC2 interaction. Here we describe a novel interaction of TAZ with the multi-PDZ-containing PALS1-associated tight junction protein (PATJ). TAZ interacts with both the N-terminal PDZ domains 1-3 and the C-terminal PDZ domains 8-10 of PATJ, suggesting two distinct TAZ binding domains. We also show that the C terminus of PC2 strongly interacts with PDZ domains 8-10 and to a weaker extent with PDZ domains 1-3 of PATJ. Finally, we demonstrate that both TAZ and PATJ impair PC2 channel activity when co-expressed with PC2 in oocytes of Xenopus laevis. These results implicate TAZ and PATJ as novel regulatory elements of the PC2 channel and might thus be involved in ADPKD pathology.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.