ArticleProceedings of the National Academy of Sciences of the United States of America2008
Syntaxin 5 regulates the endoplasmic reticulum channel-release properties of polycystin-2.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 57 citations in OpenAlex.
- An Integrated Cardiac Microtissue Proteome Map Extends Therapeutic Remodeling by Nanovesicles.Molecular & cellular proteomics : MCP · 2026Article
- The Ion channel, CFTR, assembles with HIPPO pathway proteins TAZ and YAP in polycystic kidney disease.The Journal of biological chemistry · 2026Article
- Cleavage of N-terminus of polycystin-1 increases calcium permeability of polycystin-1/2 receptor channel complexes.JCI insight · 2025Article
- Genome variation in tick infestation and cryptic divergence in Tunisian indigenous sheep.BMC genomics · 2022Article
- Article
- Polycystins as components of large multiprotein complexes of polycystin interactors.Cellular signalling · 2020Review
- Review
- COPII vesicles can affect the activity of antisense oligonucleotides by facilitating the release of oligonucleotides from endocytic pathways.Nucleic acids research · 2018Article
- Retromer associates with the cytoplasmic amino-terminus of polycystin-2.Journal of cell science · 2018Article
- Monoubiquitination of syntaxin 3 leads to retrieval from the basolateral plasma membrane and facilitates cargo recruitment to exosomes.Molecular biology of the cell · 2017Article
- Adenylyl cyclase 5 links changes in calcium homeostasis to cAMP-dependent cyst growth in polycystic liver disease.Journal of hepatology · 2017Article
- Posttranslational regulation of polycystin-2 protein expression as a novel mechanism of cholangiocyte reaction and repair from biliary damage.Hepatology (Baltimore, Md.) · 2015Article
- Vasopressin and disruption of calcium signalling in polycystic kidney disease.Nature reviews. Nephrology · 2015Review
- New and notable ion-channels in the sarcoplasmic/endoplasmic reticulum: do they support the process of intracellular Ca²⁺ release?The Journal of physiology · 2015Review
- Sec63 and Xbp1 regulate IRE1α activity and polycystic disease severity.The Journal of clinical investigation · 2015Article
- Polycystic liver diseases: advanced insights into the molecular mechanisms.Nature reviews. Gastroenterology & hepatology · 2014Review
- Altered trafficking and stability of polycystins underlie polycystic kidney disease.The Journal of clinical investigation · 2014Article
- Valosin-containing protein-interacting membrane protein (VIMP) links the endoplasmic reticulum with microtubules in concert with cytoskeleton-linking membrane protein (CLIMP)-63.The Journal of biological chemistry · 2014Article
- Modulation of the secretory pathway rescues zebrafish polycystic kidney disease pathology.Journal of the American Society of Nephrology : JASN · 2014Article
- Polycystins and partners: proposed role in mechanosensitivity.The Journal of physiology · 2014Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Polycystin-2 (PC2), the gene product of one of two genes mutated in dominant polycystic kidney disease, is a member of the transient receptor potential cation channel family and can function as intracellular calcium (Ca(2+)) release channel. We performed a yeast two-hybrid screen by using the NH(2) terminus of PC2 and identified syntaxin-5 (Stx5) as a putative interacting partner. Coimmunoprecipitation studies in cell lines and kidney tissues confirmed interaction of PC2 with Stx5 in vivo. In vitro binding assays showed that the interaction between Stx5 and PC2 is direct and defined the respective interaction domains as the t-SNARE region of Stx5 and amino acids 5 to 72 of PC2. Single channel studies showed that interaction with Stx5 specifically reduces PC2 channel activity. Epithelial cells overexpressing mutant PC2 that does not bind Stx5 had increased baseline cytosolic Ca(2+) levels, decreased endoplasmic reticulum (ER) Ca(2+) stores, and reduced Ca(2+) release from ER stores in response to vasopressin stimulation. Cells lacking PC2 altogether had reduced cytosolic Ca(2+) levels. Our data suggest that PC2 in the ER plays a role in cellular Ca(2+) homeostasis and that Stx5 functions to inactivate PC2 and prevent leaking of Ca(2+) from ER stores. Modulation of the PC2/Stx5 interaction may be a useful target for impacting dysregulated intracellular Ca(2+) signaling associated with polycystic kidney disease.
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