http://purl.uniprot.org/citations/29563216 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/29563216 | http://www.w3.org/2000/01/rdf-schema#comment | "Arf6/ARF-6 is a crucial regulator of the endosomal phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) pool in endocytic recycling. To further characterize ARF-6 regulation, we performed an ARF-6 interactor screen in Caenorhabditis elegans and identified SAC-1, the homologue of the phosphoinositide phosphatase Sac1p in yeast, as a novel ARF-6 partner. In the absence of ARF-6, basolateral endosomes show a loss of SAC-1 staining in epithelial cells. Steady-state cargo distribution assays revealed that loss of SAC-1 specifically affected apical secretory delivery and basolateral recycling. PI(4,5)P2 levels and the endosomal labeling of the ARF-6 effector UNC-16 were significantly elevated in sac-1 mutants, suggesting that SAC-1 functions as a negative regulator of ARF-6. Further analyses revealed an interaction between SAC-1 and the ARF-6-GEF BRIS-1. This interaction outcompeted ARF-6(guanosine diphosphate [GDP]) for binding to BRIS-1 in a concentration-dependent manner. Consequently, loss of SAC-1 promotes the intracellular overlap between ARF-6 and BRIS-1. BRIS-1 knockdown resulted in a significant reduction in PI(4,5)P2 levels in SAC-1-depleted cells. Interestingly, the action of SAC-1 in sequestering BRIS-1 is independent of SAC-1's catalytic activity. Our results suggest that the interaction of SAC-1 with ARF-6 curbs ARF-6 activity by limiting the access of ARF-6(GDP) to its guanine nucleotide exchange factor, BRIS-1."xsd:string |
http://purl.uniprot.org/citations/29563216 | http://purl.org/dc/terms/identifier | "doi:10.1083/jcb.201711065"xsd:string |
http://purl.uniprot.org/citations/29563216 | http://purl.uniprot.org/core/author | "Chen J."xsd:string |
http://purl.uniprot.org/citations/29563216 | http://purl.uniprot.org/core/author | "Chen D."xsd:string |
http://purl.uniprot.org/citations/29563216 | http://purl.uniprot.org/core/author | "Liu S."xsd:string |
http://purl.uniprot.org/citations/29563216 | http://purl.uniprot.org/core/author | "Shi A."xsd:string |
http://purl.uniprot.org/citations/29563216 | http://purl.uniprot.org/core/author | "Wang X."xsd:string |
http://purl.uniprot.org/citations/29563216 | http://purl.uniprot.org/core/author | "Yang C."xsd:string |
http://purl.uniprot.org/citations/29563216 | http://purl.uniprot.org/core/author | "Hang W."xsd:string |
http://purl.uniprot.org/citations/29563216 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
http://purl.uniprot.org/citations/29563216 | http://purl.uniprot.org/core/name | "J Cell Biol"xsd:string |
http://purl.uniprot.org/citations/29563216 | http://purl.uniprot.org/core/pages | "2121-2139"xsd:string |
http://purl.uniprot.org/citations/29563216 | http://purl.uniprot.org/core/title | "SAC-1 ensures epithelial endocytic recycling by restricting ARF-6 activity."xsd:string |
http://purl.uniprot.org/citations/29563216 | http://purl.uniprot.org/core/volume | "217"xsd:string |
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