{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["11(10)"],"submitter":["Dona M"],"pubmed_abstract":["Ciliopathies are Mendelian disorders caused by dysfunction of cilia, ubiquitous organelles involved in fluid propulsion (motile cilia) or signal transduction (primary cilia). Retinal dystrophy is a common phenotypic characteristic of ciliopathies since photoreceptor outer segments are specialized primary cilia. These ciliary structures heavily rely on intracellular minus-end directed transport of cargo, mediated at least in part by the cytoplasmic dynein 1 motor complex, for their formation, maintenance and function. Ninein-like protein (NINL) is known to associate with this motor complex and is an important interaction partner of the ciliopathy-associated proteins lebercilin, USH2A and CC2D2A. Here, we scrutinize the function of NINL with combined proteomic and zebrafish in vivo approache"],"journal":["PLoS genetics"],"pagination":["e1005574"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4617706"],"repository":["biostudies-literature"],"pubmed_title":["NINL and DZANK1 Co-function in Vesicle Transport and Are Essential for Photoreceptor Development in Zebrafish."],"pmcid":["PMC4617706"],"pubmed_authors":["Gibson TJ","van Beersum SE","Kremer H","Peters TA","Tonnaer EL","van Wijk E","Ueffing M","Roepman R","Keunen JE","Bachmann-Gagescu R","Slijkerman RW","Dona M","Toedt G","van Reeuwijk J","Hetterschijt L","Bergboer JG","Flik G","de Vrieze E","Texier Y","Boldt K","Horn N"],"additional_accession":[]},"is_claimable":false,"name":"NINL and DZANK1 Co-function in Vesicle Transport and Are Essential for Photoreceptor Development in Zebrafish.","description":"Ciliopathies are Mendelian disorders caused by dysfunction of cilia, ubiquitous organelles involved in fluid propulsion (motile cilia) or signal transduction (primary cilia). Retinal dystrophy is a common phenotypic characteristic of ciliopathies since photoreceptor outer segments are specialized primary cilia. These ciliary structures heavily rely on intracellular minus-end directed transport of cargo, mediated at least in part by the cytoplasmic dynein 1 motor complex, for their formation, maintenance and function. Ninein-like protein (NINL) is known to associate with this motor complex and is an important interaction partner of the ciliopathy-associated proteins lebercilin, USH2A and CC2D2A. Here, we scrutinize the function of NINL with combined proteomic and zebrafish in vivo approache","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Oct","modification":"2026-04-16T21:15:39.617Z","creation":"2019-03-26T22:46:02Z"},"accession":"S-EPMC4617706","cross_references":{"pubmed":["26485514"],"doi":["10.1371/journal.pgen.1005574"]}}