Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
TULP3 bridges the IFT-A complex and membrane phosphoinositides to promote trafficking of G protein-coupled receptors into primary cilia.
Mainzer-Saldino syndrome is a ciliopathy caused by IFT140 mutations.
Combined NGS approaches identify mutations in the intraflagellar transport gene IFT140 in skeletal ciliopathies with early progressive kidney Disease.
An organelle-specific protein landscape identifies novel diseases and molecular mechanisms.
Role for the IFT-A Complex in Selective Transport to the Primary Cilium.
Intraflagellar transport-A complex mediates ciliary entry and retrograde trafficking of ciliary G protein-coupled receptors.
Partial uniparental isodisomy of chromosome 16 unmasks a deleterious biallelic mutation in IFT140 that causes Mainzer-Saldino syndrome.
Ciliopathy-associated mutations of IFT122 impair ciliary protein trafficking but not ciliogenesis.
Human IFT-A complex structures provide molecular insights into ciliary transport.
GPR45 modulates Gα(s) at primary cilia of the paraventricular hypothalamus to control food intake.
TULP3 is required for GPR161 localization in the cilium
The IFT-A complex recruits TULP3
Assembly of IFT A complex
Assembly of the anterograde IFT train
Assembly of the retrograde IFT train
The anterograde IFT train dissociates
The retrograde IFT train dissociates