Gene Ontology annotation through association of InterPro records with GO terms
Falcon deep research report for ARL6
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Falcon deep research corroborates ARL6/BBS3 as the GTP-dependent membrane-targeting switch that recruits the BBSome coat to cilia, and refines the interface to a composite BBS1/BBS7 site exposed by a BBSome conformational change (Singh et al. 2020 cryo-EM); upstream ARL6 GEF/GAP regulators remain undefined.
"triggering a conformational change that activates the BBSome for membrane protein trafficking"
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 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
Functional dissection of Rab GTPases involved in primary cilium formation.
Large-scale proteomics and phosphoproteomics of urinary exosomes.
Bardet-Biedl syndrome-associated small GTPase ARL6 (BBS3) functions at or near the ciliary gate and modulates Wnt signaling.
The conserved Bardet-Biedl syndrome proteins assemble a coat that traffics membrane proteins to cilia.
A novel protein LZTFL1 regulates ciliary trafficking of the BBSome and Smoothened.
Bardet-Biedl syndrome 3 (Bbs3) knockout mouse model reveals common BBS-associated phenotypes and Bbs3 unique phenotypes.
The intraflagellar transport protein IFT27 promotes BBSome exit from cilia through the GTPase ARL6/BBS3.
ARL6:GTP and the BBSome bind ciliary cargo
ARL6:GTP and the BBSome target cargo to the primary cilium