Use of the ND evidence code for Gene Ontology (GO) terms
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
Combined Automated Annotation using Multiple IEA Methods
Structural Characterization of Bardet-Biedl Syndrome 9 Protein (BBS9).
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The isolated human BBS9 N-terminal domain forms a seven-bladed beta-propeller at 1.8-angstrom resolution. This supports the domain description; scaffold activity requires the separate subunit-contact and assembly experiments, and is not established by the fold alone.
"The 1.8 Å
crystal structure of the 46-kDa N-terminal domain reveals a seven-bladed
β-propeller."
A core complex of BBS proteins cooperates with the GTPase Rab8 to promote ciliary membrane biogenesis.
A BBSome subunit links ciliogenesis, microtubule stability, and acetylation.
BBS6, BBS10, and BBS12 form a complex with CCT/TRiC family chaperonins and mediate BBSome assembly.
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.
Intrinsic protein-protein interaction-mediated and chaperonin-assisted sequential assembly of stable bardet-biedl syndrome protein complex, the BBSome.
BBS mutations modify phenotypic expression of CEP290-related ciliopathies.
The centriolar satellite protein AZI1 interacts with BBS4 and regulates ciliary trafficking of the BBSome.
Nephrocystin proteins NPHP5 and Cep290 regulate BBSome integrity, ciliary trafficking and cargo delivery.
An organelle-specific protein landscape identifies novel diseases and molecular mechanisms.
Architecture of the human interactome defines protein communities and disease networks.
Protein interaction perturbation profiling at amino-acid resolution.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Multimodal cell maps as a foundation for structural and functional genomics.
ARL6:GTP and the BBSome bind ciliary cargo
ARL6:GTP and the BBSome target cargo to the primary cilium
LZTFL1 binds the BBSome and prevents its traffic to the cilium
Temporal expression pattern of Bardet-Biedl syndrome genes in adipogenesis.
Knockdown of Bardet-Biedl syndrome gene BBS9/PTHB1 leads to cilia defects.
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Bbs9 knockdown in mouse IMCD3 cells impaired ciliation and shortened remaining cilia. Zebrafish bbs9 morphants had fewer and shorter Kupffer-vesicle cilia.
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Human wild-type BBS9 mRNA improved the measured eye-size phenotype in zebrafish morphants, whereas the tested G141R mutant mRNA did not. The study did not measure heart looping or laterality markers.
Molecular architecture of the Bardet-Biedl syndrome protein 2-7-9 subcomplex.