Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Automated transfer of experimentally-verified manual GO annotation data to mouse-rat orthologs
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Automated transfer of experimentally-verified manual GO annotation data to mouse-human orthologs
Combined Automated Annotation using Multiple IEA Methods
Axial skeletal defects caused by mutation in the spondylocostal dysplasia/pudgy gene Dll3 are associated with disruption of the segmentation clock within the presomitic mesoderm.
Segmentation defects of Notch pathway mutants and absence of a synergistic phenotype in lunatic fringe/radical fringe double mutant mice.
Dll3 pudgy mutation differentially disrupts dynamic expression of somite genes.
Mind bomb 1 is essential for generating functional Notch ligands to activate Notch.
Gm364 coordinates MIB2/DLL3/Notch2 to regulate female fertility through AKT activation.
Mouse Dll3: a novel divergent Delta gene which may complement the function of other Delta homologues during early pattern formation in the mouse embryo.
Expression of Dll3 in paraxial mesoderm
Expression of Dll3 in presomitic mesoderm
The divergent DSL ligand Dll3 does not activate Notch signaling but cell autonomously attenuates signaling induced by other DSL ligands.
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Dll3 does not bind or activate Notch in trans but cell-autonomously inhibits Notch signalling.
"Therefore, Dll3 functions not as an activator as previously reported but rather as a dedicated inhibitor of N signaling."
Divergent functions and distinct localization of the Notch ligands DLL1 and DLL3 in vivo.
Notch inhibition by the ligand DELTA-LIKE 3 defines the mechanism of abnormal vertebral segmentation in spondylocostal dysostosis.
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Dll3 interacts with Notch1 in late endocytic compartment, targeting it for lysosomal degradation.
"Dll3 targeting newly synthesized Notch1 for lysosomal degradation prior to post-translational processing and cell surface presentation of the receptor."
The mouse pudgy mutation disrupts Delta homologue Dll3 and initiation of early somite boundaries.