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
Gene Ontology annotation based on curation of intracellular localizations of expressed fusion proteins in living cells
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Combined Automated Annotation using Multiple IEA Methods
Towards a proteome-scale map of the human protein-protein interaction network.
Differential use of functional domains by coiled-coil coactivator in its synergistic coactivator function with beta-catenin or GRIP1.
CCAR1/CoCoA pair-mediated recruitment of the Mediator defines a novel pathway for GATA1 function.
A proteome-scale map of the human interactome network.
A reference map of the human binary protein interactome.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Multimodal cell maps as a foundation for structural and functional genomics.
Mass spectrometry proteomics reveals a function for mammalian CALCOCO1 in MTOR-regulated selective autophagy.
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CALCOCO1 physically interacts with the ATG8-family protein MAP1LC3C, and genetic deletion of CALCOCO1 disrupts autophagy of the endoplasmic reticulum (reticulophagy), establishing CALCOCO1 as a selective-autophagy receptor in the MTOR-regulated autophagy axis.
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A canonical LIR motif (W47A abolishes LC3-family binding) and a non-canonical CLIR motif (L140A/V142A weakens MAP1LC3C binding) mediate CALCOCO1 association with ATG8-family proteins, with a preference for MAP1LC3C, and CALCOCO1 abundance is regulated by MTOR-dependent autophagy and lysosomal flux.
CCAR1, a key regulator of mediator complex recruitment to nuclear receptor transcription complexes.
Distinct, genome-wide, gene-specific selectivity patterns of four glucocorticoid receptor coregulators.
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siRNA depletion of CALCOCO1 (alongside CCAR1, CCAR2, and ZNF282) shows that CALCOCO1 acts as a gene-selective glucocorticoid-receptor coregulator with both positive and negative effects on hormone-regulated genes, rather than as a global coactivator.
YIPF3 and YIPF4 regulate autophagic turnover of the Golgi apparatus.
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In a HeLa Golgiphagy reporter assay, knockdown of CALCOCO1 alone did not decrease Golgiphagy and triple knockdown with YIPF3/YIPF4 retained activity, indicating that CALCOCO1 is not the dominant Golgiphagy receptor in this context and that Golgi turnover involves redundant or context-specific receptors.
Join the club: YIPF3 and YIPF4 act as Golgiphagy receptors.
UniProt entry Q9P1Z2 (CACO1_HUMAN)