| UniProt functional annotation for Q13137 | |||
| UniProt code: Q13137. |
| Organism: | Homo sapiens (Human). | |
| Taxonomy: | Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo. | |
| Function: | Xenophagy-specific receptor required for autophagy-mediated intracellular bacteria degradation. Acts as an effector protein of galectin-sensed membrane damage that restricts the proliferation of infecting pathogens such as Salmonella typhimurium upon entry into the cytosol by targeting LGALS8-associated bacteria for autophagy (PubMed:22246324). Initially orchestrates bacteria targeting to autophagosomes and subsequently ensures pathogen degradation by regulating pathogen-containing autophagosome maturation (PubMed:23022382, PubMed:25771791). Bacteria targeting to autophagosomes relies on its interaction with MAP1LC3A, MAP1LC3B and/or GABARAPL2, whereas regulation of pathogen-containing autophagosome maturation requires the interaction with MAP3LC3C (PubMed:23022382, PubMed:25771791). May play a role in ruffle formation and actin cytoskeleton organization and seems to negatively regulate constitutive secretion (PubMed:17635994). {ECO:0000269|PubMed:17635994, ECO:0000269|PubMed:22246324, ECO:0000269|PubMed:23022382, ECO:0000269|PubMed:23386746, ECO:0000269|PubMed:25771791}. | |
| Subunit: | Dimer (PubMed:23511477). Part of a complex consisting of CALCOCO2, TAX1BP1 and MYO6 (PubMed:17635994). Interacts with GEMIN4 (PubMed:12869526). Interacts with ATG8 family members MAP1LC3A, MAP1LC3B, GABARAP, GABARAPL1 and GABARAPL2 (PubMed:25771791). Interacts with ATG8 family member MAP1LC3C (PubMed:23022382). Interacts with LGALS8 (PubMed:22246324, PubMed:25771791, PubMed:23511477, PubMed:23386746). {ECO:0000269|PubMed:12869526, ECO:0000269|PubMed:17635994, ECO:0000269|PubMed:22246324, ECO:0000269|PubMed:23022382, ECO:0000269|PubMed:23386746, ECO:0000269|PubMed:23511477, ECO:0000269|PubMed:25771791}. | |
| Subcellular location: | Cytoplasm, perinuclear region {ECO:0000269|PubMed:12869526, ECO:0000269|PubMed:17635994, ECO:0000269|PubMed:9230084}. Cytoplasm, cytoskeleton {ECO:0000269|PubMed:17635994}. Cytoplasmic vesicle, autophagosome membrane {ECO:0000269|PubMed:25771791}; Peripheral membrane protein {ECO:0000305}. Note=According to PubMed:7540613, localizes to nuclear dots. According to PubMed:9230084 and PubMed:12869526, it is not a nuclear dot-associated protein but localizes predominantly in the cytoplasm with a coarse-grained distribution preferentially close to the nucleus. {ECO:0000269|PubMed:12869526, ECO:0000269|PubMed:7540613, ECO:0000269|PubMed:9230084}. | |
| Tissue specificity: | Expressed in all tissues tested with highest expression in skeletal muscle and lowest in brain. {ECO:0000269|PubMed:7540613}. | |
| Induction: | Treatment with IFNB1/IFN-beta and IFNG/IFN-gamma show an increase in number and size of CALCOCO2-specific dots and partial redistribution to the cytoplasm (PubMed:7540613). IFNG/IFN-gamma increases gene expression only slightly and IFNB does not increase expression (PubMed:9230084). {ECO:0000269|PubMed:7540613, ECO:0000269|PubMed:9230084}. | |
| Domain: | The MYO6-binding domain is required for autophagy-mediated degradation of infecting bacteria such as Salmonella typhimurium, but not for bacteria targeting to autophagosomes. {ECO:0000269|PubMed:25771791}. | |
| Domain: | The CLIR (LC3C-interacting region) motif is required for interaction with MAP1LC3C, but dispensable for CALCOCO2-mediated autophagosome maturation. {ECO:0000269|PubMed:23022382, ECO:0000269|PubMed:25771791}. | |
| Domain: | The LIR-like motif is required for interaction with MAP1LC3A, MAP1LC3B and GABARAPL2, as well as for CALCOCO2-mediated autophagosome maturation. {ECO:0000269|PubMed:25771791}. | |
| Domain: | The LGALS8-binding domain is essential for the recruitment to cytosol-exposed infecting bacteria. {ECO:0000269|PubMed:23386746}. | |
| Similarity: | Belongs to the CALCOCO family. {ECO:0000305}. | |
Annotations taken from UniProtKB at the EBI.