BAIT
CLN8
C8orf61, EPMR
ceroid-lipofuscinosis, neuronal 8 (epilepsy, progressive with mental retardation)
GO Process (9)
GO Function (0)
GO Component (3)
Gene Ontology Biological Process
Gene Ontology Cellular Component
Homo sapiens
PREY
GABARAPL2
ATG8, ATG8C, GATE-16, GATE16, GEF-2, GEF2
GABA(A) receptor-associated protein-like 2
GO Process (9)
GO Function (6)
GO Component (9)
Gene Ontology Biological Process
- autophagic vacuole assembly [IBA]
- autophagy [NAS]
- cellular response to nitrogen starvation [IBA]
- intra-Golgi vesicle-mediated transport [ISS]
- membrane fusion [IBA]
- mitochondrion degradation [IBA]
- negative regulation of proteasomal protein catabolic process [IMP]
- nucleophagy [IBA]
- positive regulation of ATPase activity [ISS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
Two-hybrid
Bait protein expressed as a DNA binding domain (DBD) fusion and prey expressed as a transcriptional activation domain (TAD) fusion and interaction measured by reporter gene activation.
Publication
Identifying protein partners of CLN8, an ER-resident protein involved in neuronal ceroid lipofuscinosis.
Neuronal ceroid lipofuscinoses (NCLs) are a genetically heterogeneous group of neurodegenerative diseases characterized by cognitive and motor decline, epilepsy, visual loss and by lysosomal autofluorescent inclusions. Two distinct clinical phenotypes, the progressive epilepsy with mental retardation (EPMR) and a late-infantile variant of NCLs (CLN8-vLINCL) are associated with mutations in the CLN8 gene that encodes a transmembrane protein predominantly located to ... [more]
Biochim. Biophys. Acta Mar. 01, 2013; 1833(3);529-40 [Pubmed: 23142642]
Throughput
- Low Throughput
Curated By
- BioGRID