BAIT
CLN5
NCL
ceroid-lipofuscinosis, neuronal 5
GO Process (7)
GO Function (2)
GO Component (7)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
SLC25A4
1, AAC1, ANT, ANT 1, ANT1, MTDPS12, PEO2, PEO3, T1
solute carrier family 25 (mitochondrial carrier; adenine nucleotide translocator), member 4
GO Process (9)
GO Function (2)
GO Component (4)
Gene Ontology Biological Process
- adenine transport [TAS]
- energy reserve metabolic process [TAS]
- generation of precursor metabolites and energy [TAS]
- mitochondrial genome maintenance [TAS]
- negative regulation of necroptotic process [IMP]
- regulation of insulin secretion [TAS]
- small molecule metabolic process [TAS]
- transport [TAS]
- viral process [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
Affinity Capture-MS
An interaction is inferred when a bait protein is affinity captured from cell extracts by either polyclonal antibody or epitope tag and the associated interaction partner is identified by mass spectrometric methods.
Publication
Drafting the CLN3 protein interactome in SH-SY5Y human neuroblastoma cells: a label-free quantitative proteomics approach.
Neuronal ceroid lipofuscinoses (NCL) are the most common inherited progressive encephalopathies of childhood. One of the most prevalent forms of NCL, Juvenile neuronal ceroid lipofuscinosis (JNCL) or CLN3 disease (OMIM: 204200) is caused by mutations in the CLN3 gene on chromosome 16p12.1. Despite progress in the NCL field, the primary function of ceroid-lipofuscinosis neuronal protein 3 (CLN3) remains elusive. In ... [more]
J. Proteome Res. Mar. 07, 2013; 0(0); [Pubmed: 23464991]
Throughput
- High Throughput
Curated By
- BioGRID