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
SLC25A13
ARALAR2, CITRIN, CTLN2
solute carrier family 25 (aspartate/glutamate carrier), member 13
GO Process (13)
GO Function (4)
GO Component (3)
Gene Ontology Biological Process
- ATP biosynthetic process [IDA]
- L-aspartate transmembrane transport [IDA]
- L-glutamate transmembrane transport [IDA]
- L-glutamate transport [IDA]
- aspartate transport [IDA]
- carbohydrate metabolic process [TAS]
- cellular respiration [IDA]
- gluconeogenesis [TAS]
- glucose metabolic process [TAS]
- malate-aspartate shuttle [IDA]
- response to calcium ion [IDA]
- small molecule metabolic process [TAS]
- transport [NAS]
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