BAIT
C9ORF72
ALSFTD, FTDALS
chromosome 9 open reading frame 72
GO Process (2)
GO Function (2)
GO Component (9)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
RAB8A
AA409338, Mel
RAB8A, member RAS oncogene family
GO Process (15)
GO Function (6)
GO Component (21)
Gene Ontology Biological Process
- GTP catabolic process [IBA, ISO]
- Golgi vesicle fusion to target membrane [IBA, ISO]
- Rab protein signal transduction [IBA]
- axonogenesis [ISO]
- cellular response to insulin stimulus [IBA, ISO]
- cilium assembly [ISO]
- intracellular protein transport [IBA]
- protein localization to plasma membrane [IBA, ISO]
- protein secretion [IBA]
- regulation of exocytosis [IBA]
- regulation of long-term neuronal synaptic plasticity [ISO]
- regulation of protein localization [ISO]
- regulation of protein transport [ISO]
- synaptic vesicle exocytosis [IBA]
- vesicle docking involved in exocytosis [IBA, ISO]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
- Golgi apparatus [ISO]
- centrosome [ISO]
- ciliary basal body [IDA]
- cilium [IDA, ISO]
- cytoplasmic membrane-bounded vesicle [ISO]
- dendrite [ISO]
- extracellular vesicular exosome [ISO]
- neuronal cell body [ISO]
- nonmotile primary cilium [IDA, ISO]
- nucleolus [ISO]
- nucleoplasm [ISO]
- nucleus [ISO]
- phagocytic vesicle [ISO]
- plasma membrane [IDA, ISO]
- postsynaptic density [ISO]
- primary cilium [ISO]
- recycling endosome [IDA]
- recycling endosome membrane [ISO]
- secretory granule membrane [IBA]
- synaptic vesicle [IBA]
- trans-Golgi network transport vesicle [IDA]
Mus musculus
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
Loss of C9ORF72 impairs autophagy and synergizes with polyQ Ataxin-2 to induce motor neuron dysfunction and cell death.
An intronic expansion of GGGGCC repeats within the C9ORF72 gene is the most common genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia (ALS-FTD). Ataxin-2 with intermediate length of polyglutamine expansions (Ataxin-2 Q30x) is a genetic modifier of the disease. Here, we found that C9ORF72 forms a complex with the WDR41 and SMCR8 proteins to act as a GDP/GTP exchange ... [more]
EMBO J. Dec. 15, 2015; 35(12);1276-97 [Pubmed: 27103069]
Throughput
- Low Throughput
Curated By
- BioGRID