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
RB1CC1
2900055E04Rik, 5930404L04Rik, Cc1, FIP200, LaXp180
RB1-inducible coiled-coil 1
GO Process (9)
GO Function (2)
GO Component (8)
Gene Ontology Biological Process
- JNK cascade [IGI]
- autophagic vacuole assembly [IMP]
- heart development [IMP]
- liver development [IMP]
- negative regulation of apoptotic process [IMP]
- negative regulation of extrinsic apoptotic signaling pathway [IMP]
- positive regulation of cell size [IMP]
- positive regulation of protein phosphorylation [IMP]
- regulation of autophagy [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
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