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
PRKAA1
AI194361, AI450832, AL024255, AMPKalpha1, C130083N04Rik
protein kinase, AMP-activated, alpha 1 catalytic subunit
GO Process (29)
GO Function (9)
GO Component (6)
Gene Ontology Biological Process
- cellular response to glucose starvation [IDA]
- cellular response to nutrient levels [IDA]
- cellular response to prostaglandin E stimulus [IGI]
- cold acclimation [ISO]
- fatty acid homeostasis [ISO]
- fatty acid oxidation [IMP]
- glucose homeostasis [IMP]
- glucose metabolic process [IMP]
- histone-serine phosphorylation [IDA]
- lipid biosynthetic process [IDA]
- negative regulation of TOR signaling [IMP]
- negative regulation of apoptotic process [IMP]
- negative regulation of glucose import in response to insulin stimulus [ISO]
- negative regulation of lipid catabolic process [IDA]
- positive regulation of autophagy [IMP]
- positive regulation of cell proliferation [ISO]
- positive regulation of gene expression [ISO]
- positive regulation of glycolytic process [ISO]
- protein heterooligomerization [ISO]
- protein phosphorylation [IMP, ISO]
- regulation of circadian rhythm [IMP]
- regulation of energy homeostasis [ISO]
- regulation of vesicle-mediated transport [ISO]
- response to UV [IMP]
- response to activity [ISO]
- response to caffeine [ISO]
- response to camptothecin [IMP]
- response to gamma radiation [IMP]
- response to hydrogen peroxide [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