BAIT
ATG3
APG3, APG3-LIKE, APG3L, PC3-96
autophagy related 3
GO Process (8)
GO Function (5)
GO Component (2)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
ALS2
ALS2CR6, ALSJ, IAHSP, PLSJ
amyotrophic lateral sclerosis 2 (juvenile)
GO Process (9)
GO Function (8)
GO Component (9)
Gene Ontology Biological Process
- endosome organization [IGI, NAS]
- neuron projection morphogenesis [IDA]
- positive regulation of Rab GTPase activity [IDA]
- positive regulation of Rac GTPase activity [IDA]
- positive regulation of Rac protein signal transduction [IC]
- positive regulation of Ran GTPase activity [NAS]
- positive regulation of protein kinase activity [IDA]
- positive regulation of protein serine/threonine kinase activity [IDA]
- regulation of endosome size [IEP]
Gene Ontology Molecular Function- Rab GTPase binding [IDA, NAS]
- Rab guanyl-nucleotide exchange factor activity [IDA]
- Rac guanyl-nucleotide exchange factor activity [IDA]
- Ran guanyl-nucleotide exchange factor activity [NAS]
- guanyl-nucleotide exchange factor activity [IDA]
- protein binding [IPI]
- protein homodimerization activity [IPI]
- protein serine/threonine kinase activator activity [IDA]
- Rab GTPase binding [IDA, NAS]
- Rab guanyl-nucleotide exchange factor activity [IDA]
- Rac guanyl-nucleotide exchange factor activity [IDA]
- Ran guanyl-nucleotide exchange factor activity [NAS]
- guanyl-nucleotide exchange factor activity [IDA]
- protein binding [IPI]
- protein homodimerization activity [IPI]
- protein serine/threonine kinase activator activity [IDA]
Gene Ontology Cellular Component
Homo sapiens
Phenotypic Enhancement
A genetic interaction is inferred when mutation or overexpression of one gene results in enhancement of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.
Publication
Receptor-mediated clustering of FIP200 bypasses the role of LC3 lipidation in autophagy.
Autophagosome formation requires multiple autophagy-related (ATG) factors. However, we find that a subset of autophagy substrates remains robustly targeted to the lysosome in the absence of several core ATGs, including the LC3 lipidation machinery. To address this unexpected result, we performed genome-wide CRISPR screens identifying genes required for NBR1 flux in ATG7KO cells. We find that ATG7-independent autophagy still requires ... [more]
EMBO J Dec. 15, 2019; 39(24);e104948 [Pubmed: 33226137]
Throughput
- High Throughput
Ontology Terms
- cell component: autophagy (GO:0006914)
Additional Notes
- CRISPR GI screen
- Cell Line:K-562 (BTO:0000664)
- Experimental Setup: Timecourse; fluorescent ratio read-out as autophagy reporter
- Library:Brunello (ADDGENE:73179)
- Significance Threshold: -0.5>Beta Score>0.5
Curated By
- BioGRID