BAIT
ATG7
APG7-LIKE, APG7L, GSA7
autophagy related 7
GO Process (17)
GO Function (5)
GO Component (4)
Gene Ontology Biological Process
- C-terminal protein lipidation [IBA]
- cellular protein modification process [TAS]
- cellular response to hyperoxia [IDA]
- cellular response to nitrogen starvation [IBA]
- cellular response to starvation [IDA]
- late nucleophagy [IBA]
- membrane fusion [TAS]
- mitochondrion degradation [IBA]
- piecemeal microautophagy of nucleus [IBA]
- positive regulation of apoptotic process [IMP]
- positive regulation of autophagy [IMP]
- positive regulation of macroautophagy [IMP]
- positive regulation of protein catabolic process [IMP]
- positive regulation of protein modification process [IDA]
- protein catabolic process [IBA]
- protein lipidation [IDA]
- protein modification by small protein conjugation [IBA]
Gene Ontology Molecular Function
Homo sapiens
PREY
RAB7A
PRO2706, RAB7
RAB7A, member RAS oncogene family
GO Process (16)
GO Function (4)
GO Component (8)
Gene Ontology Biological Process
- GTP catabolic process [IDA, TAS]
- Rab protein signal transduction [IBA]
- antigen processing and presentation of exogenous peptide antigen via MHC class II [TAS]
- early endosome to late endosome transport [IMP]
- endocytosis [TAS]
- endosome to lysosome transport [IMP]
- epidermal growth factor catabolic process [IMP]
- phagosome acidification [IMP]
- phagosome maturation [TAS]
- phagosome-lysosome fusion [IMP]
- positive regulation of exosomal secretion [IMP]
- protein targeting to lysosome [IMP]
- protein to membrane docking [IDA]
- protein transport [TAS]
- regulation of autophagic vacuole assembly [IMP]
- retrograde transport, endosome to Golgi [IMP]
Gene Ontology Molecular Function
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
- 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