BAIT
FBXL4
FBL4, FBL5, MTDPS13
F-box and leucine-rich repeat protein 4
GO Process (1)
GO Function (0)
GO Component (3)
Gene Ontology Biological Process
Gene Ontology Cellular Component
Homo sapiens
PREY
HSPA5
BIP, GRP78, HEL-S-89n, MIF2
heat shock 70kDa protein 5 (glucose-regulated protein, 78kDa)
GO Process (14)
GO Function (10)
GO Component (12)
Gene Ontology Biological Process
- ATP catabolic process [ISS]
- ER-associated ubiquitin-dependent protein catabolic process [TAS]
- activation of signaling protein activity involved in unfolded protein response [TAS]
- blood coagulation [TAS]
- cellular protein metabolic process [TAS]
- cellular response to glucose starvation [IDA]
- endoplasmic reticulum unfolded protein response [TAS]
- maintenance of protein localization in endoplasmic reticulum [IMP]
- negative regulation of apoptotic process [IMP, TAS]
- platelet activation [TAS]
- platelet degranulation [TAS]
- positive regulation of cell migration [IMP]
- regulation of protein folding in endoplasmic reticulum [TAS]
- substantia nigra development [IEP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
- COP9 signalosome [IDA]
- endoplasmic reticulum [IDA, IMP, TAS]
- endoplasmic reticulum chaperone complex [IDA]
- endoplasmic reticulum lumen [TAS]
- endoplasmic reticulum membrane [TAS]
- endoplasmic reticulum-Golgi intermediate compartment [IDA]
- extracellular vesicular exosome [IDA]
- focal adhesion [IDA]
- integral component of endoplasmic reticulum membrane [IDA]
- membrane [IDA]
- midbody [IDA]
- nucleus [IDA, IMP]
Homo sapiens
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
A mitochondrial SCF-FBXL4 ubiquitin E3 ligase complex degrades BNIP3 and NIX to restrain mitophagy and prevent mitochondrial disease.
Mitophagy is a fundamental quality control mechanism of mitochondria. Its regulatory mechanisms and pathological implications remain poorly understood. Here, via a mitochondria-targeted genetic screen, we found that knockout (KO) of FBXL4, a mitochondrial disease gene, hyperactivates mitophagy at basal conditions. Subsequent counter screen revealed that FBXL4-KO hyperactivates mitophagy via two mitophagy receptors BNIP3 and NIX. We determined that FBXL4 functions ... [more]
EMBO J Jul. 03, 2023; 42(13);e113033 [Pubmed: 36896912]
Throughput
- High Throughput
Curated By
- BioGRID