Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Combined Automated Annotation using Multiple IEA Methods
A novel adenovirus E1B19K-binding protein B5 inhibits apoptosis induced by Nip3 by forming a heterodimer through the C-terminal hydrophobic region.
Towards a proteome-scale map of the human protein-protein interaction network.
An empirical framework for binary interactome mapping.
Hypoxia-induced autophagy is mediated through hypoxia-inducible factor induction of BNIP3 and BNIP3L via their BH3 domains.
Nix, a receptor protein for mitophagy in mammals.
Possible existence of lysosome-like organella within mitochondria and its role in mitochondrial quality control.
Mieap, a p53-inducible protein, controls mitochondrial quality by repairing or eliminating unhealthy mitochondria.
Next-generation sequencing to generate interactome datasets.
Identification of novel ATP13A2 interactors and their role in α-synuclein misfolding and toxicity.
Orphan nuclear receptor TR3 acts in autophagic cell death via mitochondrial signaling pathway.
Human-chromatin-related protein interactions identify a demethylase complex required for chromosome segregation.
A proteome-scale map of the human interactome network.
Widespread macromolecular interaction perturbations in human genetic disorders.
Pooled-matrix protein interaction screens using Barcode Fusion Genetics.
Architecture of the human interactome defines protein communities and disease networks.
Extensive disruption of protein interactions by genetic variants across the allele frequency spectrum in human populations.
A reference map of the human binary protein interactome.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Quantitative high-confidence human mitochondrial proteome and its dynamics in cellular context.
BNIP3L/NIX regulates both mitophagy and pexophagy.
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NIX, anchored in the mitochondrial outer membrane, also independently localizes to peroxisomes and drives their selective autophagic clearance (pexophagy), and Nix-null mouse tissue has increased peroxisomal content, showing that NIX acts as a selective autophagy receptor for more than one organelle.
FBXL4 ubiquitin ligase deficiency promotes mitophagy by elevating NIX levels.
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A CRISPR screen of human E3 ubiquitin ligases identified VHL and FBXL4 as the strongest negative regulators of basal mitophagy, both converging on the mitophagy receptors BNIP3 and BNIP3L/NIX; FBXL4 destabilizes NIX/BNIP3 directly while VHL acts by suppressing HIF-1alpha-mediated transcription, and depletion of NIX is sufficient to restore mitophagy levels.
FBXL4 suppresses mitophagy by restricting the accumulation of NIX and BNIP3 mitophagy receptors.
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The SCF(FBXL4) ubiquitin ligase complex localizes to the mitochondrial outer membrane in unstressed cells and constitutively ubiquitylates and degrades the mitophagy receptors NIX and BNIP3 to suppress basal mitophagy; pathogenic FBXL4 variants causing mtDNA depletion syndrome (MTDPS13) fail to mediate this turnover, linking dysregulated NIX accumulation to excessive basal mitophagy.
Nix interacts with WIPI2 to induce mitophagy.
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In addition to its LIR motif that binds ATG8 proteins, NIX contains a minimal essential region (MER) that binds and recruits the autophagy effector WIPI2 to mitochondria; both the MER and the LIR are required for robust mitophagy, with the LIR reorganizing WIPI2 into puncta even in the absence of ATG8 proteins.
Dual-localized PPTC7 limits mitophagy through proximal and dynamic interactions with BNIP3 and NIX.
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A pool of the mitochondrial phosphatase PPTC7 localizes to the outer mitochondrial membrane, dynamically associates with BNIP3 and NIX, and promotes their proteasomal turnover to limit basal mitophagy, acting post-transcriptionally and independently of HIF-1alpha stabilization.
PPTC7 antagonizes mitophagy by promoting BNIP3 and NIX degradation via SCF(FBXL4).
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PPTC7 is an essential cofactor for SCF(FBXL4)-mediated degradation of the BNIP3 and NIX mitophagy receptors, acting as an outer-mitochondrial-membrane adaptor that links BNIP3/NIX to FBXL4 to suppress both steady-state and induced mitophagy, with the turnover function independent of PPTC7 phosphatase activity.
SARS-CoV-2 ORF10 suppresses the antiviral innate immune response by degrading MAVS through mitophagy.
A comprehensive two-hybrid analysis to explore the Legionella pneumophila effector-effector interactome.
BNIP3alpha: a human homolog of mitochondrial proapoptotic protein BNIP3.
TP53 stimulates BNIP3L expression
BNIP3L (NIX) UniProtKB record O60238
Manual BNIP3L curation notes