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FLASH GENE
Symbol BNIP3L contributors: mct - updated : 04-10-2017
HGNC name BCL2/adenovirus E1B 19kDa interacting protein 3-like
HGNC id 1085
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • a ligand domain
  • a conserved BH3 domain
  • a C terminal membrane anchoring segment
  • mono polymer homomer , dimer
    HOMOLOGY
    interspecies homolog to murine Bnip3l (97.7pc)
    homolog to rattus Bnip3l (97.7pc)
    intraspecies homolog to BNIP3
    Homologene
    FAMILY
  • BCL2/adenovirus E1B 19kd interacting protein (BNIP) family
  • NIP3 family
  • CATEGORY tumor suppressor , receptor
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,organelle,mitochondria,outer
    intracellular,cytoplasm,organelle,membrane
    intracellular,cytoplasm,organelle,endoplasmic reticulum
    intracellular,cytoplasm,cytosolic
    intracellular,nucleus,nucleoplasm,nuclear bodies,nuclear speckles
    intracellular,nuclear envelope
    text
  • expressed in target of the mitochondria, when inducing apoptosis
  • colocalizing with HSPD1
  • basic FUNCTION
  • inhibiting growth of cancer cells
  • promoting apoptosis and repressing survival genes
  • playing a role in tumor suppression
  • required for the selective elimination of mitochondria
  • playing a critical role in programmed mitochondrial clearance during reticulocyte maturation
  • crucial for hypoxia-induced autophagy by disrupting the Bcl2-beclin1 complex without inducing cell death, promoting tumor progression
  • may function simultaneously with BNIP320
  • can overcome the suppressors BCL2 and BCLXL, although high levels of BCLXL expression will inhibit apoptosis
  • functioning as a mitophagy-specific receptor through the direct interaction with the Atg8 homologues
  • functions by causing mitochondrial depolarization, activating autophagy, or engaging the autophagy machinery
  • plays a critical role in pressure overload-induced cardiac remodeling and heart failure through mediating cardiomyocyte apoptosis
  • is a mitochondrial outer membrane protein that is required for the selective clearance of mitochondria 2)
  • BNIP3 regulates mitophagy during hypoxia, whereas BNIP3L is required for mitophagy during development of the erythroid lineage
  • temporally regulated role for BNIP3 and BNIP3L in the generation of robust NK cell memory
  • BNIP3L-dependent mitophagy results in a metabolic shift towards glycolysis essential for retinal ganglion cell (RGC) neurogenesis
  • BNIP3L-dependent mitophagy regulates cell differentiation via metabolic reprogramming
  • involvement of BNIP3L/NIX in cerebral ischemia-reperfusion (I-R)-induced mitophagy
  • CELLULAR PROCESS cell life, proliferation/growth
    cell life, cell death/apoptosis
    PHYSIOLOGICAL PROCESS
    text highly regulated effector of growth during erythroid cells, terminal maturation
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • heterodimerizing with BCL2L7P1 (BCLX) binding adenovirus E1B, BCL3, BCL2, BCL2L1
  • colocolazing with mitochondrial HSPD1
  • part of a pathway in which IGFBP7 increases expression of SMARCB1, which in turn leads to increased expression of BNIP3L culminating in apoptosis
  • interacting with STEAP3
  • binding to GABARAP
  • SPATA18, BNIP3 and BNIP3L at the mitochondrial outer membrane may play a critical role in the translocation of lysosomal proteins from the cytoplasm to the mitochondrial matrix
  • partners of CLN8 are VAPA, C14orf1/hERG28, STX8, GABARAPL2, BNIP3 and BNIP3L proteins and are associated with biologically relevant processes such as synthesis and transport of lipids, vesicular/membrane trafficking, autophagy/mitophagy and apoptosis
  • BNIP3L is a substrate of PRKN to drive PRKN-mediated mitophagy, and promoting mitophagy in the PINK1/PRKN pathway associated with Parkinson Disease pathogenesis
  • different mitophagy effectors, including the mitophagy receptors BNIP3L, BNIP3 and FUNDC1 and the PINK1/Parkin pathway, have been identified to participate in the selective clearance of mitochondria
  • roles of BNIP3L-mediated mitophagy are independent from PRKN
  • cell & other
    REGULATION
    induced by hypoxia in tumor cells
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral   LOH    
    LOH in carcinomas of the colon, prostate, liver and lung
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
  • may be a novel therapeutic target for intervention because of its pathological roles in regulating cell deth in disease states
  • ANIMAL & CELL MODELS
  • Nix(-/-) mice developed anaemia with reduced mature erythrocytes and compensatory expansion of erythroid precursors
  • retinas from Nix-deficient mice displayed increased mitochondrial mass, reduced expression of glycolytic enzymes and decreased neuronal differentiation