Affinage

BNIP3L

BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like · UniProt O60238

Length
219 aa
Mass
23.9 kDa
Annotated
2026-06-09
100 papers in source corpus 48 papers cited in narrative 46 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BNIP3L/NIX is a mitochondrial outer-membrane protein that functions both as a pro-death effector and as a dedicated receptor for selective autophagy of mitochondria and other organelles (PMID:10467396, PMID:18048346, PMID:20010802). It was first identified as a NIP3-homologous candidate tumor suppressor whose overexpression suppresses cancer cell growth (PMID:9523198), and shown to be a BH3- and transmembrane-anchored mitochondrial protein that homodimerizes, binds Bcl-2/Bcl-xL, and triggers cytochrome c release and apoptosis (PMID:10467396, PMID:9867803). Depending on subcellular localization, NIX executes distinct death programs: mitochondrial NIX drives Bax/Bak- and caspase-dependent apoptosis, whereas ER/SR-localized NIX raises calcium and activates MPTP-dependent necrosis, with full protection requiring blockade of both arms (PMID:19065046, PMID:20418503). In its receptor role, NIX engages LC3/GABARAP through an N-terminal LIR motif whose affinity is enhanced ~100-fold by serine 34/35 phosphorylation, and recruits the early autophagy effector WIPI2 through a separate minimal essential region (MER); both modules are needed for robust mitophagy, and transmembrane glycine-mediated homodimerization further potentiates autophagosome engagement (PMID:20010802, PMID:28442745, PMID:37621214, PMID:32286918, PMID:22906961). NIX is the dominant mitophagy receptor (with BNIP3) across diverse settings—programmed mitochondrial clearance in maturing reticulocytes, somatic-cell reprogramming, platelets, keratinocyte and lens-fiber differentiation—and also independently localizes to peroxisomes to mediate pexophagy and to the ER/Golgi to clear those organelles (PMID:18048346, PMID:20010802, PMID:38519771, PMID:28722510, PMID:31391167, PMID:33535046, PMID:29879393, PMID:36215693). Beyond degradation, NIX initiates DRP1-dependent mitochondrial fragmentation during differentiation (PMID:33535046) and restrains insulin signaling via mTOR–IRS1, an activity reversed by PKA phosphorylation that relocalizes NIX to the cytosol (PMID:33044904). Steady-state NIX is held low by proteasomal turnover, principally through a PPTC7-scaffolded SCF-FBXL4 ubiquitin ligase complex at the outer mitochondrial membrane; loss of this circuit causes pathogenic hyperactive mitophagy, and Nix deletion rescues Fbxl4- and Pptc7-null lethality (PMID:36896912, PMID:37161784, PMID:37102372, PMID:38151018). NIX transcription is induced by hypoxic and stress signals through HIF-1, p53, EGR2, PKCα/Sp1, FoxO3a, and KDM3A (PMID:11559532, PMID:15607964, PMID:12687019, PMID:16291751, PMID:28006775, PMID:27472901).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1998 Medium

    Established BNIP3L as a discrete gene whose product suppresses cancer cell growth, framing it as a candidate tumor suppressor before any pathway was known.

    Evidence cDNA isolation and gain-of-function transfection growth-suppression assay with FISH mapping to 8p21

    PMID:9523198

    Open questions at the time
    • No mechanism linking growth suppression to a defined pathway
    • Tumor-suppressor role not tested in vivo
  2. 1999 High

    Defined NIX as a mitochondrial BH3/transmembrane protein that homodimerizes, binds Bcl-2/Bcl-xL, and induces apoptosis via cytochrome c release, placing it in the BCL-2 family pro-death subfamily.

    Evidence Transfection, co-IP with Bcl-2/Bcl-xL, domain mutagenesis, colocalization with HSP60, and in vitro isolated-mitochondria assays

    PMID:10467396 PMID:9867803

    Open questions at the time
    • Physiological trigger for apoptotic activity not defined
    • Relationship between dimerization and death activity unresolved
  3. 2002 High

    Showed NIX-driven apoptosis has organ-level consequences and is antagonized by a non-mitochondrial isoform, linking NIX to cardiomyopathy.

    Evidence Cardiac-specific transgenic mice, cytochrome c/caspase-3 assays, and sNix heterodimerization rescue

    PMID:12053174

    Open questions at the time
    • Endogenous regulation of sNix splicing unknown
    • Upstream signals to cardiac NIX not defined here
  4. 2001 High

    Identified the transcriptional logic placing NIX downstream of hypoxia and stress signaling through multiple transcription factors.

    Evidence HIF-1/VHL genetic cell lines, ChIP and reporter assays for p53/CBP, EGR2, PKCα/Sp1, FoxO3a, and KDM3A

    PMID:11559532 PMID:12687019 PMID:15607964 PMID:16166289 PMID:16291751 PMID:27472901 PMID:28006775

    Open questions at the time
    • Combinatorial integration of these inputs not resolved
    • Cell-type specificity of each regulator incompletely mapped
  5. 2007 High

    Reassigned NIX from a generic pro-death protein to a selective mitophagy receptor required for programmed mitochondrial clearance, independent of canonical BCL-2 family members and of autophagy induction itself.

    Evidence NIX-knockout mice, reticulocyte flow cytometry/EM, and epistasis with BAX/BAK/BCL-XL/BIM/PUMA knockouts plus depolarization assays

    PMID:17420462 PMID:18048346 PMID:18623629

    Open questions at the time
    • Molecular bridge to the autophagy machinery not yet identified
    • How NIX achieves cargo selectivity unresolved at this stage
  6. 2008 High

    Resolved how localization dictates death mode—mitochondrial NIX drives caspase apoptosis while ER/SR NIX drives calcium- and MPTP-dependent necrosis—explaining its dual lethal output.

    Evidence Localization-specific NIX mutants in reconstituted KO cells, cyclosporine A, Ppif/Bax/Bak ablation, and cardiac transgenics; extended to β-cell and hypertrophy models

    PMID:18178777 PMID:19065046 PMID:20418503 PMID:20978346

    Open questions at the time
    • What partitions NIX between mitochondria and ER/SR in vivo is unclear
    • Trigger switching between necrosis and mitophagy not defined
  7. 2009 High

    Identified the molecular receptor mechanism: NIX binds LC3/GABARAP via an N-terminal LIR, providing the physical link between cargo and autophagosome.

    Evidence Co-IP, phage display, pull-downs, LIR mutagenesis, and in vivo reticulocyte clearance in LIR-mutant mice; BH3-peptide disruption of Bcl-2–Beclin1

    PMID:19273585 PMID:19363302 PMID:20010802

    Open questions at the time
    • LIR engagement alone insufficient to explain selectivity
    • Regulation of LIR availability not yet known
  8. 2012 High

    Mapped a second cytoplasmic functional element (the MER) distinct from the LIR, indicating NIX uses more than ATG8 binding to drive clearance.

    Evidence MER mutagenesis with in vivo reticulocyte clearance rescue and structural bioinformatics; plus Mieap/BNIP3 co-IP and membrane-potential studies

    PMID:22292033 PMID:22906961

    Open questions at the time
    • MER binding partner unidentified at this stage
    • Structural state of MER upon binding only predicted
  9. 2015 High

    Connected NIX to the PINK1/Parkin axis, showing NIX can act downstream of PINK1 and be ubiquitinated by Parkin to recruit NBR1.

    Evidence Ubiquitination/co-IP assays, Drosophila pink1/park rescue, and complex I inhibitor treatments

    PMID:25612572

    Open questions at the time
    • Relative contribution of Parkin-dependent vs receptor-intrinsic mitophagy unclear
    • Direct ubiquitination sites not defined
  10. 2017 High

    Revealed phosphoregulation of the LIR—S34/35 phosphorylation strengthens LC3B binding ~100-fold—providing a switch that licenses autophagosome recruitment.

    Evidence ITC, NMR, crystal structure of LC3B–phosphomimetic NIX LIR, and live-cell imaging with LC3B point mutants

    PMID:28442745

    Open questions at the time
    • Kinase responsible for S34/35 phosphorylation not identified
    • Dynamics of phospho-switching in vivo unknown
  11. 2020 High

    Established that transmembrane glycine-mediated dimerization (G204/G208, S212) is required alongside LIR phosphorylation for robust mitophagy, and that dimers are preferentially degraded.

    Evidence TM-residue mutagenesis, dimerization co-IP, phosphomimetic S212E analysis, and proteasome-inhibitor rescue in ischemic brain models

    PMID:32286918 PMID:32722981

    Open questions at the time
    • How dimerization mechanically enhances engulfment unresolved
    • Coupling between dimer state and degradation incompletely defined
  12. 2022 High

    Broadened NIX cargo scope beyond mitochondria, showing independent peroxisomal localization driving pexophagy and ER/Golgi clearance during differentiation.

    Evidence Subcellular fractionation, immunofluorescence, and organelle-content quantification in NIX-knockout mouse tissues; lens organelle elimination

    PMID:28722510 PMID:29879393 PMID:33535046 PMID:36215693

    Open questions at the time
    • Targeting signals distinguishing organelle destinations unknown
    • Whether peroxisomal and mitochondrial pools are regulated independently unclear
  13. 2023 High

    Defined the dominant degradative control of NIX—a PPTC7-scaffolded SCF-FBXL4 ligase at the outer membrane—whose disruption causes pathogenic hyperactive mitophagy rescued by Nix deletion.

    Evidence Mitochondria-targeted CRISPR screen, biochemical complex assembly, ubiquitination assays, and Fbxl4-/- / Pptc7-/- genetic rescue with Nix knockout

    PMID:36896912 PMID:37102372 PMID:37161784 PMID:38151018

    Open questions at the time
    • Signals that relieve FBXL4/PPTC7 repression physiologically not fully mapped
    • Interplay between degradation and LIR/dimer activation unresolved
  14. 2023 Medium

    Identified spatial and effector partners (WIPI2 via MER, TMEM11, prohibitin 1) that organize NIX-driven mitophagosome formation.

    Evidence CID systems, co-IP, WIPI2 live-cell recruitment, TMEM11/PHB1 knockout mitophagy assays

    PMID:36593241 PMID:36795401 PMID:37621214

    Open questions at the time
    • Hierarchy among WIPI2/TMEM11/PHB1 inputs not established
    • Direct vs scaffolded nature of some interactions not fully validated
  15. 2024 High

    Demonstrated that NIX (with BNIP3) constitutes the dominant mitophagy machinery whose loss elevates ROS and sensitizes cells to ferroptosis, linking mitophagy to redox homeostasis and disease.

    Evidence BNIP3/NIX double-knockout HeLa cells, multi-stimulus mitophagy assays, Nrf2/ROS readouts, and ferroptosis rescue with mitophagy-competent vs mutant NIX; UVB fibroblast and KRAS pancreatic cancer models

    PMID:31263025 PMID:38519771 PMID:38761001

    Open questions at the time
    • Therapeutic window for modulating NIX in cancer vs neuroprotection undefined
    • Tissue-specific reliance on NIX vs other receptors incompletely mapped

Open questions

Synthesis pass · forward-looking unresolved questions
  • How NIX integrates phospho-LIR activation, dimerization, organelle-selective targeting, and FBXL4/PPTC7-mediated turnover into a single regulated decision to clear a given organelle remains unresolved.
  • Kinase(s) driving LIR and the deactivating PKA phosphorylation not unified into one model
  • Mechanism partitioning NIX among mitochondria, ER/Golgi, and peroxisomes unknown
  • Coupling of cargo recognition to degradative control not mechanistically defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 2 GO:0008289 lipid binding 1
Localization
GO:0005739 mitochondrion 4 GO:0005783 endoplasmic reticulum 2 GO:0005777 peroxisome 1 GO:0005794 Golgi apparatus 1 GO:0005829 cytosol 1
Pathway
R-HSA-5357801 Programmed Cell Death 3 R-HSA-9612973 Autophagy 3 R-HSA-1852241 Organelle biogenesis and maintenance 2 R-HSA-8953897 Cellular responses to stimuli 2
Partners
BCL2L1FBXL4GABARAPMAP1LC3BPARK2PPTC7TMEM11WIPI2
Complex memberships
PPTC7-SCFFBXL4 holocomplex (substrate)SCF-FBXL4 ubiquitin ligase complex (substrate)TMEM11-BNIP3-BNIP3L outer-membrane complex

Evidence

Reading pass · 46 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 BNIP3L encodes a 219 amino acid protein homologous to NIP3; introduction of BNIP3L into cancer cell lines caused significant growth suppression, identifying it as a candidate tumor suppressor on chromosome 8p21. cDNA isolation, transfection into cancer cell lines (gain-of-function growth suppression assay), FISH chromosomal mapping Genes, chromosomes & cancer Medium 9523198
1999 BNIP3L (Nix) is a mitochondrial protein that homodimerizes, is localized to mitochondria via its C-terminal transmembrane domain, interacts with anti-apoptotic proteins Bcl-2 and Bcl-xL, and induces apoptosis; both the BH3 domain and the transmembrane/membrane-anchoring domain are required for cell death induction; recombinant BNIP3L added to isolated mitochondria induces membrane potential loss and cytochrome c release. Transfection, immunofluorescence microscopy, co-immunoprecipitation with Bcl-2/Bcl-xL, mutational analysis of BH3 and transmembrane domains, in vitro mitochondrial assay (cytochrome c release, membrane potential) Oncogene High 10467396
1999 Nix and Nip3 form a pro-apoptotic mitochondrial protein subfamily; Nix colocalizes with mitochondrial HSP60, homodimerizes (expressed as ~48 kDa dimer from 23.8 kDa monomer), undergoes proteasomal degradation to an 11 kDa C-terminal fragment, and its transmembrane domain is required for mitochondrial localization and apoptosis induction; Nix can overcome Bcl-2 and Bcl-xL but high Bcl-xL levels inhibit its apoptotic activity. Transfection, immunofluorescence colocalization with HSP60, transmembrane domain deletion mutants, proteasome inhibitor (lactacystin) treatment, Western blot The Journal of biological chemistry High 9867803
2001 HIF-1-dependent transcriptional regulation of BNIP3L (NIX) in response to hypoxia; regulation is HIF-1-dependent and suppressed by VHL in normoxic cells. cDNA arrays, SAGE, Northern blot, analysis of HIF-1 and VHL mutant cell lines Cancer research Medium 11559532
2002 Nix localizes to mitochondria in cardiomyocytes, causes release of cytochrome c and caspase-3 activation when expressed in HEK293 cells, and triggers apoptotic cardiomyopathy in vivo; a truncated isoform sNix lacks mitochondrial targeting, heterodimerizes with Nix, and protects against Nix-mediated apoptosis; forced myocardial Nix expression causes apoptotic cardiomyopathy. Transfection, subcellular localization, cytochrome c release assay, caspase-3 activation, cardiac-specific transgenic mouse overexpression, in vivo peripartum model rescue by sNix Nature medicine High 12053174
2003 EGR2 directly transactivates BNIP3L expression as part of the PTEN-EGR2 apoptotic pathway; EGR2-induced BNIP3L expression leads to cytochrome c release and caspase activation. Adenovirus-mediated gene transfer, cDNA microarray, chromatin immunoprecipitation/reporter assays, functional apoptosis assays Oncogene Medium 12687019
2003 TSAP6 physically interacts with Nix (confirmed by yeast two-hybrid, GST pull-down, and co-immunoprecipitation); TSAP6 cooperates with Nix to enhance apoptosis susceptibility. Yeast two-hybrid, GST pull-down, co-immunoprecipitation, functional apoptosis assays Proceedings of the National Academy of Sciences of the United States of America Medium 12606722
2004 p53 directly upregulates BNIP3L expression during hypoxia via increased recruitment of p53 and CBP to the BNIP3L promoter; BNIP3L knockdown reduces hypoxia-induced apoptosis in p53 wild-type cells and promotes tumorigenicity in vivo. Chromatin immunoprecipitation (ChIP), siRNA knockdown, apoptosis assays, in vivo tumor growth experiments Cancer cell High 15607964
2005 Nix transcription is induced by Gαq-mediated hypertrophic stimuli via PKCα signaling through Sp1 transcription factor binding to GC boxes in the Nix promoter; mithramycin (Sp1 inhibitor) suppresses Nix promoter activity in vivo. Luciferase reporter gene assays in neonatal rat cardiomyocytes, adenoviral PKC expression, mithramycin inhibition, NixP transgenic mice in cardiac stress models The Journal of biological chemistry High 16291751
2005 Blockade of EGFR/HER2 specifically induces BNIP3L transcription via FoxO3a; FoxO3a transcriptionally activates the BNIP3L gene, and BNIP3L is required for chemosensitization induced by EGFR/HER2 blockade in breast cancer cells. Antibody blockade (cetuximab, trastuzumab), siRNA knockdown of BNIP3L, constitutively active FoxO3a transfection, apoptosis assays Cancer research Medium 16166289
2006 Nix physically interacts with POSH (a scaffold protein for JNK activation) via co-immunoprecipitation and in vitro binding; Nix promotes apoptosis through POSH-dependent JNK/c-Jun pathway activation; Nix does not promote JNK/c-Jun phosphorylation or apoptosis in cells lacking POSH. Yeast two-hybrid screen, co-immunoprecipitation, in vitro binding assay, JNK/c-Jun phosphorylation assays, POSH-deficient cells, PC12 cell model of Parkinson's disease The Journal of biological chemistry Medium 17095503
2007 NIX is required for programmed mitochondrial clearance in reticulocytes; NIX-deficient reticulocytes show arrest of mitochondrial incorporation into autophagosomes and autophagosome maturation; NIX functions independently of BAX, BAK, BCL-XL, BIM, or PUMA, and is not required for autophagy induction but specifically for selective mitochondrial incorporation. Gene targeting (NIX knockout mice), flow cytometry of reticulocyte mitochondria, electron microscopy, epistasis analysis with BAX/BAK/BCL-XL/BIM/PUMA knockouts Proceedings of the National Academy of Sciences of the United States of America High 18048346
2007 Nix-mediated apoptosis in erythroblasts regulates erythrocyte production; Nix-null mice exhibit massive erythroblastosis and reduced apoptosis; Nix null erythroid cells are hypersensitive to Epo and resistant to cytokine deprivation-induced apoptosis, establishing Nix as a cell-autonomous pro-apoptotic regulator opposing Epo survival signaling. Gene targeting (NIX knockout mice), peripheral blood counts, bone marrow/spleen analysis, in vitro cultured Nix-null erythroid cells, cytokine deprivation and calcium ionophore apoptosis assays Proceedings of the National Academy of Sciences of the United States of America High 17420462
2008 NIX localizes to both mitochondria and ER/sarcoplasmic reticulum; NIX at the ER/SR regulates calcium stores and activates mitochondrial permeability transition pore (MPTP)-dependent necrosis, while mitochondrial NIX activates Bax/Bak- and caspase-dependent apoptosis; ER/SR-targeted NIX causes dissipation of mitochondrial membrane potential preventable by cyclosporine A or Ppif ablation. Subcellular fractionation, NIX localization-specific mutants (ER/SR vs. mitochondria), cyclosporine A treatment, Ppif/Bax/Bak ablation in genetic mouse models, calcium measurements The Journal of clinical investigation High 19065046
2008 Nix-mediated cardiomyocyte apoptosis is a major determinant of adverse remodeling in pathological hypertrophy; Nix ablation reduces cardiomyocyte apoptosis and improves cardiac function in Gq transgenic and transverse aortic constriction models; conditional Nix overexpression synergizes with Gq to cause lethal cardiomyopathy. Conditional/germ-line NIX knockout mice, cardiac-specific Nix transgenic mice, echocardiography, MRI, TUNEL/apoptosis assays, pressure overload model Circulation High 18178777
2008 NIX induces mitochondrial depolarization in wild-type reticulocytes; NIX-deficient reticulocytes fail to depolarize mitochondria; NIX is required for selective incorporation of mitochondria into autophagosomes but is not required for induction of autophagy per se. NIX-knockout mice, mitochondrial membrane potential assays in reticulocytes, autophagosome formation assays Autophagy High 18623629
2009 BNIP3L (NIX) functions as a selective autophagy receptor by binding LC3/GABARAP proteins via an amino-terminal LC3-interacting region (LIR); Nix recruits GABARAP-L1 to damaged mitochondria; ablation of the Nix:LC3/GABARAP interaction retards mitochondrial clearance in maturing reticulocytes. Co-immunoprecipitation, pull-down assays, colocalization studies, site-directed mutagenesis of LIR, reticulocyte mitochondrial clearance assay in NIX LIR mutant mice EMBO reports High 20010802
2009 Nix directly binds to GABARAP (a ubiquitin-like autophagy modifier) in mammalian cells; interaction was identified by phage display and confirmed by in vitro binding studies, pull-down analysis, co-immunoprecipitation, and colocalization studies. Phage display screening, in vitro binding studies, GST pull-down, co-immunoprecipitation, colocalization microscopy Autophagy High 19363302
2009 BNIP3 and BNIP3L are required for hypoxia-induced autophagy; their combined (not individual) silencing suppresses hypoxia-mediated autophagy; ectopic expression of both activates autophagy in normoxia; 20-mer BH3 peptides of BNIP3L are sufficient to initiate autophagy by disrupting the Bcl-2–Beclin1 complex without inducing cell death. siRNA knockdown, ectopic expression, BH3 peptide treatment, autophagy (LC3, acidic vesicle) assays, Beclin1 ablation Molecular and cellular biology High 19273585
2010 Mitochondrial Nix activates Bax/Bak- and caspase-dependent apoptosis, while ER-targeted Nix activates Bax/Bak-independent, MPTP-dependent necrosis; complete protection against Nix-mediated cell death requires simultaneous inhibition of both pathways (caspases + MPTP). Nix-deficient fibroblasts reconstituted with subcellular-targeted Nix mutants, cytochrome c release, caspase activation, annexin V/TUNEL, cyclosporine A, Ppif ablation, combined Bax/Bak double knockout, conditional cardiac transgenic mice Proceedings of the National Academy of Sciences of the United States of America High 20418503
2010 Loss of Nix in Pdx1-haploinsufficient mice prevents β cell apoptosis and necrosis; forced Nix expression in β cells activates both apoptotic and MPTP-dependent necrotic pathways simultaneously; Nix ablation normalizes islet architecture, β cell mass, and insulin secretion in Pdx1+/- diabetic mice. Nix shRNA in MIN6 cells, forced Nix expression in islet β cells, Nix/Pdx1 double-mutant mice, in vivo glucose challenge, β cell mass quantification The Journal of clinical investigation High 20978346
2012 BNIP3L activity in reticulocyte mitochondrial clearance maps to a short cytoplasmic 'minimal essential region' (MER) comprising three contiguous hydrophobic residues flanked by charged residues; mutation of the central leucine causes complete loss of BNIP3L activity and failure to rescue mitochondrial clearance; structural bioinformatics predicts the MER forms an α-helix upon binding to a partner protein. Mutagenesis of MER residues, reticulocyte mitochondrial clearance rescue assays in NIX-KO mice, structural bioinformatics Autophagy High 22906961
2012 BNIP3 and NIX interact with Mieap (a p53-inducible mitochondrial quality control protein) and together mediate accumulation of lysosomal proteins within mitochondria (MALM); co-expression of Mieap, BNIP3, and NIX causes dramatic mitochondrial membrane potential reduction, suggesting a pore-forming complex at the outer mitochondrial membrane. Co-immunoprecipitation, co-expression studies, mitochondrial membrane potential measurement, siRNA knockdown of BNIP3 PloS one Medium 22292033
2015 BNIP3L is a substrate of PARK2 (Parkin) E3 ubiquitin ligase; PARK2-mediated ubiquitination of BNIP3L recruits NBR1 to mitochondria to drive mitophagy; BNIP3L acts downstream of PINK1 but requires PARK2 for mitochondrial clearance (rescue of pink1 but not park mutant Drosophila); BNIP3L is improperly degraded in cells treated with mitochondrial complex I inhibitors (rotenone, 6-OHDA, MPP+). Co-immunoprecipitation, ubiquitination assays, genetic rescue in Drosophila pink1 and park mutants, siRNA/overexpression in mammalian cells, mitophagy assays Human molecular genetics High 25612572
2016 KDM3A (a histone H3K9 demethylase) directly transcriptionally activates BNIP3 and BNIP3L to promote anoikis; KDM3A expression is maintained low by integrin signaling in attached cells; following detachment, increased KDM3A drives BNIP3/BNIP3L expression; KDM3A knockdown substantially reduces detachment-induced apoptosis. RNAi screening, KDM3A knockdown/ectopic expression, ChIP, gene expression analysis, anoikis assays, breast cancer metastasis mouse models eLife High 27472901
2016 FoxO3a binds directly to the BNIP3L promoter region (confirmed by ChIP and luciferase assay) and activates BNIP3L transcription; FGF-2 suppresses BNIP3L via the PI3K/Akt/FoxO3a pathway, protecting cardiomyocytes from H2O2-induced necrosis and mitochondrial dysfunction. ChIP analysis, luciferase reporter assay, PI3K inhibitor treatment, Western blot, Seahorse metabolic analysis Cellular physiology and biochemistry Medium 28006775
2017 Phosphorylation of Nix at serine 34/35 within its LIR domain enhances affinity to LC3B ~100-fold and forms a rigid complex; crystal structure of LC3B with phosphomimetic Nix LIR peptide reveals two additional hydrogen bonds with Arg11, Lys49, and Lys51 in LC3B; S34/35 phosphorylation enhances autophagosome recruitment to mitochondria in HeLa cells; Lys51Ala substitution in LC3B abrogates phosphomimetic Nix binding. Isothermal titration calorimetry, NMR, crystal structure of LC3B-Nix LIR complex, site-directed mutagenesis, live-cell imaging in HeLa cells Scientific reports High 28442745
2017 BNIP3L-dependent mitophagy accounts for mitochondrial clearance during Sox2/Klf4/Oct4-mediated (SKO) somatic cell reprogramming; this mitophagy is independent of mitochondrial membrane potential dissipation; RAB5 (endosome-related) is involved in mitophagosome formation in this context. SKO reprogramming, BNIP3L knockdown, mitochondrial mass assays, mitochondrial membrane potential measurement, RAB5 manipulation Autophagy Medium 28722510
2018 BNIP3L/NIX localizes to the endoplasmic reticulum and Golgi apparatus in addition to mitochondria in lens cells; BNIP3L deletion leads to retention of mitochondria, ER, and Golgi apparatus (but not nuclei) during lens fiber cell organelle elimination, establishing BNIP3L as required for elimination of multiple organelle types during lens OFZ formation. BNIP3L knockout mice, immunofluorescence colocalization, organelle fractionation from adult mouse liver, electron microscopy of lens sections Experimental eye research High 29879393
2019 HHV-8 vIRF-1 directly binds NIX on mitochondria and activates NIX-mediated mitophagy to promote mitochondrial clearance and support virus replication; genetic or pharmacological disruption of vIRF-1/NIX-activated mitophagy inhibits HHV-8 productive replication. Co-immunoprecipitation (vIRF-1/NIX direct binding), genetic interference with vIRF-1 expression, mitophagy assays, viral replication assays Nature communications Medium 31324791
2019 Oncogenic KRAS induces BNIP3L/NIX expression and a selective mitophagy program in pancreatic cancer that restricts glucose flux to mitochondria and enhances redox capacity; NIX deletion restores functional mitochondria, increases NADPH demand, and markedly delays pancreatic cancer progression in the KPC mouse model. KRAS-driven NIX induction studies, conditional Nix knockout in KPC (KrasG12D/Trp53R172H/Pdx1-Cre) mice, mitochondrial functional assays, redox assays, tumor progression analysis Cancer discovery High 31263025
2019 Rhes (a striatal-enriched protein) promotes mitophagy via Nix; Rhes interacts with Nix via its SUMO E3-ligase domain; Nix depletion totally abrogates Rhes-mediated mitophagy and cell death; Rhes traveling via tunneling nanotubes interacts with dysfunctional mitochondria in neighboring cells in a Nix-dependent manner. In vivo interactome/co-IP, density fractionation, live-cell imaging, Nix siRNA knockdown, 3-NP model, Rhes KO mice, ultrastructural analysis Proceedings of the National Academy of Sciences of the United States of America Medium 31676548
2019 Nix mediates mitophagy in platelets; genetic ablation of Nix impairs mitochondrial quality, platelet activation, and arterial thrombosis; Nix loss increases platelet lifespan likely by preventing autophagic degradation of mitochondrial Bcl-xL; platelet-autonomous Nix role confirmed by bone marrow transplant. NIX knockout mice, platelet function assays, FeCl3-induced thrombosis model, metabolic analysis (membrane potential, ROS, OCR, ATP), bone marrow transplantation Blood advances High 31391167
2020 BNIP3L dimerization via transmembrane domain residues (G204, G208) is essential for robust autophagosome recruitment; monomeric BNIP3L mutants (G204A, G208V) show reduced LC3A binding and lower mitophagy; serine 212 at the C-terminus (intermembrane space-facing) is the main dimerization residue; phosphomimetic S212E mutation abolishes dimerization; combined LIR phosphorylation and receptor dimerization are needed for proper mitophagy initiation. Site-directed mutagenesis of TM residues, co-immunoprecipitation for dimer formation, mitophagy induction assays, phosphomimetic mutation analysis Autophagy High 32286918
2020 BNIP3L accumulation triggers mitochondrial depolarization, calcium-dependent activation of DRP1/DNM1L, and mitophagy in myotubes; BNIP3L inhibits insulin signaling through MTOR-RPS6KB/p70S6K-mediated IRS1 inhibition contingent on phosphatidic acids and RHEB; PRKA/PKA directly phosphorylates BNIP3L, causing its translocation from mitochondria/SR to the cytosol and reversing BNIP3L-induced mitophagy and glucose uptake impairment. Gain- and loss-of-function in rodent/human myotubes, DRP1/DNM1L inhibition, PKA activation/inhibition, IRS1 signaling assays, subcellular fractionation showing BNIP3L translocation Autophagy High 33044904
2020 In ischemic brains, BNIP3L is degraded by proteasomes, causing mitophagy deficiency; BNIP3L monomers (S195A, G203A mutations) fail to induce mitophagy; wild-type (dimeric) but not monomeric BNIP3L rescues mitophagy deficiency; the dimeric form is more prone to proteasomal degradation; proteasome inhibition (MG132, carfilzomib) prevents BNIP3L loss, restores mitophagy, and protects against ischemic brain injury in bnip3l-/- null-rescue experiments. Site-specific BNIP3L mutations (S195A, G203A), proteasome inhibitors (MG132, carfilzomib), bnip3l-/- mice, in vivo cerebral ischemia models (tMCAO, pMCAO, photothrombosis), AAV-mediated overexpression Autophagy High 32722981
2021 NIX initiates mitochondrial fragmentation via DRP1 (GTPase) in keratinocytes; NIX depletion compromises epidermal maturation and mitochondrial elimination; ectopic NIX expression accelerates keratinocyte differentiation and induces premature mitochondrial fragmentation via DRP1; inhibiting DRP1 blocks NIX-mediated mitochondrial breakdown and disrupts epidermal development. Live imaging of organotypic human epidermal cultures, NIX siRNA depletion, ectopic NIX expression, DRP1 inhibition, mitochondrial fragmentation/depolarization/acidification assays Cell reports High 33535046
2022 BNIP3L/NIX independently localizes to peroxisomes (in addition to mitochondria) and drives pexophagy; NIX-dependent pexophagy occurs in vivo (mouse tissue lacking NIX has higher peroxisomal content); pexophagy is stimulated under the same physiological conditions (iron chelation, cardiomyocyte and erythrocyte differentiation) that activate mitophagy. Subcellular fractionation, immunofluorescence, NIX-knockout mouse tissues (peroxisome content), iron chelation assays, selective autophagy pathway analysis The EMBO journal High 36215693
2023 SCF-FBXL4 ubiquitin E3 ligase complex ubiquitinates BNIP3L/NIX and BNIP3 to target them for proteasomal degradation, restraining basal mitophagy; FBXL4 functions as an integral outer-membrane protein; pathogenic FBXL4 mutations disrupt SCF-FBXL4 assembly and impair NIX/BNIP3 degradation; Bnip3 or Nix knockout rescues metabolic derangements and lethality in Fbxl4-/- mice. CRISPR mitochondria-targeted genetic screen, co-IP/biochemical SCF complex assembly, ubiquitination assays, Fbxl4-/- and Bnip3/Nix double-KO mice, metabolic phenotyping The EMBO journal High 36896912 37102372 37161784
2023 PPTC7, a mitochondrial matrix phosphatase, scaffolds assembly of a substrate-PPTC7-SCFFBXL4 holocomplex at the outer mitochondrial membrane to degrade BNIP3 and NIX; PPTC7 has an unusually weak mitochondrial targeting sequence facilitating outer membrane retention; starvation upregulates PPTC7 to repress mitophagy and maintain hepatic mitochondrial mass and gluconeogenesis; NIX knockout rescues perinatal lethality of Pptc7-/- mice. Biochemical complex assembly/co-IP, PPTC7 KO and Nix/PPTC7 double KO mice, metabolic phenotyping, subcellular fractionation, starvation experiments Molecular cell High 38151018
2023 Nix MER interacts with the autophagy effector WIPI2, recruiting WIPI2 to mitochondria; the Nix LIR motif is also required for robust mitophagy and converts homogeneous WIPI2 distribution into puncta even without ATG8s; both LIR and MER are required for robust NIX-induced mitophagy. Chemically induced dimerization (CID) of Nix, co-immunoprecipitation of WIPI2, live-cell imaging of WIPI2 recruitment, LIR and MER mutant analysis, ATG8-independent WIPI2 puncta assay The EMBO journal High 37621214
2023 TMEM11 forms a complex with BNIP3 and BNIP3L at the outer mitochondrial membrane and co-enriches at sites of mitophagosome formation; TMEM11 loss leads to hyper-active mitophagy due to increased BNIP3/BNIP3L mitophagy sites, establishing TMEM11 as a spatial restrictor of BNIP3L-mediated mitophagosome formation. Co-immunoprecipitation (TMEM11/BNIP3/BNIP3L complex), TMEM11 knockout cells, mitophagy quantification under normoxia and hypoxia-mimetic conditions, colocalization at mitophagosome sites The Journal of cell biology Medium 36795401
2023 CC-885 (a cereblon modulator) causes CRL4-CRBN E3 ligase-dependent ubiquitination and proteasomal degradation of BNIP3L; degradation is CRBN-dependent (not occurring in CRBN-/- cells); BNIP3L degradation by CC-885 inhibits mitophagy and sensitizes AML cells to mitochondria-targeting drugs. MS-based quantitative proteomics, dose-response degradation assays in CRBN+/+ vs CRBN-/- cells, mitophagy assays, drug sensitivity assays Acta pharmacologica Sinica Medium 32210356
2023 Prohibitin 1 (inner mitochondrial membrane protein) binds to Nix/BNIP3L and is required for ROS-induced Nix localization to mitochondria, driving Parkin-independent mitophagy in intestinal epithelial cells. Co-immunoprecipitation (PHB1-Nix binding), Nix localization by immunofluorescence in PHB1-deficient cells, Parkin-independent mitophagy assays in gastrointestinal epithelial model Scientific reports Medium 36593241
2024 In HeLa cells lacking both BNIP3 and NIX (DKO), mitophagy is completely abolished under multiple conditions; cells deficient in the other three mitophagy receptors show normal mitophagy; BNIP3/NIX DKO leads to elevated mitochondrial ROS and Nrf2 antioxidant pathway activation; DKO cells are highly sensitive to ferroptosis when Nrf2 antioxidant enzymes are compromised; wild-type but not mitophagy-incompetent BNIP3/NIX mutants rescue ferroptosis sensitivity. BNIP3/NIX double knockout HeLa cells, mitophagy assays under multiple stimuli, ROS measurement, Nrf2 pathway assays, ferroptosis sensitivity assays, rescue with WT vs. mitophagy-deficient mutants Cell death and differentiation High 38519771
2024 NIX is the main mitophagy receptor mediating elimination of UVB-damaged mitochondria in human dermal fibroblasts; NIX depletion increases cell death under UVB conditions and leads to enhanced release of extracellular vesicles as an alternative mitochondrial quality control mechanism. NIX siRNA depletion in human dermal fibroblasts, UVB irradiation, mitophagy assays, extracellular vesicle quantification, cell survival assays Aging cell Medium 38761001

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 Hypoxia-induced autophagy is mediated through hypoxia-inducible factor induction of BNIP3 and BNIP3L via their BH3 domains. Molecular and cellular biology 1252 19273585
2009 Nix is a selective autophagy receptor for mitochondrial clearance. EMBO reports 1066 20010802
2009 Role of BNIP3 and NIX in cell death, autophagy, and mitophagy. Cell death and differentiation 851 19229244
2007 NIX is required for programmed mitochondrial clearance during reticulocyte maturation. Proceedings of the National Academy of Sciences of the United States of America 759 18048346
2001 HIF-1-dependent regulation of hypoxic induction of the cell death factors BNIP3 and NIX in human tumors. Cancer research 619 11559532
2008 Hypoxia signals autophagy in tumor cells via AMPK activity, independent of HIF-1, BNIP3, and BNIP3L. Cell death and differentiation 270 18551130
2015 BNIP3- and BNIP3L-Mediated Mitophagy Promotes the Generation of Natural Killer Cell Memory. Immunity 265 26253785
2019 BNIP3L/NIX and FUNDC1-mediated mitophagy is required for mitochondrial network remodeling during cardiac progenitor cell differentiation. Autophagy 254 30741592
2002 Mitochondrial death protein Nix is induced in cardiac hypertrophy and triggers apoptotic cardiomyopathy. Nature medicine 254 12053174
1999 Nix and Nip3 form a subfamily of pro-apoptotic mitochondrial proteins. The Journal of biological chemistry 249 9867803
2017 Phosphorylation of the mitochondrial autophagy receptor Nix enhances its interaction with LC3 proteins. Scientific reports 243 28442745
2004 Bnip3L is induced by p53 under hypoxia, and its knockdown promotes tumor growth. Cancer cell 196 15607964
2015 The mitochondrial protein BNIP3L is the substrate of PARK2 and mediates mitophagy in PINK1/PARK2 pathway. Human molecular genetics 194 25612572
2009 Nix directly binds to GABARAP: a possible crosstalk between apoptosis and autophagy. Autophagy 193 19363302
2010 Mitochondrial pruning by Nix and BNip3: an essential function for cardiac-expressed death factors. Journal of cardiovascular translational research 182 20559783
2020 Dimerization of mitophagy receptor BNIP3L/NIX is essential for recruitment of autophagic machinery. Autophagy 170 32286918
2021 BNIP3L/NIX-mediated mitophagy: molecular mechanisms and implications for human disease. Cell death & disease 167 34930907
2017 Nix restores mitophagy and mitochondrial function to protect against PINK1/Parkin-related Parkinson's disease. Scientific reports 165 28281653
2021 BNIP3L/NIX-mediated mitophagy protects against glucocorticoid-induced synapse defects. Nature communications 155 33473105
2019 Oncogenic KRAS Induces NIX-Mediated Mitophagy to Promote Pancreatic Cancer. Cancer discovery 155 31263025
2008 Nix-mediated apoptosis links myocardial fibrosis, cardiac remodeling, and hypertrophy decompensation. Circulation 150 18178777
1999 Bcl-2/E1B 19 kDa-interacting protein 3-like protein (Bnip3L) interacts with bcl-2/Bcl-xL and induces apoptosis by altering mitochondrial membrane permeability. Oncogene 146 10467396
2020 BNIP3L/NIX degradation leads to mitophagy deficiency in ischemic brains. Autophagy 144 32722981
2007 Unrestrained erythroblast development in Nix-/- mice reveals a mechanism for apoptotic modulation of erythropoiesis. Proceedings of the National Academy of Sciences of the United States of America 132 17420462
2008 Endoplasmic reticulum-mitochondria crosstalk in NIX-mediated murine cell death. The Journal of clinical investigation 131 19065046
2010 Dual autonomous mitochondrial cell death pathways are activated by Nix/BNip3L and induce cardiomyopathy. Proceedings of the National Academy of Sciences of the United States of America 118 20418503
2007 The role of the hypoxia-inducible BH3-only proteins BNIP3 and BNIP3L in cancer. Cancer metastasis reviews 114 17805942
2003 Expression of the cell death genes BNip3 and NIX in ductal carcinoma in situ of the breast; correlation of BNip3 levels with necrosis and grade. The Journal of pathology 112 14648660
2024 Mitophagy mediated by BNIP3 and NIX protects against ferroptosis by downregulating mitochondrial reactive oxygen species. Cell death and differentiation 111 38519771
2005 Distinct pathways regulate proapoptotic Nix and BNip3 in cardiac stress. The Journal of biological chemistry 110 16291751
2018 BNIP3L/NIX-dependent mitophagy regulates cell differentiation via metabolic reprogramming. Autophagy 101 28614042
1998 Isolation, mapping, and functional analysis of a novel human cDNA (BNIP3L) encoding a protein homologous to human NIP3. Genes, chromosomes & cancer 101 9523198
2023 A mitochondrial SCF-FBXL4 ubiquitin E3 ligase complex degrades BNIP3 and NIX to restrain mitophagy and prevent mitochondrial disease. The EMBO journal 98 36896912
2003 The p53-inducible TSAP6 gene product regulates apoptosis and the cell cycle and interacts with Nix and the Myt1 kinase. Proceedings of the National Academy of Sciences of the United States of America 95 12606722
2003 EGR2 induces apoptosis in various cancer cell lines by direct transactivation of BNIP3L and BAK. Oncogene 95 12687019
2012 A short linear motif in BNIP3L (NIX) mediates mitochondrial clearance in reticulocytes. Autophagy 87 22906961
2003 The proapoptotic factor Nix is coexpressed with Bcl-xL during terminal erythroid differentiation. Blood 87 12663450
2020 BNIP3L/Nix-induced mitochondrial fission, mitophagy, and impaired myocyte glucose uptake are abrogated by PRKA/PKA phosphorylation. Autophagy 86 33044904
2022 BNIP3L/NIX regulates both mitophagy and pexophagy. The EMBO journal 82 36215693
2008 NIX induces mitochondrial autophagy in reticulocytes. Autophagy 82 18623629
2021 BNIP3L-mediated mitophagy is required for mitochondrial remodeling during the differentiation of optic nerve oligodendrocytes. Autophagy 80 33404293
2019 Mitochondrial NIX Promotes Tumor Survival in the Hypoxic Niche of Glioblastoma. Cancer research 76 31488423
2023 FBXL4 suppresses mitophagy by restricting the accumulation of NIX and BNIP3 mitophagy receptors. The EMBO journal 68 37161784
2023 A mitophagy sensor PPTC7 controls BNIP3 and NIX degradation to regulate mitochondrial mass. Molecular cell 67 38151018
2018 BNIP3L/NIX is required for elimination of mitochondria, endoplasmic reticulum and Golgi apparatus during eye lens organelle-free zone formation. Experimental eye research 67 29879393
2020 BNIP3L-Dependent Mitophagy Promotes HBx-Induced Cancer Stemness of Hepatocellular Carcinoma Cells via Glycolysis Metabolism Reprogramming. Cancers 65 32168902
2022 Baicalin ameliorates CUMS-induced depression-like behaviors through activating AMPK/PGC-1α pathway and enhancing NIX-mediated mitophagy in mice. European journal of pharmacology 64 36463946
2020 Effects of NIX-mediated mitophagy on ox-LDL-induced macrophage pyroptosis in atherosclerosis. Cell biology international 63 32181963
2017 BNIP3L-dependent mitophagy accounts for mitochondrial clearance during 3 factors-induced somatic cell reprogramming. Autophagy 63 28722510
2019 Activation of NIX-mediated mitophagy by an interferon regulatory factor homologue of human herpesvirus. Nature communications 60 31324791
2020 Nix alone is sufficient to convert female Aedes aegypti into fertile males and myo-sex is needed for male flight. Proceedings of the National Academy of Sciences of the United States of America 59 32661163
2021 NIX initiates mitochondrial fragmentation via DRP1 to drive epidermal differentiation. Cell reports 58 33535046
2005 Blockade of epidermal growth factor receptors chemosensitizes breast cancer cells through up-regulation of Bnip3L. Cancer research 58 16166289
2022 BNIP3 and Nix: Atypical regulators of cell fate. Biochimica et biophysica acta. Molecular cell research 56 35863652
2010 Nix, a receptor protein for mitophagy in mammals. Autophagy 56 20200478
2021 A brief overview of BNIP3L/NIX receptor-mediated mitophagy. FEBS open bio 52 34597467
2017 MiR-30c regulates cisplatin-induced apoptosis of renal tubular epithelial cells by targeting Bnip3L and Hspa5. Cell death & disease 49 28796263
2012 BNIP3 and NIX mediate Mieap-induced accumulation of lysosomal proteins within mitochondria. PloS one 48 22292033
2008 Cardiac reanimation: targeting cardiomyocyte death by BNIP3 and NIX/BNIP3L. Oncogene 45 19641501
2023 FBXL4 ubiquitin ligase deficiency promotes mitophagy by elevating NIX levels. The EMBO journal 44 37102372
2019 Nix-mediated mitophagy regulates platelet activation and life span. Blood advances 43 31391167
2023 BNIP3L/NIX-mediated mitophagy alleviates passive stress-coping behaviors induced by tumor necrosis factor-α. Molecular psychiatry 41 36914810
2020 Nix-Mediated Mitophagy Modulates Mitochondrial Damage During Intestinal Inflammation. Antioxidants & redox signaling 41 32103677
2019 Nix/BNIP3L-dependent mitophagy accounts for airway epithelial cell injury induced by cigarette smoke. Journal of cellular physiology 41 30618073
2010 Loss of Nix in Pdx1-deficient mice prevents apoptotic and necrotic β cell death and diabetes. The Journal of clinical investigation 40 20978346
2019 Rhes, a striatal-enriched protein, promotes mitophagy via Nix. Proceedings of the National Academy of Sciences of the United States of America 39 31676548
2023 Nix interacts with WIPI2 to induce mitophagy. The EMBO journal 38 37621214
2023 The outer mitochondrial membrane protein TMEM11 demarcates spatially restricted BNIP3/BNIP3L-mediated mitophagy. The Journal of cell biology 37 36795401
2023 FBXL4 mutations cause excessive mitophagy via BNIP3/BNIP3L accumulation leading to mitochondrial DNA depletion syndrome. Cell death and differentiation 36 37568009
2020 The novel cereblon modulator CC-885 inhibits mitophagy via selective degradation of BNIP3L. Acta pharmacologica Sinica 36 32210356
2019 Nix is a male-determining factor in the Asian tiger mosquito Aedes albopictus. Insect biochemistry and molecular biology 36 31901476
2017 Cutting Edge: NANOG Activates Autophagy under Hypoxic Stress by Binding to BNIP3L Promoter. Journal of immunology (Baltimore, Md. : 1950) 35 28093523
2003 Analysis of the candidate 8p21 tumour suppressor, BNIP3L, in breast and ovarian cancer. British journal of cancer 35 12610513
2018 NIX-mediated mitophagy protects against proteinuria-induced tubular cell apoptosis and renal injury. American journal of physiology. Renal physiology 33 30207166
2007 Mitochondrial proteins Bnip3 and Bnip3L are involved in anthrax lethal toxin-induced macrophage cell death. The Journal of biological chemistry 33 17623653
2006 Proapoptotic Nix activates the JNK pathway by interacting with POSH and mediates death in a Parkinson disease model. The Journal of biological chemistry 32 17095503
2022 HIF-1α/BNIP3L induced cognitive deficits in a mouse model of sepsis-associated encephalopathy. Frontiers in immunology 31 36569834
2018 Protective roles of autophagy in retinal pigment epithelium under high glucose condition via regulating PINK1/Parkin pathway and BNIP3L. Biological research 31 30012208
2021 Baicalein Mediates Mitochondrial Autophagy via miR-30b and the NIX/BNIP3 Signaling Pathway in Parkinson's Disease. Biochemistry research international 28 34457363
2019 Potential Roles of NIX/BNIP3L Pathway in Rat Traumatic Brain Injury. Cell transplantation 28 30961359
2016 The histone H3K9 demethylase KDM3A promotes anoikis by transcriptionally activating pro-apoptotic genes BNIP3 and BNIP3L. eLife 28 27472901
2016 FGF-2 Transcriptionally Down-Regulates the Expression of BNIP3L via PI3K/Akt/FoxO3a Signaling and Inhibits Necrosis and Mitochondrial Dysfunction Induced by High Concentrations of Hydrogen Peroxide in H9c2 Cells. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 28 28006775
2014 Central role of Nix in the autophagic response to ochratoxin A. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association 28 24755393
2016 Novel p53-dependent anticancer strategy by targeting iron signaling and BNIP3L-induced mitophagy. Oncotarget 27 26517689
2022 Transgenic expression of Nix converts genetic females into males and allows automated sex sorting in Aedes albopictus. Communications biology 26 35256751
2020 BCL2 Interacting Protein 3-like/NIX-mediated Mitophagy Plays an Important Role in the Process of Age-related Hearing Loss. Neuroscience 26 33346118
2019 Knockdown of BNIP3L or SQSTM1 alters cellular response to mitochondria target drugs. Autophagy 24 30563411
2022 Tanshinone I inhibits metastasis of cervical cancer cells by inducing BNIP3/NIX-mediated mitophagy and reprogramming mitochondrial metabolism. Phytomedicine : international journal of phytotherapy and phytopharmacology 23 35124382
2005 Differential profile of Nix upregulation and translocation during hypoxia/ischaemia in vivo versus in vitro. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 23 15902200
2021 Puerarin alleviates cadmium-induced mitochondrial mass decrease by inhibiting PINK1-Parkin and Nix-mediated mitophagy in rat cortical neurons. Ecotoxicology and environmental safety 22 34979308
2019 Mitophagy mediated by BNIP3 and BNIP3L/NIX in urothelial cells of the urinary bladder of cattle harbouring bovine papillomavirus infection. Veterinary microbiology 22 31500722
2018 DNA methylation of the promoter region of bnip3 and bnip3l genes induced by metabolic programming. BMC genomics 22 30223788
2017 BNIP3L promotes cardiac fibrosis in cardiac fibroblasts through [Ca2+]i-TGF-β-Smad2/3 pathway. Scientific reports 21 28507335
2024 Elimination of damaged mitochondria during UVB-induced senescence is orchestrated by NIX-dependent mitophagy. Aging cell 20 38761001
2023 Host cell egress of Brucella abortus requires BNIP3L-mediated mitophagy. The EMBO journal 20 37232029
2022 MiR-30a-5p Alters Epidermal Terminal Differentiation during Aging by Regulating BNIP3L/NIX-Dependent Mitophagy. Cells 20 35269458
2022 N, N-dimethylformamide exposure induced liver abnormal mitophagy by targeting miR-92a-1-5p-BNIP3L pathway in vivo and vitro. The Science of the total environment 20 35623527
2021 Circ-BNIP3L knockdown alleviates LPS-induced renal tubular epithelial cell injury during sepsis-associated acute kidney injury by miR-370-3p/MYD88 axis. Journal of bioenergetics and biomembranes 20 34731384
2020 NIX compensates lost role of parkin in cd-induced mitophagy in HeLa cells through phosphorylation. Toxicology letters 20 32142837
2023 Inner mitochondrial membrane protein Prohibitin 1 mediates Nix-induced, Parkin-independent mitophagy. Scientific reports 19 36593241

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