Affinage

BCL2L13

Bcl-2-like protein 13 · UniProt Q9BXK5

Length
485 aa
Mass
52.7 kDa
Annotated
2026-06-09
45 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BCL2L13 (Bcl-rambo/MIL1) is an outer mitochondrial membrane protein of the Bcl-2 family that operates two distinct effector programs—apoptosis and mitophagy—through structurally separable modules (PMID:11262395, PMID:26506896). Its pro-apoptotic activity is driven not by canonical BH-domain interactions with other Bcl-2 family members, which it does not engage, but by its unique C-terminal membrane-anchored domain, and the resulting cell death is caspase-dependent and blocked by IAPs (PMID:11262395). This caspase-activating function is amplified by physical partners at the outer membrane and intermembrane space: VDAC1/2 cooperatively promote effector caspase activation, PGAM5 binds the transmembrane domain to favor caspase activity over mitophagy, and GRP75/mortalin binds the No-BH domain to facilitate executioner caspase activation, PARP-1 cleavage, and cytochrome c release (PMID:31102594, PMID:36075447, PMID:37640805). Independently of apoptosis, BCL2L13 acts as a mammalian functional analog of the yeast mitophagy receptor Atg32, using its BH domains for mitochondrial fragmentation and its WXXL/LIR motif for mitophagy, and complementing atg32Δ yeast (PMID:26506896). The LIR motif selectively engages LC3C, GABARAP, and GABARAPL1 and recruits the FIP200/ULK1 complex to nucleate autophagosome biogenesis, operating independently of Parkin and, for fragmentation, of DNM1L (PMID:26506896, PMID:30625316, PMID:32828302). Its mitophagy activity is switched on by phosphorylation: PRKAA2/AMPKα2 phosphorylates Ser272 to drive mitophagy in pressure-overloaded heart, TBK1 phosphorylates Ser275 under mitochondrial stress, and MAP2K6/MKK6 phosphorylates Ser426 to strengthen the BCL2L13–LC3B interaction (PMID:39995141, PMID:40672348, PMID:41886451). Through its C-terminal insert BCL2L13 also binds and inhibits ceramide synthases CerS2/CerS6, blocking ceramide-induced apoptosis upstream of BAX (PMID:24706805). Physiologically, BCL2L13 contributes to germline purifying selection against pathogenic heteroplasmic mtDNA (PMID:36608143) and localizes to mitochondria-associated membranes where it shapes ER–mitochondria calcium signaling and mitochondrial complex activity in skeletal muscle (PMID:39175772).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2001 High

    Established that BCL2L13 is a mitochondrial Bcl-2 family member whose death activity is mechanistically unusual—driven by its C-terminal anchor and caspases rather than BH-domain heterodimerization.

    Evidence Overexpression, subcellular fractionation, domain deletion, and caspase/IAP inhibitor rescue in mammalian cells, plus interaction screens against Bcl-2 family members

    PMID:11262395

    Open questions at the time
    • Did not identify the caspase activation pathway or direct molecular partners
    • Mechanism by which the C-terminal domain triggers death left unresolved
  2. 2003 Medium

    Showed a splice variant generates a cytosolic BH4-only protein, indicating isoform-dependent control of BCL2L13 pro-apoptotic output.

    Evidence Cloning/sequencing of Bcl-rambo beta, localization, mutagenesis removing the Alu insert, and drug-induced cell death assays

    PMID:12527362

    Open questions at the time
    • Single lab; physiological abundance of the variant unknown
    • Mechanism by which the cytosolic variant promotes death not defined
  3. 2014 High

    Identified a non-canonical anti-apoptotic role: BCL2L13 inhibits ceramide synthases CerS2/6 via its C-terminal insert, blocking ceramide-driven apoptosis upstream of BAX.

    Evidence Co-IP with domain mapping, in vitro ceramide synthase activity assays, siRNA loss-of-function, and in vivo tumor growth

    PMID:24706805

    Open questions at the time
    • How the same protein reconciles pro- and anti-apoptotic activities not resolved
    • No structural basis for CerS binding
  4. 2015 High

    Defined BCL2L13 as a mammalian mitophagy receptor functionally equivalent to yeast Atg32, with separable domains for fragmentation versus mitophagy.

    Evidence Domain mutagenesis (BH and LIR mutants), knockdown, mitophagy flux assays, and cross-species complementation in atg32Δ yeast

    PMID:26506896

    Open questions at the time
    • Did not identify the downstream autophagy machinery recruited
    • Physiological mitophagy contexts not established
  5. 2015 Medium

    Linked BCL2L13 to non-apoptotic caspase regulation in neural progenitors under microRNA control.

    Evidence Proteomics, siRNA knockdown, caspase-3 and cytochrome c release assays, and miR-124/miR-137 target validation

    PMID:26207921

    Open questions at the time
    • Single lab
    • Direct molecular mechanism connecting BCL2L13 to caspase-3 control not defined
  6. 2019 High

    Resolved the autophagy initiation machinery, showing BCL2L13 recruits the ULK1 complex with LC3B bridging BCL2L13 and ULK1.

    Evidence Yeast ATG mutant screening, mammalian ULK1 complex knockout, reciprocal Co-IP, and mitophagy flux assays

    PMID:30625316

    Open questions at the time
    • Selectivity among ATG8 family members not yet defined here
    • How recruitment is regulated upstream unknown
  7. 2019 Medium

    Defined VDAC1/2 as outer-membrane partners that cooperatively amplify BCL2L13-driven caspase activation, separating the apoptotic and morphological roles.

    Evidence Co-IP, Drosophila genetic screen, caspase assays, VDAC siRNA, and live-cell mitochondrial imaging

    PMID:31102594

    Open questions at the time
    • Single lab
    • Direct vs indirect nature of VDAC contribution to caspase activation unclear
  8. 2020 Medium

    Established the structural basis of ATG8 selectivity, showing BCL2L13's LIR selectively binds LC3C/GABARAP/GABARAPL1.

    Evidence In vitro binding assays, LIR X2 and HP1/HP2 mutagenesis, and mitophagy assays in cells

    PMID:32828302

    Open questions at the time
    • Single lab
    • Functional consequence of selectivity in vivo not established
  9. 2022 Medium

    Showed PGAM5 binds the transmembrane domain to bias BCL2L13 toward caspase activation and away from mitophagy, revealing a partner-controlled switch between its two programs.

    Evidence Co-IP with domain mapping, Drosophila epistasis/rescue, caspase assays, and LC3B-II immunoblot

    PMID:36075447

    Open questions at the time
    • Single lab
    • Mechanism by which PGAM5 toggles output not biochemically defined
  10. 2023 High

    Identified GRP75/mortalin as a No-BH-domain partner that potentiates executioner caspase activation and cytochrome c release.

    Evidence Co-IP and GST pull-down with domain mapping, siRNA knockdown, caspase/PARP-1/cytochrome c assays, and Drosophila epistasis

    PMID:37640805

    Open questions at the time
    • How GRP75 binding couples to caspase machinery not resolved
  11. 2023 Medium

    Connected BCL2L13 to DNM1L-mediated fission in cancer, with targeting of DNM1L Ser616 promoting mitophagy and tumor cell aggression.

    Evidence OE/KD in GBM cells, phospho-DNM1L-Ser616 immunoblot, mitochondrial morphology and mitophagy flux, and xenografts

    PMID:37660127

    Open questions at the time
    • Single lab; reconciles incompletely with prior DNM1L-independent fragmentation report
    • Whether BCL2L13 directly modifies DNM1L unclear
  12. 2023 High

    Demonstrated an in vivo physiological role: BCL2L13-dependent mitophagy contributes to germline purifying selection against pathogenic mtDNA.

    Evidence Mouse Bcl2l13 knockout with heteroplasmy quantification across generations, benchmarked against Parkin/Ulk1/Ulk2 KO lines

    PMID:36608143

    Open questions at the time
    • Cell-type and developmental window of selection not defined
    • Relative contribution versus other receptors not quantified
  13. 2024 High

    Placed BCL2L13 at MAMs and assigned a calcium-handling and bioenergetic role in skeletal muscle.

    Evidence Organelle fractionation, immunolocalization, zebrafish bcl2l13 knockout, calcium imaging, complex activity assays, and C2C12 knockdown

    PMID:39175772

    Open questions at the time
    • Molecular mechanism linking BCL2L13 to Ca2+ flux unknown
    • Relationship between MAM localization and mitophagy not established
  14. 2024 Medium

    Showed BCL2L13-LC3 receptor mitophagy operates in endothelial oxidative stress under microRNA control.

    Evidence Proteomics, BCL2L13-LC3 Co-IP, KD/OE mitophagy assays, and o8G-modified miR-6513-5p target analysis

    PMID:39307929

    Open questions at the time
    • Single lab
    • Direct contribution of BCL2L13 to endothelial protection not isolated
  15. 2025 High

    Identified PRKAA2/AMPKα2 as the kinase phosphorylating Ser272 to activate cardiac mitophagy, with phospho-mutant knock-in mice confirming functional requirement.

    Evidence Bcl2l13 KO and BCL2L13-S272A knock-in mice, transverse aortic constriction, in vitro kinase assay, mitophagy flux, and ATP measurement

    PMID:39995141

    Open questions at the time
    • How Ser272 phosphorylation activates the receptor structurally unknown
    • Interplay with other phospho-sites not addressed
  16. 2026 High

    Defined MAP2K6/MKK6 phosphorylation of Ser426 as a switch strengthening BCL2L13-LC3B binding and suppressing tumor growth via mitophagy.

    Evidence In vitro kinase assay, BCL2L13-S426 mutant Co-IP, MKK6 fractionation, LUAD loss-of-function, mitophagy/OXPHOS readouts, and tumor growth

    PMID:41886451

    Open questions at the time
    • How three distinct kinases coordinate distinct phospho-sites unresolved
    • Context determining which kinase dominates unknown
  17. 2026 Medium

    Linked GDF15 signaling to BCL2L13 induction driving bystander T-cell apoptosis in viral infection.

    Evidence Recombinant GDF15 treatment, BCL2L13 knockdown, apoptosis assays, and co-culture with Omicron-infected epithelial cells

    PMID:41896204

    Open questions at the time
    • Single lab
    • Signaling intermediate between GDF15 and BCL2L13 transcription unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • How BCL2L13 partitions between its pro-apoptotic and pro-mitophagic programs—and how partner binding, isoform choice, and multi-kinase phosphorylation are integrated into a single decision—remains unresolved.
  • No structural model of full-length BCL2L13 or its domain switch
  • Hierarchy and crosstalk among AMPK/TBK1/MKK6 phospho-sites undefined
  • Mechanism coupling MAM calcium signaling to mitophagy unestablished

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3
Localization
GO:0005739 mitochondrion 3 GO:0005783 endoplasmic reticulum 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
Partners
CERS2CERS6HSPA9MAP2K6MAP3K6PGAM5VDAC1VDAC2
Complex memberships
FIP200/ULK1 complex

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 BCL2L13 (Bcl-rambo) localizes to mitochondria and induces apoptosis via its unique C-terminal membrane-anchored domain (not via its BH motifs). The cell death activity is specifically blocked by caspase inhibitors and IAPs, but not by Bcl-xL, FLIP, or FADD-DN. No interaction was detected with either anti-apoptotic (Bcl-2, Bcl-xL, Bcl-w, A1, MCL-1, E1B-19K, BHRF1) or pro-apoptotic (Bax, Bak, Bik, Bid, Bim, Bad) Bcl-2 family members. Overexpression in mammalian cells, subcellular fractionation/localization, domain deletion analysis, caspase/IAP inhibitor rescue assays, yeast two-hybrid/co-IP for interaction studies The Journal of biological chemistry High 11262395
2003 A splice variant of BCL2L13, Bcl-rambo beta, contains a 98 bp Alu-like insertion creating a premature stop codon, producing a BH4-only protein of 104 aa that lacks BH1/BH2/BH3 and the C-terminal membrane anchor. This cytosol-localized variant promotes etoposide- and Taxol-induced cell death; removal of the Alu sequence from Bcl-rambo beta abrogates its pro-apoptotic capability. Cloning and sequencing of splice variant, subcellular localization assay, domain deletion/mutagenesis, cell death assays with drug treatment FEBS letters Medium 12527362
2014 BCL2L13 binds to pro-apoptotic ceramide synthases CerS2 and CerS6 via its unique C-terminal 250-aa sequence (between BH and membrane anchor domains), blocking CerS2/6 homo- and heteromeric complex formation and their enzymatic activity, thereby inhibiting ceramide-induced apoptosis upstream of BAX activation and mitochondrial outer membrane permeabilization. Co-immunoprecipitation, in vitro ceramide synthase activity assay, domain deletion mapping, loss-of-function (siRNA/shRNA) in vitro and in vivo tumor growth assays Proceedings of the National Academy of Sciences of the United States of America High 24706805
2015 BCL2L13 functions as a mammalian homolog of yeast mitophagy receptor Atg32. Its BH domains are required for mitochondrial fragmentation, while its WXXL/LIR motif is required for mitophagy. BCL2L13 induces mitochondrial fragmentation and mitophagy independently of DNM1L/Drp1 and PARK2/Parkin, respectively, and can complement Atg32 deficiency in yeast. Overexpression and siRNA knockdown in HEK293 cells, domain mutagenesis (BH domain mutants, LIR motif mutants), mitophagy flux assays, cross-species complementation in atg32Δ yeast Autophagy High 26506896
2015 BCL2L13 controls caspase-3 activity and cytochrome C release in hippocampal neural stem/progenitor cells. miR-124 and miR-137 cooperatively target BCL2L13 to fine-tune its expression, thereby modulating non-apoptotic caspase-3 functions. Comparative proteomics, siRNA knockdown, caspase-3 activity assay, cytochrome C release assay, microRNA target validation Scientific reports Medium 26207921
2016 Human BCL2L13 localizes to mitochondria in Drosophila S2 cells and induces apoptosis (effector caspase activation) when overexpressed; this requires its C-terminal transmembrane domain. BCL2L13 genetically interacts with Drosophila adenine nucleotide translocators (ANT) and Atg8 (autophagy-related 8 protein) in vivo. Ectopic expression in Drosophila (GAL4-UAS system), immunofluorescence localization, caspase activity assay in eye imaginal discs, genetic epistasis/interaction screen, p35/DIAP rescue experiments PloS one Medium 27348811
2018 BCL2L13 promotes beige adipocyte biogenesis and browning of white adipose tissue. BCL2L13 disruption inhibits the browning program (reduced Prdm16, Ucp1, Dio2, Adrb3), through regulation of mitochondrial dynamics and biogenesis (decreased fission/fusion genes, PGC-1α, mitochondrial respiratory chain complexes), independently of autophagy activity. siRNA knockdown in preadipocytes, cold exposure and β3-adrenergic agonist treatment in vivo, qPCR/western blot for browning markers and mitochondrial dynamics genes Biochemical and biophysical research communications Medium 30352689
2019 BCL2L13 recruits the ULK1 complex to initiate mitophagy. The ULK1 complex (but not ULK1's yeast counterpart components for starvation autophagy) is required for BCL2L13-mediated mitophagy in mammalian cells. Interaction of LC3B with both ULK1 and BCL2L13 is important for this process. Yeast ATG mutant screening, mammalian cell ULK1 complex knockdown/knockout, co-immunoprecipitation of BCL2L13 with ULK1 complex components, mitophagy flux assays Cell reports High 30625316
2019 Human BCL2L13 binds to VDAC1 (and previously reported ANT1/ANT2) at the outer mitochondrial membrane. VDAC1 and VDAC2 cooperatively promote effector caspase activation when co-expressed with BCL2L13. BCL2L13 (with its LIR motif mutated W276A/I279A) still causes mitochondrial fragmentation and perinuclear accumulation of fragmented mitochondria; VDAC knockdown also promotes this perinuclear accumulation. Co-immunoprecipitation, Drosophila genetic screen, caspase activity assay in 293T cells, siRNA knockdown of VDACs, live cell imaging of mitochondrial morphology Experimental cell research Medium 31102594
2020 BCL2L13 (Bcl-rambo) selectively binds LC3C, GABARAP, and GABARAPL1 over other LC3/GABARAP family members. The selectivity depends on residues at the X2 position of BCL2L13's LIR motif and the HP1/HP2 sites of the LC3/GABARAP proteins. Disrupting this selective binding alters mitophagy induction in cells. In vitro binding assays, bioinformatics, site-directed mutagenesis of LIR and HP1/HP2 sites, mitophagy assays in cells with mutant constructs Biochemical and biophysical research communications Medium 32828302
2022 PGAM5 interacts with BCL2L13 (Bcl-rambo) via the BCL2L13 transmembrane domain. PGAM5 co-expression promotes BCL2L13-dependent effector caspase activity but interferes with BCL2L13-dependent mitophagy (decreases LC3B-II accumulation induced by BCL2L13). The genetic interaction was confirmed in Drosophila where pgam5-2 knockdown partially rescues BCL2L13-induced rough eye phenotype. Co-immunoprecipitation, Drosophila genetic screen and rescue, caspase activity assay, LC3B-II immunoblot, domain mapping Experimental cell research Medium 36075447
2023 BCL2L13 interacts with GRP75 (mortalin/HSPA9) via its No-BH domain, as confirmed by co-immunoprecipitation and GST pull-down. GRP75 co-expression facilitates elevated executioner caspase activity and PARP-1 cleavage induced by BCL2L13, and GRP75 knockdown suppresses BCL2L13-dependent caspase activation and cytochrome c release. Genetic interaction confirmed in Drosophila. Co-immunoprecipitation, GST pull-down, domain mapping, siRNA knockdown, caspase activity assay, PARP-1 cleavage assay, cytochrome c release assay, Drosophila genetic epistasis Scientific reports High 37640805
2023 BCL2L13 promotes mitophagy through DNM1L (Drp1)-mediated mitochondrial fission in glioblastoma cells. BCL2L13 targets DNM1L at the Ser616 phosphorylation site, leading to mitochondrial fission and increased mitophagy flux, which promotes GBM cell proliferation and invasion. Overexpression and knockdown in GBM cell lines, phospho-DNM1L-Ser616 immunoblot, mitochondrial morphology assay, mitophagy flux assay, in vitro proliferation/invasion assays, in vivo xenograft Cell death & disease Medium 37660127
2023 Knockout of Bcl2l13 in mice has a statistically robust effect on germline purifying selection against transmission of a pathogenic heteroplasmic mtDNA mutation (C5024T in tRNAAla), establishing BCL2L13-dependent mitophagy as a contributor to maternal mtDNA quality control. Mouse knockout genetics, heteroplasmy quantification across generations, comparison with Parkin KO, Ulk1 KO, and Ulk2 KO mouse models PLoS genetics High 36608143
2024 BCL2L13 is localized at mitochondria, ER, and mitochondria-associated membranes (MAMs) in mammalian cells. Loss of Bcl2l13 in zebrafish impairs skeletal muscle structure and function, alters cytosolic Ca2+ release and mitochondrial Ca2+ uptake, and decreases mitochondrial complex activity, without changing ER-mitochondria contact site number. Organelle fractionation, immunolocalization, zebrafish bcl2l13 knockout, calcium imaging, mitochondrial complex activity assay, siRNA knockdown in C2C12 cells iScience High 39175772
2024 BCL2L13 interacts with LC3 to regulate receptor-mediated mitophagy in human saphenous vein endothelial cells during oxidative stress. o8G modification of miR-6513-5p causes it to lose targeted regulation of BCL2L13, contributing to BCL2L13 upregulation during oxidative stress. Proteomics, Co-IP of BCL2L13 with LC3, BCL2L13 knockdown/overexpression, mitophagy assays, miRNA target validation with o8G modification analysis Advanced biology Medium 39307929
2024 BCL2L13 exclusively uses the FIP200/ULK1 complex (not the WIPI-ATG13 complex) to initiate autophagosome biogenesis for mitophagy, distinguishing it from BNIP3/NIX receptors which use WIPI-ATG13, and from FKBP8 and TEX264 which can use both pathways. Reconstitution of autophagy initiation with purified components, genetic epistasis in cells with FIP200/ULK1 vs WIPI-ATG13 pathway perturbations bioRxivpreprint Medium bio_10.1101_2024.08.28.609967
2025 PRKAA2 (AMPKα2) is the kinase responsible for phosphorylating BCL2L13 at Ser272, which is required for BCL2L13-mediated mitophagy activation in pressure-overloaded heart. bcl2l13 knockout and non-phosphorylatable BCL2L13-S272A knock-in mice show suppressed mitochondrial fission and mitophagy under pressure overload, leading to reduced ATP production. No additive effects were found in bcl2l13/prkn double knockout. Bcl2l13 knockout mice, knock-in mice (BCL2L13-S272A), transverse aortic constriction model, in vitro kinase assay identifying PRKAA2 as the kinase, mitophagy flux assays, ATP production measurement Autophagy High 39995141
2025 BCL2L13 phosphorylation at Ser261 and Ser275 is induced by mitochondrial stress (CCCP) in an AMPK-dependent manner. TBK1, not ULK1, directly phosphorylates BCL2L13 at Ser275, revealing that BCL2L13 is uniquely regulated by both AMPK and innate immune stimuli among mitophagy receptors. Mass spectrometry phospho-mapping, phospho-specific antibody development, genetic studies with AMPK/ULK1/TBK1 knockout or inhibition, CCCP treatment bioRxivpreprint Medium 40672348
2026 MAP2K6 (MKK6) directly phosphorylates BCL2L13 at Ser426, enhancing the interaction between BCL2L13 and LC3B and thereby promoting mitophagy, inhibiting oxidative phosphorylation, and suppressing tumor growth in lung adenocarcinoma. MKK6 localizes to mitochondria and autophagosome interaction sites, and its pro-mitophagy function requires kinase activity but not p38 signaling. In vitro kinase assay, Co-IP of BCL2L13-LC3B with phospho-mutant BCL2L13-S426, subcellular fractionation of MKK6, loss-of-function studies in LUAD cells, mitophagy flux assay, OXPHOS measurement, in vivo tumor growth Cell reports High 41886451
2026 GDF15 secreted by Omicron-stimulated epithelial cells upregulates BCL2L13 in T cells, driving bystander T-cell apoptosis. Genetic dampening of BCL2L13 blunts Omicron-specific high-intensity bystander apoptosis, and recombinant GDF15 increases BCL2L13 expression and apoptosis. Recombinant GDF15 treatment, BCL2L13 genetic knockdown, apoptosis assays, co-culture experiments with Omicron-infected epithelial cells Cell death discovery Medium 41896204

Source papers

Stage 0 corpus · 45 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2001 Bcl-rambo, a novel Bcl-2 homologue that induces apoptosis via its unique C-terminal extension. The Journal of biological chemistry 119 11262395
2019 A Mammalian Mitophagy Receptor, Bcl2-L-13, Recruits the ULK1 Complex to Induce Mitophagy. Cell reports 109 30625316
2014 Bcl2L13 is a ceramide synthase inhibitor in glioblastoma. Proceedings of the National Academy of Sciences of the United States of America 84 24706805
2015 BCL2L13 is a mammalian homolog of the yeast mitophagy receptor Atg32. Autophagy 78 26506896
2002 Developmentally regulated expression of mil-1 and mil-2, mouse interferon-induced transmembrane protein like genes, during formation and differentiation of primordial germ cells. Mechanisms of development 76 14516695
2004 Regulation of expression of mouse interferon-induced transmembrane protein like gene-3, Ifitm3 (mil-1, fragilis), in germ cells. Developmental dynamics : an official publication of the American Association of Anatomists 65 15254899
2015 MicroRNA-124 and -137 cooperativity controls caspase-3 activity through BCL2L13 in hippocampal neural stem cells. Scientific reports 58 26207921
2019 Upregulation of miR-874-3p decreases cerebral ischemia/reperfusion injury by directly targeting BMF and BCL2L13. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 48 31200256
2020 BCL2L13: physiological and pathological meanings. Cellular and molecular life sciences : CMLS 45 33201252
2020 Long non-coding RNA SNHG15 is a competing endogenous RNA of miR-141-3p that prevents osteoarthritis progression by upregulating BCL2L13 expression. International immunopharmacology 37 32247266
2020 LncRNA FOXD3-AS1 knockdown protects against cerebral ischemia/reperfusion injury via miR-765/BCL2L13 axis. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 35 33068927
2023 BCL2L13 promotes mitophagy through DNM1L-mediated mitochondrial fission in glioblastoma. Cell death & disease 33 37660127
2003 Bcl-rambo beta, a special splicing variant with an insertion of an Alu-like cassette, promotes etoposide- and Taxol-induced cell death. FEBS letters 30 12527362
2016 The Human Bcl-2 Family Member Bcl-rambo Localizes to Mitochondria and Induces Apoptosis and Morphological Aberrations in Drosophila. PloS one 27 27348811
2018 A novel role for Bcl2l13 in promoting beige adipocyte biogenesis. Biochemical and biophysical research communications 24 30352689
2020 Selective binding of mitophagy receptor protein Bcl-rambo to LC3/GABARAP family proteins. Biochemical and biophysical research communications 23 32828302
2021 By targeting apoptosis facilitator BCL2L13, microRNA miR-484 alleviates cerebral ischemia/reperfusion injury-induced neuronal apoptosis in mice. Bioengineered 22 33724167
2002 Developmentally regulated expression of mil-1 and mil-2, mouse interferon-induced transmembrane protein like genes, during formation and differentiation of primordial germ cells. Gene expression patterns : GEP 19 12617817
2013 Widespread but tissue-specific patterns of interferon-induced transmembrane protein 3 (IFITM3, FRAGILIS, MIL-1) in the mouse gastrula. Gene expression patterns : GEP 17 23639725
2022 The protective effect of inhibiting mitochondrial fission on the juvenile rat brain following PTZ kindling through inhibiting the BCL2L13/LC3 mitophagy pathway. Metabolic brain disease 16 36094724
2015 The alternate AP-1 adaptor subunit Apm2 interacts with the Mil1 regulatory protein and confers differential cargo sorting. Molecular biology of the cell 14 26658609
2023 A role for BCL2L13 and autophagy in germline purifying selection of mtDNA. PLoS genetics 13 36608143
2022 Biological properties of the BCL-2 family protein BCL-RAMBO, which regulates apoptosis, mitochondrial fragmentation, and mitophagy. Frontiers in cell and developmental biology 13 36589739
2021 MIL-1, a novel antitumor agent derived from natural product millepachine, acts as tubulin polymerization inhibitor for the treatment of hepatocellular carcinoma. European journal of pharmacology 13 33647258
2022 LncRNA SNHG14 is beneficial to oxygen glucose deprivation/reoxygenation-induced neuro-2a cell injury via mir-98-5p sequestration-caused BCL2L13 upregulation. Metabolic brain disease 12 35678981
2021 Circ_0062166 aggravates cerebral ischemia-reperfusion injury through targeting miR-526b-5p/BCL2L13 axis. Brain injury 12 34495821
2022 PGAM5 interacts with Bcl-rambo and regulates apoptosis and mitophagy. Experimental cell research 9 36075447
2019 The human Bcl-2 family member Bcl-rambo and voltage-dependent anion channels manifest a genetic interaction in Drosophila and cooperatively promote the activation of effector caspases in human cultured cells. Experimental cell research 9 31102594
2025 TAM-derived exosomal miR-589-3p accelerates ovarian cancer progression through BCL2L13. Journal of ovarian research 8 39985077
2024 BCL2L13 at endoplasmic reticulum-mitochondria contact sites regulates calcium homeostasis to maintain skeletal muscle function. iScience 8 39175772
2023 Significant role of circRNA BBS9 in chronic obstructive pulmonary disease via miRNA-103a-3p/BCL2L13. BMC pulmonary medicine 8 37442983
2025 Phosphorylation of BCL2L13 by PRKAA2/AMPKα2 activates mitophagy in pressure-overloaded heart. Autophagy 7 39995141
2023 The role of BCL2L13 in glioblastoma: turning a need into a target. Biochemistry and cell biology = Biochimie et biologie cellulaire 7 37988705
2022 A Single Amino Acid Substitution in MIL1 Leads to Activation of Programmed Cell Death and Defense Responses in Rice. International journal of molecular sciences 7 36012116
2021 Silencing of H19 alleviates oxygen-glucose deprivation/reoxygenation-triggered injury through the regulation of the miR-1306-5p/BCL2L13 axis. Metabolic brain disease 5 34436746
2023 The BCL-2 family protein BCL-RAMBO interacts and cooperates with GRP75 to promote its apoptosis signaling pathway. Scientific reports 4 37640805
2022 Small Peptides from Periplaneta americana Inhibits Oxidative Stress-Induced KGN Cell Apoptosis by Regulating Mitochondrial Function Through Bcl2L13. Reproductive sciences (Thousand Oaks, Calif.) 4 36085549
2025 Epimedii Folium and Ligustri Lucidi Fructus synergistically delay renal aging through AMPK/ULK1/Bcl2L13-mediated mitophagy. Journal of ethnopharmacology 3 40122318
2024 BCL2L13 Influences Autophagy and Ceramide Metabolism without Affecting Temozolomide Resistance in Glioblastoma. bioRxiv : the preprint server for biology 3 39253475
2025 Multi-site phosphorylation of BCL2L13 in a TBK1- and AMPK-dependent manner reveals new modes of mitophagy regulation. bioRxiv : the preprint server for biology 2 40672348
2024 Molecular Characterization and Expression Changes of the bcl2l13 Gene in Response to Hypoxia in Megalobrama amblycephala. Current issues in molecular biology 1 38392190
2026 MAP2K6 directly phosphorylates BCL2L13 to mediate mitophagy for suppressing tumorigenicity. Cell reports 0 41886451
2026 Variant-divergent death: Omicron intensifies bystander T-cell apoptosis via GDF15-BCL2L13. Cell death discovery 0 41896204
2024 MiR-449b-5p Ameliorates Hypoxia-induced Cardiomyocyte Injury through Activating PI3K/AKT Pathway by Targeting BCL2L13. Applied biochemistry and biotechnology 0 38581629
2024 o8G-miR-6513-5p/BCL2L13 Axis Regulates Mitophagy during Oxidative Stress in the Human Saphenous Vein Endothelial Cells. Advanced biology 0 39307929

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