| Study / source | Identity | Domains / motifs | Localization | Molecular functions | Key interactors | Pathway position | Physiological roles | Disease contexts | Recent 2023–2024 findings with citations and dates | Quantitative / statistical notes |
|---|---|---|---|---|---|---|---|---|---|---|
| Murakawa et al., 2015 | Human/mammalian BCL2L13, also called Bcl-rambo/Bcl2-L-13; identified as a mammalian functional homologue of yeast Atg32 (pqac-00000003) | BH1–BH4 domains; two WXXL/I motifs, with the second motif at 273–276 functioning as the LC3-interacting region required for mitophagy (pqac-00000003, pqac-00000009) | Outer mitochondrial membrane protein with C-terminal transmembrane anchor (pqac-00000003, pqac-00000009) | Induces mitochondrial fragmentation and mitophagy; BH domains required for fragmentation, LIR required for mitophagy; fragmentation can occur independent of Drp1 and mitophagy in Parkin-deficient cells (pqac-00000003) | LC3B binding shown by GST pull-down / yeast two-hybrid; LC3 interaction enhanced after CCCP (pqac-00000003, pqac-00000009) | Receptor-mediated, ubiquitin-independent mitophagy at the mitochondrial outer membrane; engages core autophagy machinery (pqac-00000003) | Mitochondrial quality control; rescue of mitophagy in Atg32-deficient yeast supports conserved quality-control role (pqac-00000003) | Primarily mechanistic foundational study rather than disease-focused (pqac-00000003) | Foundational primary paper establishing BCL2L13 as a mitophagy receptor and fragmentation factor, July 2015 (pqac-00000003) | Motif positions 147–150 and 273–276 defined; figure evidence shows W273A/I276A mutation weakens LC3B binding and LIR-dependent mitophagy (pqac-00000009) |
| Yamaguchi et al., 2016 review | Reviews BCL2L13/Bcl-rambo as a mammalian mitophagy receptor protein (pqac-00000002) | Highlights second LIR motif at residues 273–276 and adjacent Ser272 phosphorylation site regulating LC3 binding (pqac-00000002) | Outer mitochondrial membrane, TM-domain anchored (pqac-00000002) | Separates mitochondrial fission and mitophagy functions: BH1–4 support fission, LIR/LC3 binding specifically supports mitophagy (pqac-00000002) | LC3; core autophagy factor Atg7 required in yeast rescue experiments; Parkin not required (pqac-00000002) | Places BCL2L13 within receptor-mediated mitophagy, distinct from PINK1/Parkin ubiquitin-driven pathway (pqac-00000002) | Mitochondrial homeostasis under stress, especially damage-induced mitophagy after CCCP (pqac-00000002) | Review links mitophagy dysregulation broadly to cardiac and other diseases but not with disease-specific BCL2L13 statistics (pqac-00000002) | Review synthesis published June 2016; emphasizes Ser272-dependent tuning of LC3 interaction and mitophagic activity (pqac-00000002) | S272A mutant retains fragmentation but shows reduced LC3 interaction and mitophagy; knockdown attenuates CCCP-induced fragmentation/mitophagy (pqac-00000002) |
| Kataoka, 2022 review | Human BCL2L13/BCL-RAMBO described as a BCL-2 family protein involved in apoptosis, mitochondrial fragmentation, and mitophagy (pqac-00000004, pqac-00000008) | Human protein 485 aa; BH1–BH4, BHNo domain, C-terminal TM domain; human LIR sequence WQQI at residues 276–279; Ser272 phosphorylation promotes mitophagy (pqac-00000004, pqac-00000005, pqac-00000007) | Integral mitochondrial outer membrane protein; N-terminal domains exposed to cytosol; TM domain needed for mitochondrial targeting and PGAM5 binding (pqac-00000001, pqac-00000007) | Context-dependent apoptosis regulation, mitochondrial fragmentation, mitophagy receptor activity, and likely ULK1 recruitment to the MOM (pqac-00000005, pqac-00000007) | PGAM5, ULK1, LC3/GABARAP family, ANT, VDAC, CERS2/CERS6; does not co-IP with many canonical BCL-2 family partners (pqac-00000005, pqac-00000006, pqac-00000007) | Positioned as a MOM-anchored receptor in ubiquitin-independent mitophagy; may recruit ULK1 complex and ATG8-family proteins (pqac-00000004, pqac-00000005) | Broad expression, relatively high in heart, skeletal muscle, pancreas; roles proposed in embryonic development, adipocyte browning, and mitochondrial quality control (pqac-00000001) | Review summarizes roles across cancer, ischemia/reperfusion injury, and metabolism, but notes mechanistic complexity and cell-type dependence (pqac-00000005, pqac-00000006) | State-of-the-field review published December 2022 consolidating apoptosis/mitophagy/fragmentation evidence (pqac-00000004, pqac-00000005) | Notes apparent SDS-PAGE migration around ~85 kDa despite predicted 485 aa size; limited precise effect sizes in excerpted review text (pqac-00000004) |
| Wang et al., 2023 GBM | Human BCL2L13 investigated in glioblastoma as an upregulated mitochondrial quality-control factor (pqac-00000016, pqac-00000019) | Not a motif-mapping study, but functionally linked to DNM1L Ser616-driven mitochondrial fission and mitophagy flux (pqac-00000019, pqac-00000037) | Acts at mitochondria in GBM cells, consistent with mitophagy receptor role (pqac-00000016) | Promotes mitophagy, proliferation, migration, and invasion; knockdown increases apoptosis and impairs tumor growth (pqac-00000016, pqac-00000035, pqac-00000038) | DNM1L/Drp1, BECN1, LC3B, and mitophagy/autophagy factors including NDP52, PINK1, Parkin, OPTN, BNIP3L/NIX, BNIP3 (pqac-00000016, pqac-00000035) | Supports pro-tumor mitochondrial fission–mitophagy axis in GBM; autophagy inhibitors reverse BCL2L13-driven phenotypes (pqac-00000016, pqac-00000038) | In tumor cells, BCL2L13 appears to maintain mitochondrial quality control that supports survival and invasiveness rather than cell death (pqac-00000016) | GBM: expression higher than normal brain, associated with higher grade and mesenchymal subtype; proposed biomarker/therapeutic target (pqac-00000016, pqac-00000019, pqac-00000037) | Key 2023 advance: Cell Death & Disease study (Sep 2023) linked BCL2L13 mechanistically to DNM1L-mediated fission and protective mitophagy in GBM (pqac-00000019, pqac-00000038) | Orthotopic mouse tumor bioluminescence reported ~55 × 10^8 vs ~30 × 10^8 photons/s for control vs BCL2L13 knockdown, with Kaplan–Meier survival benefit after knockdown (P < 0.05) (pqac-00000038) |
| Jiang et al., 2024 cardiomyocyte hypoxia | Human BCL2L13 identified as a direct target of miR-449b-5p in AC16 cardiomyocytes under hypoxia (pqac-00000014, pqac-00000017) | Study leverages 3'UTR targeting rather than structural mapping; prior BCL2L13 BH/TM/LIR architecture acknowledged in background (pqac-00000017) | Studied in human cardiomyocytes under hypoxic stress; mitochondrial/apoptotic role inferred from known biology and downstream apoptotic signaling changes (pqac-00000014, pqac-00000017) | BCL2L13 promotes hypoxia-induced injury/apoptosis and oxidative stress in this model; suppression is protective (pqac-00000014, pqac-00000017) | miR-449b-5p directly targets BCL2L13; downstream PI3K/AKT, Bcl-2, Bax altered (pqac-00000014, pqac-00000017) | Positions BCL2L13 upstream of stress injury signaling in hypoxic cardiomyocytes, intersecting apoptosis and PI3K/AKT survival pathways (pqac-00000017) | Suggests BCL2L13 contributes to cardiomyocyte vulnerability during hypoxia/ischemic stress (pqac-00000017) | Cardiomyocyte hypoxia / ischemic heart disease model; therapeutic implication is inhibition of BCL2L13 via miR-449b-5p (pqac-00000014, pqac-00000017) | Important 2024 paper (Apr 2024) showing miRNA-mediated repression of BCL2L13 ameliorates hypoxia injury in human cardiomyocytes (pqac-00000014, pqac-00000017) | miR mimic/inhibitor doses reported (50 nM mimic, 100 nM inhibitor; co-transfection with 2 µg pcDNA3.1-BCL2L13); statistics from three independent experiments with p < 0.05 threshold, though exact fold-changes not in excerpt (pqac-00000014) |
| Luo et al., 2024 DKD | Human/mammalian BCL2L13 implicated as a mitophagy receptor downstream of YME1L in diabetic kidney disease models (pqac-00000022, pqac-00000023, pqac-00000026) | Focus on phosphorylation state rather than primary motif mapping; phosphorylated BCL2L13 decreases in HG/DKD and rises with YME1L overexpression (pqac-00000023, pqac-00000024) | Studied in HK2 renal tubular epithelial cells and diabetic mouse kidneys; mitochondrial outer membrane mitophagy receptor role is central (pqac-00000022, pqac-00000023) | BCL2L13 supports mitophagy that restrains renal tubular senescence; loss impairs LC3 recruitment and worsens senescence markers (pqac-00000022, pqac-00000023) | YME1L interacts with BCL2L13; BCL2L13-LC3 binding strengthened by YME1L-mediated phosphorylation (pqac-00000022, pqac-00000023) | Places BCL2L13 in a YME1L→BCL2L13 phosphorylation→LC3 binding→mitophagy pathway that protects tubules under diabetic stress (pqac-00000023, pqac-00000024) | Renal tubular mitochondrial quality control and anti-senescence function under high glucose (pqac-00000022, pqac-00000024) | Diabetic kidney disease; potential therapeutic axis through YME1L/BCL2L13-mediated mitophagy (pqac-00000022, pqac-00000025, pqac-00000026) | Important 2024 advance (Mar 2024): Biological Research study connected BCL2L13 phosphorylation and mitophagy with protection from DKD-associated tubular senescence (pqac-00000022, pqac-00000023) | Cellular assays typically n = 3–4; in vivo groups n = 8–10; significance annotations reported (*p < 0.05, **p < 0.01, ***p < 0.001), but excerpt lacks exact effect sizes for LC3II, SA-β-Gal, UACR, creatinine (pqac-00000025) |
| Grepper et al., 2024 skeletal muscle / ER-mito contacts | BCL2L13 studied as a mammalian ER–mitochondria contact-site protein in muscle, extending beyond its classic mitophagy annotation (pqac-00000015, pqac-00000021) | Not primarily a motif study; relies on known BCL2L13 identity while functionally mapping ERMC localization and calcium-regulatory role (pqac-00000015, pqac-00000021) | Localizes to mitochondria, ER, and mitochondria-associated membranes / ER–mitochondria contact sites (pqac-00000015, pqac-00000021) | Regulates calcium homeostasis, muscle bioenergetics, and muscle integrity; knockdown lowers cytosolic Ca2+ release and raises mitochondrial Ca2+ uptake without increasing ERMC number (pqac-00000015, pqac-00000021, pqac-00000029) | Functional links to calcium-handling machinery and mitochondrial respiratory complexes; broader background notes connection to mitophagy and apoptosis (pqac-00000015, pqac-00000030) | Positions BCL2L13 at ER–mitochondria signaling interfaces controlling Ca2+ flux and downstream mitochondrial metabolism in skeletal muscle (pqac-00000021, pqac-00000029) | Maintains skeletal muscle function and endurance-associated mitochondrial physiology (pqac-00000015, pqac-00000021) | Skeletal muscle dysfunction phenotype in zebrafish KO model; potentially relevant to exercise adaptation and myopathy-like states (pqac-00000021, pqac-00000028) | Major 2024 advance (Aug 2024): iScience study expanded BCL2L13 biology from mitophagy receptor to ER–mitochondria calcium regulator in muscle (pqac-00000015, pqac-00000021) | n = 16 fish/group for physiology; tubular aggregates in 11% of KO fibers and 0% of WT; ERMC SPLICS assays used n = 30 cells from four transfections; EM quantification used 27 micrographs/condition; significance range *p < 0.05 to ****p < 0.0001 (pqac-00000021, pqac-00000028, pqac-00000029, pqac-00000030) |


*Table: This table summarizes core and recent evidence on human BCL2L13/Bcl-rambo, covering identity, domains, localization, molecular function, interactors, pathway role, physiology, and disease relevance. It is useful as a compact evidence map linking foundational mitophagy studies to newer 2023–2024 disease and physiology findings.*