BCL2L13
- Known as:
- BCL2L13
- Catalog number:
- 002471A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- BCL2L13
Related genes to: BCL2L13
- Gene:
- BCL2L13 NIH gene
- Name:
- BCL2 like 13
- Previous symbol:
- -
- Synonyms:
- MIL1, BCL-RAMBO
- Chromosome:
- 22q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-20
- Date modifiied:
- 2016-10-05
Related products to: BCL2L13
Related articles to: BCL2L13
- Mitochondrial quality control is essential for cellular homeostasis, particularly in neurons, where mitochondrial dysfunction is implicated in the pathogenesis of neurodegenerative diseases. Mitophagy, the selective degradation of damaged or superfluous mitochondria, plays a central role in maintaining mitochondrial integrity and metabolic balance. This review provides a comprehensive overview of the best-characterized PINK1-PRKN/parkin-dependent mitophagy pathway and the expanding repertoire of PRKN-independent mechanisms, including additional ubiquitin-dependent, receptor-mediated, and lipid-mediated pathways. We explore how these pathways intersect and compensate for one another, highlighting the complexity and adaptability of mitochondrial quality control networks. Furthermore, we discuss how dysregulated mitophagy contributes to the onset and progression of neurodegenerative diseases. By examining the interplay between mitophagy pathways and their regulation under physiological and pathological conditions, this review underscores the therapeutic potential of targeting mitophagy in neurodegeneration. Future studies should aim to decode the spatiotemporal dynamics of these pathways to uncover novel opportunities for clinical intervention. AD: Alzheimer disease; ALS: amyotrophic lateral sclerosis; AMBRA1: autophagy and beclin 1 regulator 1; AMFR/GP78: autocrine motility factor receptor; AMPK: AMP-activated protein kinase; ARIH1: ariadne RBR E3 ubiquitin protein ligase 1; ATG: autophagy related; Aβ: amyloid beta; BCL2L13: BCL2 like 13; BNIP3: BCL2 interacting protein 3; BNIP3L/NIX: BCL2 interacting protein 3 like; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; CAMc: core autophagy machinery components; CSNK2/CK2: casein kinase 2; DUB: deubiquitinase; DNM1L/DRP1: dynamin 1 like; FKBP8: FKBP prolyl isomerase 8; FUNDC1: FUN14 domain containing 1; GABARAP: GABA type A receptor-associated protein; GLP-1: glucagon-like peptide 1; HD: Huntington disease; HUWE1: HECT, UBA and WWE domain containing E3 ubiquitin protein ligase 1; IMM: inner mitochondrial membrane; iPSC: induced pluripotent stem cell; LIR: LC3-interacting region; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MARCHF5: membrane associated ring-CH-type finger 5; MCL1: MCL1 apoptosis regulator, BCL2 family member; MDV: mitochondria-derived vesicle; MFN1: mitofusin 1; MFN2: mitofusin 2; MQC: mitochondrial quality control; mtDNA: mitochondrial DNA; MUL1: mitochondrial E3 ubiquitin protein ligase 1; NBR1: NBR1 autophagy cargo receptor; OMM: outer mitochondrial membrane; OMMAD: outer mitochondrial membrane-associated degradation; OPA1: OPA1 mitochondrial dynamin like GTPase; OPTN: optineurin; OXPHOS: oxidative phosphorylation; PARL: presenilin associated rhomboid like; PD: Parkinson disease; PE: phosphatidylethanolamine; PG: phagophore; PGAM5: PGAM family member 5, mitochondrial serine/threonine protein phosphatase; PINK1: PTEN induced kinase 1; PPARGC1A/PGC-1α: PPARG coactivator 1 alpha; PRKN/parkin: parkin RBR E3 ubiquitin protein ligase; PtdIns3K: phosphatidylinositol 3-kinase; RB1CC1/FIP200: RB1 inducible coiled-coil 1; RHOT1/Miro1: ras homolog family member T1; ROS: reactive oxygen species; SIAH1: siah E3 ubiquitin protein ligase 1; SMURF1: SMAD specific E3 ubiquitin protein ligase 1; SOD1: superoxide dismutase 1; SQSTM1/p62: sequestosome 1; TAX1BP1: Tax1 binding protein 1; TBK1: TANK binding kinase 1; TCA: tricarboxylic acid cycle; TFAM: transcription factor A, mitochondrial; TIMM: translocase of inner mitochondrial membrane; TOMM: translocase of outer mitochondrial membrane; Ub: ubiquitin; ULK1: unc-51 like autophagy activating kinase 1; UPRmt: mitochondrial unfolded protein response; UPS: ubiquitin-proteasome system; USP30: ubiquitin specific peptidase 30; VCP: valosin containing protein; VDAC: voltage dependent anion channel; WIPI: WD repeat domain, phosphoinositide interacting. - Source: PubMed
Publication date: 2026/08/13
Rasmussen Laura KristineGomes Moreira DianaOkarmus JustynaSimonsen AnneMeyer Morten - Exosomes derived from bone marrow mesenchymal stem cells (BMSCs) represent a promising cell-free strategy for intervertebral disc degeneration (IDD). Here, we obtained oxidative stress-preconditioned exosomes (O-Exos) from BMSCs exposed to low-concentration hydrogen peroxide. Compared with exosomes from untreated cells (N-Exos), O-Exos more effectively delayed nucleus pulposus (NP) cell senescence and attenuated IDD and . The superior effects of O-Exos were associated with restoration of mitophagy and improved mitochondrial homeostasis in TNF/TNF-α-treated NP cells. BMF (Bcl2 modifying factor) was identified as a functionally relevant downstream target suppressed by O-Exos, and deficiency promoted mitophagy and alleviated IDD. Further analyses showed that O-Exos relieved the inhibitory effect of BMF on BCL2L13-LC3B coupling, thereby restoring mitophagy. In addition, exosomal was required for BMF suppression and the superior activity of O-Exos. Together, these findings identify oxidative stress preconditioning as an effective strategy to enhance exosome potency against IDD. ACAN: aggrecan; BCL2L13: BCL2 like 13; BMF: Bcl2 modifying factor; BMSCs: bone marrow mesenchymal stem cells; BNIP3: BCL2 interacting protein 3; CDKN1A: cyclin dependent kinase inhibitor 1A; CDKN2A: cyclin dependent kinase inhibitor 2A; COL2A1: collagen type II alpha 1 chain; DHI: disc height index; FUNDC1: FUN14 domain containing 1; HO: hydrogen peroxide; IDD: intervertebral disc degeneration; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MMP3: matrix metallopeptidase 3; MRI: nuclear magnetic resonance imaging; N-Exos: exosomes derived from untreated BMSCs; NP: nucleus pulposus; O-Exos: exosomes derived from HO-preconditioned BMSCs; OCR: oxygen consumption rate; PINK1: PTEN induced kinase 1; PRKN: parkin RBR E3 ubiquitin protein ligase; ROS: reactive oxygen species; RT-qPCR: reverse transcription quantitative polymerase chain reaction; SA-GLB1/β-gal: senescence-associated galactosidase beta 1; TEM: transmission electron microscopy; TNF/TNF-alpha: tumor necrosis factor; TOMM20: translocase of outer mitochondrial membrane 20; TP53: tumor protein p53; WT: wild type. - Source: PubMed
Publication date: 2026/06/29
Teng YunWu TianyiWu YanglinGe JunChen RuiSun XiaoZhao LeyuZhong XiangguYan QiZhang QiYang HuilinNiu JunjieZou Jun - The canine transmissible venereal tumor (CTVT) is a naturally occurring clonal cancer that offers a unique model to study tumor evolution, immune evasion, and chemoresistance. Although vincristine induces complete remission in most cases, some tumors show partial response or resistance, and the molecular drivers of this variability remain unclear. While genomic and epigenetic studies have implicated multidrug resistance and immune modulation, transcriptional mechanisms underlying therapeutic outcomes are not fully characterized. - Source: PubMed
Publication date: 2026/04/15
López-Valbuena Fabián DOsorio-Zambrano William FDebiaso Rossi André LMontoya-Flórez Luis MRocha Noeme S - Severe Omicron cases present profound lymphocytopenia, suggesting variant-specific immune injury. - Source: PubMed
Publication date: 2026/03/28
Gao ChaoChen HanbingChi YingLu XinxingLi JiahuangTang YingYu RuixuanShi NanLiu LingXie JianfengQiu HaiboChao JieLi Shufeng - The mitogen-activated protein kinase (MAPK) pathway widely regulates development and cancer. However, the subcellular localization and function of the secondary kinases in the MAPK pathway remain unclear. Here, we identified mitogen-activated protein kinase kinase 6 or 3 (MKK6/MKK3) as tumor suppressors that could significantly activate mitophagy and suppress tumor growth in lung adenocarcinoma (LUAD). Mechanistically, among MKK1-7, only MKK6/MKK3 exhibited subcellular organellar localization in mitochondria and autophagosome interaction site. The function of MKK6 in mitophagy and tumorigenicity was dependent on its kinase activity, but not through p38. MKK6 directly phosphorylated BCL2L13 at serine 426, enhancing the interaction between BCL2L13 and LC3B, which, in turn, promoted mitophagy, inhibited oxidative phosphorylation (OXPHOS), and prevented tumor growth. Our studies not only revealed that MKK6-BCL2L13 phosphorylation at the interorganellar site can affect mitochondrial quality in tumorigenicity but also might provide a potential therapeutic strategy for LUAD treatment. - Source: PubMed
Publication date: 2026/03/24
Xing GuangsuoHuang YileLiu XiwenLi LinpengLiu ZichaoWu YiZhou YanshuangDing YingzheChen BaodanXue GuanruLi ZijingHao ZhihongLiu YangFan WenhuiDing HaolinLiang ShanHe JingcaiWang JunweiZhang JianQin DajiangWang WumingLu GangChan Wai-YeeRan PixinJu HuaiqiangDong MingLiang WenhuaLiu XingguoChen Keshi