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Showing YME1L1 — YME1L is a alias.

YME1L1

ATP-dependent zinc metalloprotease YME1L1 · UniProt Q96TA2

Length
773 aa
Mass
86.5 kDa
Annotated
2026-06-11
32 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

YME1L1 is an ATP-dependent inner mitochondrial membrane protease that governs mitochondrial morphology and proteostasis by exposing a catalytic domain to the intermembrane space and assembling into large (600–1100 kDa) complexes (PMID:17709429, PMID:22262461). It constitutively cleaves OPA1 at site S2 and, together with OMA1, generates the balance of long and short OPA1 isoforms that set the equilibrium between mitochondrial fusion and fission (PMID:17709429, PMID:24616225). Beyond this central dynamics role, YME1L1 performs quality-control proteolysis of a broad substrate set including non-assembled respiratory chain subunits, where this activity maintains cristae morphology, respiration, proliferation, and apoptotic resistance (PMID:22262461), the TIM23 translocase channel components TIMM17A and TIMM23 when their import channel is unoccupied (PMID:39774271), lipid transfer proteins and metabolic enzymes (PMID:31695197), and the MICOS subunit MIC13 (PMID:40338741). This proteolysis is mobilized as an adaptive program: mTORC1 inhibition activates LIPIN1, lowering mitochondrial phosphatidylethanolamine and triggering YME1L1-mediated remodeling of the mitochondrial proteome to limit biogenesis while supporting growth under hypoxia or starvation (PMID:31695197). YME1L1 is anchored within the SLP2–PARL–YME1L (SPY) scaffold at the inner membrane (PMID:24176854, PMID:27737933) and is selectively imported through a ROMO1-dependent TIM23 pathway (PMID:30598479). In vivo, loss of YME1L1 causes neurodegeneration driven by impaired proteostasis rather than fragmentation per se (PMID:30389680) and depletes neural stem/progenitor pools by forcing premature differentiation (PMID:35172139). Human homozygous YME1L1 mutations that abolish or impair function cause defective OPA1 processing, mitochondrial fragmentation, and a mitochondriopathy classified as a form of secondary 3-methylglutaconic aciduria (PMID:27495975, PMID:40255048).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 2007 High

    Establishing which protease produces a specific OPA1 isoform answered how a single dynamin-related GTPase is post-translationally diversified to control fusion; YME1L was identified as the S2-cleaving enzyme.

    Evidence shRNA knockdown of Yme1L and OPA1 isoform analysis in OPA1-null reconstituted cells

    PMID:17709429

    Open questions at the time
    • Did not resolve full substrate spectrum beyond OPA1
    • Did not establish the regulatory inputs controlling S2 cleavage
  2. 2012 High

    Defining YME1L topology and catalytic requirement showed it is a bona fide proteolytic quality-control enzyme rather than a passive scaffold, linking its activity to respiratory chain integrity and cell survival.

    Evidence shRNA knockdown with wild-type vs. catalytically dead rescue, EM, respiration assays in HEK293

    PMID:22262461

    Open questions at the time
    • Substrate recognition mechanism not defined
    • Composition of the 600–1100 kDa complexes not resolved
  3. 2014 High

    Double-knockout epistasis with OMA1 clarified how two proteases jointly set the long/short OPA1 ratio and demonstrated that long OPA1 forms suffice for fusion.

    Evidence Yme1l/Oma1 single and double genetic deletion, morphology imaging, co-localization of short OPA1 with fission machinery

    PMID:24616225

    Open questions at the time
    • Did not establish how cleavage choice between OMA1 and YME1L is partitioned
    • Stoichiometry of short-OPA1 action at fission sites unresolved
  4. 2013 Medium

    Characterizing the SLP-2 interaction and the Drp1/Mff-dependent fragmentation phenotype showed YME1L influences fission through the recruitment machinery, not only via OPA1 processing.

    Evidence shRNA knockdown in MEFs, live imaging, Co-IP of SLP-2, epistasis with Drp1/Mff knockout

    PMID:24176854

    Open questions at the time
    • Single lab
    • Mechanistic link between YME1L loss and elevated MiD49/Mff not defined
  5. 2016 High

    Identifying the SPY complex placed YME1L within a defined inner-membrane proteolytic scaffold alongside SLP2 and PARL, contextualizing how multiple processing reactions are spatially organized.

    Evidence Reciprocal Co-IP, blue-native PAGE, SLP2 deletion with PINK1/PGAM5/OPA1 processing assays

    PMID:27737933

    Open questions at the time
    • Direct biochemical architecture of the SPY complex not solved
    • How SLP2 binding modulates YME1L catalysis specifically not dissected
  6. 2016 High

    A patient pre-sequence mutation that blocks MPP cleavage established YME1L1 as a human disease gene and demonstrated that loss of mature protein recapitulates OPA1 and morphology defects.

    Evidence Patient fibroblast studies, precursor/mature western blot, OPA1 analysis, genetic complementation

    PMID:27495975

    Open questions at the time
    • Full clinical-molecular spectrum not defined from a single family
    • Tissue-specific vulnerability not explained
  7. 2018 High

    Discovering the ROMO1-dependent TIM23 import route explained how YME1L is selectively delivered to the inner membrane and why its unusual targeting sequence creates a specific import dependency.

    Evidence MS identification of TIM23 components, ROMO1 KO, import assays, quantitative proteomics, EM

    PMID:30598479

    Open questions at the time
    • Biochemical basis of ROMO1 recognition of the YME1L pre-sequence not solved
    • Whether other inner-membrane proteins share this route not fully mapped
  8. 2019 High

    Linking mTORC1–LIPIN1–phosphatidylethanolamine signaling to YME1L proteolysis revealed how the protease acts as an adaptive sensor that remodels the mitochondrial proteome in response to nutrient and oxygen stress.

    Evidence Quantitative proteomics and lipidomics under hypoxia/starvation, mTORC1 inhibition, LIPIN1 manipulation, YME1L KO, xenografts

    PMID:31695197

    Open questions at the time
    • How lowered PE mechanistically activates YME1L not resolved at the molecular level
    • Substrate selectivity rules under remodeling not defined
  9. 2019 High

    Nervous-system conditional knockout with Oma1 epistasis separated YME1L's proteostasis function from morphology, showing that proteostatic failure—not fragmentation—drives neurodegeneration.

    Evidence Conditional Yme1l KO mice, Yme1l/Oma1 double KO, histology, behavior, morphology imaging

    PMID:30389680

    Open questions at the time
    • Specific substrate(s) responsible for axonal degeneration not identified
    • Cell-type basis of proprioceptive selectivity unexplained
  10. 2019 Medium

    Identifying KIF1Bβ as a stimulatory binding partner provided a mechanism for inducible YME1L activation during apoptotic signaling.

    Evidence Co-IP, domain mapping, OPA1 cleavage assay, siRNA, NGF-withdrawal apoptosis model in PC12

    PMID:30859632

    Open questions at the time
    • No in vitro reconstitution of stimulated protease activity
    • Single lab
  11. 2019 Medium

    Muscle-cell depletion connected YME1L loss to AMPK/FoxO3a-driven atrophy programs, extending its physiological reach to muscle homeostasis.

    Evidence shRNA in C2C12 myotubes, immobilization mouse model, western blots for OPA1/AMPK/FoxO3a/MuRF1/myostatin

    PMID:31725201

    Open questions at the time
    • No epistasis to place YME1L upstream of AMPK
    • Direct substrate driving atrophy not identified
  12. 2020 Medium

    Biochemical study of ATP binding showed nucleotide stabilizes the hexameric catalytic assembly, beginning the mechanistic dissection of allosteric control.

    Evidence Urea unfolding fluorescence and stopped-flow nucleotide-binding assays on purified protein

    PMID:32340357

    Open questions at the time
    • Single in vitro study
    • Did not link nucleotide state to substrate processing on membranes
  13. 2022 High

    Conditional knockout in neural stem/progenitor cells demonstrated YME1L sets a metabolic state required for quiescence, with its loss forcing premature differentiation and pool depletion.

    Evidence In vivo conditional Yme1l KO, mitochondrial proteomics, metabolic profiling, fate-mapping

    PMID:35172139

    Open questions at the time
    • Key substrate controlling the fatty-acid-oxidation state not pinpointed
    • Reversibility window not defined
  14. 2022 Medium

    Identifying Sirt3-mediated deacetylation of YME1L1 established a post-translational regulatory layer coupling NAD+-dependent signaling to mitochondrial fusion.

    Evidence Sirt3 KO mice + LPS, HK-2 overexpression, Co-IP, deacetylation and OPA1 processing assays

    PMID:36433732

    Open questions at the time
    • Acetylation site not mapped by mutagenesis
    • Direct effect of acetylation on catalytic activity not measured biochemically
  15. 2024 High

    An import-blocking system revealed YME1L1 degrades unoccupied TIM23 channel subunits via an exposed degron, defining a surveillance role over the translocase itself.

    Evidence DHFR-MIC60 import-block, YME1L1 KO cells, western blots for TIMM17A/TIMM23, growth assays

    PMID:39774271

    Open questions at the time
    • Degron sequence not precisely defined
    • Whether degradation is direct (not via cofactor) not biochemically reconstituted
  16. 2024 Medium

    Identifying SLC25A38 as a short-lived YME1L1 substrate linked the protease to control of a mitochondrial glycine transporter and tied turnover to membrane potential.

    Evidence Half-life analysis, pharmacological/genetic YME1L1 depletion, CCCP depolarization, western blot (preprint)

    PMID:38979268

    Open questions at the time
    • No in vitro reconstitution of direct cleavage
    • Preprint, not peer-reviewed
  17. 2024 Low

    A reported interaction with the mitophagy receptor BCL2L13 raised the possibility that YME1L participates in mitophagy regulation.

    Evidence LC-MS/MS interactome, Co-IP, phosphorylation assay, AAV overexpression, mitophagy flux assays

    PMID:38494498

    Open questions at the time
    • Single lab with limited mechanistic follow-up on the phosphorylation step
    • Whether the effect requires YME1L catalytic activity not established
  18. 2025 Medium

    A second human homozygous variant (p.Leu667Val) expanded the disease phenotype, linking defective OPA1 and PRELID1 processing to impaired Krebs cycle activity and classifying the deficiency within 3-methylglutaconic aciduria.

    Evidence Patient fibroblast OPA1/PRELID1 processing, morphology imaging, Krebs cycle enzyme and respiration assays

    PMID:40255048

    Open questions at the time
    • Genotype-phenotype correlation across patients not established
    • Mechanism linking PRELID1 mis-processing to metabolic defect not dissected
  19. 2025 Medium

    Structural-dynamics analysis defined an inter-domain salt bridge mediating AAA+-to-protease allostery, explaining how ATP and Zn2+ binding are communicated to control substrate degradation.

    Evidence HDX-MS, NMR, salt-bridge mutagenesis, in vitro degradation assay with soluble hexameric construct (preprint)

    PMID:bio_10.1101_2025.01.30.635686

    Open questions at the time
    • Preprint, not peer-reviewed
    • Full-length membrane-embedded enzyme not structurally resolved
  20. 2025 Medium

    Identifying GCN5L1 as an intermembrane-space partner that promotes YME1L-mediated MIC13 degradation connected the protease to diet-induced cristae remodeling.

    Evidence GCN5L1 KO interactome, Co-IP, MIC13 degradation assay, EM, adipose-specific KO metabolic phenotyping

    PMID:40338741

    Open questions at the time
    • Single lab
    • Direct vs. cofactor-assisted MIC13 cleavage not reconstituted

Open questions

Synthesis pass · forward-looking unresolved questions
  • How YME1L's substrate selectivity is encoded—what degrons and recognition features distinguish its many membrane substrates and how lipid, nucleotide, and partner inputs converge on a single processing decision—remains unresolved.
  • No unified substrate-recognition code defined
  • No structure of the full membrane-embedded SPY-assembled enzyme
  • Quantitative integration of PE, ATP, acetylation, and partner regulation not achieved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 5 GO:0016787 hydrolase activity 3 GO:0140657 ATP-dependent activity 2
Pathway
R-HSA-1852241 Organelle biogenesis and maintenance 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-9609507 Protein localization 2
Partners
BCL2L13GCN5L1KIF1BΒPARLROMO1SIRT3SLP2
Complex memberships
SPY complex (SLP2-PARL-YME1L)

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 YME1L (Yme1L) is the protease responsible for OPA1 cleavage at site S2 in the mitochondrial inner membrane. Loss of membrane potential destabilizes OPA1 long isoforms and enhances cleavage at S1 (but not S2), while S2 cleavage is specifically regulated by Yme1L. Cellular reconstitution in OPA1-null cells; shRNA knockdown of Yme1L; analysis of OPA1 isoform patterns by western blot The Journal of cell biology High 17709429
2012 Human YME1L is an integral inner mitochondrial membrane protein that exposes its carboxy-terminus to the intermembrane space and exists in large complexes of 600–1100 kDa. Its proteolytic activity is required for degrading non-assembled respiratory chain subunits (Ndufb6, ND1, Cox4), maintaining cristae morphology, supporting cell proliferation, and conferring apoptotic resistance. Stable shRNA knockdown in HEK293 cells; rescue with wild-type vs. proteolytically inactive YME1L mutant; electron microscopy; western blot; respiration assay Molecular biology of the cell High 22262461
2014 YME1L performs constitutive cleavage of OPA1, and together with OMA1 generates both long and short OPA1 forms that maintain mitochondrial fusion. Short OPA1 forms produced by OMA1/YME1L processing promote mitochondrial fission and partially co-localize with ER-mitochondria contact sites and the fission machinery. Long OPA1 forms alone are sufficient to mediate fusion in the absence of both YME1L and OMA1. Genetic deletion of Yme1l, Oma1, or both; mitochondrial morphology imaging; epistasis analysis; co-localization of GTPase-inactive short OPA1 with fission machinery The Journal of cell biology High 24616225
2013 Endogenous Yme1L localizes to punctate structures on mitochondria. Loss of Yme1L causes mitochondrial fragmentation through increased Drp1 recruitment (via elevated MiD49/Mff), not via OPA1 S1/S2 processing; shYme1L stabilizes L-OPA1 and exogenous OPA1/L-OPA1 further promotes fragmentation. SLP-2 interacts with Yme1L. Loss of Drp1 or Mff rescues shYme1L-induced fragmentation. shRNA knockdown in MEF cells; live-cell mitochondrial dynamics imaging; co-immunoprecipitation of SLP-2 with Yme1L; epistasis with Drp1/Mff KO Cell death & disease Medium 24176854
2016 SLP2 anchors a large protease complex (SPY complex) at the mitochondrial inner membrane comprising PARL and YME1L. Association with SLP2 regulates PARL-mediated processing of PINK1 and PGAM5, and SLP2 inhibits OMA1-mediated OPA1 cleavage, thereby enabling stress-induced mitochondrial hyperfusion. SLP2 restricts OMA1 activity by direct binding. Co-immunoprecipitation; blue-native PAGE complex analysis; genetic deletion/knockdown of SLP2; processing assays for PINK1, PGAM5, OPA1; mitochondrial morphology imaging under starvation stress EMBO reports High 27737933
2016 A homozygous missense mutation in the mitochondrial pre-sequence of YME1L1 inhibits its cleavage by the mitochondrial processing peptidase (MPP), leading to rapid degradation of the YME1L1 precursor protein. This abolishes YME1L1 function, causes abnormal OPA1 processing, mitochondrial network fragmentation, and a proliferation defect in patient-derived cells. Patient fibroblast studies; western blot for precursor vs. mature YME1L1; OPA1 isoform analysis; mitochondrial morphology imaging; genetic complementation eLife High 27495975
2018 ROMO1 is a constituent of the human TIM23 presequence translocase that is specifically required for import of YME1L into the inner mitochondrial membrane. Loss of ROMO1 causes selective loss of YME1L (but not general presequence import), leading to aberrant OPA1 processing and inner membrane structural defects. This selective requirement is linked to the unusually long and charge-distributed targeting sequence of YME1L. Mass spectrometry identification of TIM23 complex components; ROMO1 knockout cell line; quantitative proteomics; protein import assays; OPA1 processing assay; inner membrane morphology by EM The Journal of cell biology High 30598479
2019 YME1L rewires the mitochondrial proteome in response to hypoxia or nutrient starvation via a lipid signalling cascade. Inhibition of mTORC1 activates LIPIN1 phosphatidic acid phosphatase, which decreases mitochondrial phosphatidylethanolamine levels and promotes YME1L-mediated proteolysis of mitochondrial protein translocases, lipid transfer proteins, and metabolic enzymes, acutely limiting mitochondrial biogenesis while supporting cell growth. Quantitative mitochondrial proteomics under hypoxia/starvation; mTORC1 inhibition; LIPIN1 genetic manipulation; lipid mass spectrometry for PE levels; YME1L KO; xenograft tumor models Nature High 31695197
2019 YME1L-deficient mice lacking YME1L in the nervous system develop ocular dysfunction and selective degeneration of spinal cord proprioceptive axons. Deletion of Oma1 in Yme1l-null mice restores tubular mitochondria but worsens axonal degeneration, establishing that impaired mitochondrial proteostasis (not mitochondrial fragmentation per se) causes the neurological defects. Conditional nervous-system-specific Yme1l KO mice; double Yme1l/Oma1 KO epistasis; histological and behavioral analysis; mitochondrial morphology imaging EMBO molecular medicine High 30389680
2019 KIF1Bβ physically interacts with YME1L1 through its death-inducing region and stimulates YME1L1 protease activity to cleave long OPA1 forms, causing mitochondrial fragmentation and apoptosis. Both KIF1Bβ and YME1L1 are upregulated upon NGF withdrawal in PC12 cells, and knockdown of either protein inhibits NGF-depletion-induced apoptosis. Co-immunoprecipitation of KIF1Bβ with YME1L1; domain-mapping with deletion constructs; OPA1 cleavage assay; siRNA knockdown of each protein; NGF-withdrawal apoptosis model Molecular carcinogenesis Medium 30859632
2019 Loss of Yme1L in C2C12 myotubes activates AMPK and FoxO3a and increases expression of MuRF1 and myostatin, contributing to muscle atrophy. Yme1L depletion causes accumulation of short OPA1 forms and mitochondrial fragmentation, and this effect is specific to Yme1L (not LonP1). shRNA knockdown of Yme1L in C2C12 myotubes; hindlimb-immobilized mouse model; western blot for OPA1 isoforms, AMPK, FoxO3a, MuRF1, myostatin; mitochondrial morphology Journal of cellular and molecular medicine Medium 31725201
2020 ATP binding stabilizes the hexameric structure of the YME1L catalytic domain and protects it from urea-induced unfolding and loss of active hexamers, as measured by fluorescence unfolding and stopped-flow nucleotide-binding assays. Protein unfolding fluorescence assay with urea; stopped-flow fluorescence for nucleotide binding and unfoldase activity; multiple fluorophore systems Biomolecules Medium 32340357
2022 YME1L controls the abundance of numerous mitochondrial substrates in quiescent neural stem and progenitor cells (NSPCs). Conditional Yme1l deletion activates a differentiation program with broad metabolic changes, irreversibly shifting NSPCs away from a fatty-acid-oxidation-dependent state and causing premature differentiation and NSPC pool depletion in vivo. Conditional Yme1l KO in adult NSPCs in vivo; quantitative mitochondrial proteomics; metabolic profiling; fate-mapping and self-renewal assays Cell reports High 35172139
2022 Sirt3 deacetylates YME1L1, and this deacetylation promotes OPA1-mediated mitochondrial fusion. Loss of Sirt3 increases YME1L1 acetylation and impairs fusion; Sirt3 overexpression rescues LPS-induced mitochondrial damage and apoptosis in renal tubular epithelial cells via the YME1L1-OPA1 axis. Sirt3 KO mice + LPS model; Sirt3 overexpression in HK-2 cells; co-immunoprecipitation; deacetylation assay; OPA1 processing analysis; mitochondrial morphology by immunofluorescence and electron microscopy Cell proliferation Medium 36433732
2024 Plugging the TOM complex in mammalian cells induces YME1L1-dependent degradation of TIM23 channel components TIMM17A and TIMM23. Unoccupied TIM23 complexes appear to expose a C-terminal degron on TIMM17A that is recognized by YME1L1 for proteolysis. Loss of YME1L1 exacerbates the growth defect caused by TOM channel plugging. DHFR-MIC60 import-blocking system stabilized by methotrexate; YME1L1 KO cell lines; western blot for TIMM17A/TIMM23 levels; cell growth assays Nature cell biology High 39774271
2024 YME1L1 directly degrades SLC25A38, a short-lived mitochondrial glycine transporter (half-life ~4 h). Pharmacological inhibition or genetic depletion of YME1L1 stabilizes SLC25A38. Depolarization of mitochondrial membrane potential by CCCP prevents SLC25A38 degradation, linking its turnover to inner membrane integrity. Protein half-life analysis; pharmacological inhibition of proteolytic systems; YME1L1 genetic depletion; CCCP depolarization experiment; western blot for SLC25A38 stability bioRxivpreprint Medium 38979268
2024 YME1L interacts with BCL2L13 (a mitophagy receptor) and promotes its phosphorylation, thereby enhancing mitophagy in renal tubular epithelial cells. LC-MS/MS identified BCL2L13 as a YME1L-interacting protein. LC-MS/MS interactome analysis; co-immunoprecipitation; phosphorylation assay; in vivo AAV-mediated YME1L overexpression; mitophagy flux assays Biological research Low 38494498
2025 A novel homozygous YME1L1 variant (p.Leu667Val) causes defective proteolytic processing of OPA1 and PRELID1 (PRELI domain containing 1), enhanced mitochondrial fission, attenuated Krebs cycle enzyme activities, and reduced mitochondrial respiration in patient fibroblasts, classifying YME1L1 deficiency as a form of secondary 3-methylglutaconic aciduria. Patient fibroblast functional studies; OPA1 and PRELID1 processing assays; mitochondrial morphology imaging; Krebs cycle enzyme activity assays; mitochondrial respiration measurement Journal of inherited metabolic disease Medium 40255048
2025 Nucleotide (ATP) binding reduces backbone flexibility and modulates side-chain dynamics of the AAA+ domain of YME1L, while Zn²⁺ binding stabilizes the protease domain. Long-range allostery between the AAA+ and protease domains is mediated by a critical salt bridge at the inter-domain interface, and disruption of this salt bridge impairs ATP-dependent substrate degradation. HDX-MS; NMR spectroscopy; site-directed mutagenesis of salt bridge residue; in vitro substrate degradation assay with hexameric soluble YME1L construct bioRxivpreprint Medium bio_10.1101_2025.01.30.635686
2025 GCN5L1 physically associates with YME1L in the mitochondrial intermembrane space and facilitates YME1L-mediated degradation of the MICOS component MIC13, thereby promoting cristae disassembly during obesity. A high-fat diet triggers GCN5L1 accumulation in the intermembrane space, activating this pathway. Protein interactome analysis (GCN5L1 KO mice); co-immunoprecipitation; MIC13 degradation assay; cristae morphology by EM; metabolic phenotyping of adipose-specific KO mice Cell reports Medium 40338741

Source papers

Stage 0 corpus · 32 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 OPA1 processing controls mitochondrial fusion and is regulated by mRNA splicing, membrane potential, and Yme1L. The Journal of cell biology 678 17709429
2014 The i-AAA protease YME1L and OMA1 cleave OPA1 to balance mitochondrial fusion and fission. The Journal of cell biology 652 24616225
2016 The membrane scaffold SLP2 anchors a proteolytic hub in mitochondria containing PARL and the i-AAA protease YME1L. EMBO reports 155 27737933
2019 Lipid signalling drives proteolytic rewiring of mitochondria by YME1L. Nature 143 31695197
2012 YME1L controls the accumulation of respiratory chain subunits and is required for apoptotic resistance, cristae morphogenesis, and cell proliferation. Molecular biology of the cell 141 22262461
2016 Homozygous YME1L1 mutation causes mitochondriopathy with optic atrophy and mitochondrial network fragmentation. eLife 99 27495975
2018 ROMO1 is a constituent of the human presequence translocase required for YME1L protease import. The Journal of cell biology 52 30598479
2022 Sirt3 mitigates LPS-induced mitochondrial damage in renal tubular epithelial cells by deacetylating YME1L1. Cell proliferation 46 36433732
2022 Metabolic control of adult neural stem cell self-renewal by the mitochondrial protease YME1L. Cell reports 42 35172139
2019 Loss of the mitochondrial i-AAA protease YME1L leads to ocular dysfunction and spinal axonopathy. EMBO molecular medicine 42 30389680
2013 Loss of Yme1L perturbates mitochondrial dynamics. Cell death & disease 42 24176854
2000 Identification and characterization of YME1L1, a novel paraplegin-related gene. Genomics 39 10843804
2020 GDF11 enhances therapeutic efficacy of mesenchymal stem cells for myocardial infarction via YME1L-mediated OPA1 processing. Stem cells translational medicine 31 32515551
2025 Mitochondrial YME1L1 governs unoccupied protein translocase channels. Nature cell biology 29 39774271
2018 Loss of Mitochondrial AAA Proteases AFG3L2 and YME1L Impairs Mitochondrial Structure and Respiratory Chain Biogenesis. International journal of molecular sciences 28 30544562
2019 Tumor suppressor KIF1Bβ regulates mitochondrial apoptosis in collaboration with YME1L1. Molecular carcinogenesis 25 30859632
2024 YME1L-mediated mitophagy protects renal tubular cells against cellular senescence under diabetic conditions. Biological research 14 38494498
2005 Mutation detection in four candidate genes (OXA1L, MRS2L, YME1L and MIPEP) for combined deficiencies in the oxidative phosphorylation system. Journal of inherited metabolic disease 12 16435202
2024 Targeting the mitochondrial protein YME1L to inhibit osteosarcoma cell growth in vitro and in vivo. Cell death & disease 10 38769124
2019 Down-regulation of the mitochondrial i-AAA protease Yme1L induces muscle atrophy via FoxO3a and myostatin activation. Journal of cellular and molecular medicine 10 31725201
2024 SREBP1c-Mediated Transcriptional Repression of YME1L1 Contributes to Acute Kidney Injury by Inducing Mitochondrial Dysfunction in Tubular Epithelial Cells. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 9 39680752
2025 Reduced Expression of UPRmt Proteins HSP10, HSP60, HTRA2, OMA1, SPG7, and YME1L Is Associated with Accelerated Heart Failure in Humans. Biomedicines 7 40426970
2024 Expression and functional implications of YME1L in nasopharyngeal carcinoma. Cell death & disease 7 38890304
2025 Macrophage polarization-mediated PKM2/mTORC1/YME1L signaling pathway activation in fibrosis associated with Cardiorenal syndrome. Cellular signalling 4 39961408
2025 Mitochondrial GCN5L1 coordinates with YME1L and MICOS to remodel mitochondrial cristae in white adipocytes and modulate obesity. Cell reports 4 40338741
2023 Knock-down of YME1L1 induces mitochondrial dysfunction during early porcine embryonic development. Frontiers in cell and developmental biology 4 37123411
2024 Wnt/β-catenin Pathway Aggravates Renal Fibrosis by Activating PUM2 Transcription to Repress YME1L-mediated Mitochondrial Homeostasis. Biochemical genetics 3 38564095
2023 OMA1 and YME1L as a Diagnostic Panel in Hepatocellular Carcinoma. The Yale journal of biology and medicine 3 38161580
2024 The iAAA-mitochondrial protease YME1L1 regulates the degradation of the short-lived mitochondrial transporter SLC25A38. bioRxiv : the preprint server for biology 2 38979268
2020 Fluorescence Methods Applied to the Description of Urea-Dependent YME1L Protease Unfolding. Biomolecules 2 32340357
2025 YME1L1 Dysfunction Associated With 3-Methylglutaconic Aciduria. Journal of inherited metabolic disease 0 40255048
2025 YME1L facilitates the development of non-small cell lung cancer by promoting activation of mitochondria-Gαi1-Akt pathway. Cancer genetics 0 41166794

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