Affinage

VPS41

Vacuolar protein sorting-associated protein 41 homolog · UniProt P49754

Length
854 aa
Mass
98.6 kDa
Annotated
2026-06-11
33 papers in source corpus 18 papers cited in narrative 18 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

VPS41 is a membrane-tethering factor that governs the delivery and fusion of cargo with the lysosome/vacuole and the biogenesis of regulated secretory granules, operating both as a subunit of the multisubunit HOPS tethering complex and as a coat-like adaptor for AP-3 vesicles (PMID:10559961, PMID:24210660). In yeast it is required for post-Golgi sorting of vacuolar hydrolases and for the formation of AP-3 transport vesicles at the late Golgi, binding directly to the AP-3 δ-adaptin subunit (PMID:10559961, PMID:9159129). Its activity is gated by phosphorylation: an amphipathic lipid-packing-sensor (ALPS) motif inserts into highly curved endosomal membranes to mask the AP-3-binding site, and casein kinase Yck3 phosphorylation of this motif at the less-curved vacuole exposes the site, switching VPS41 between curvature-sensing (endosome-vacuole fusion) and coat-recognition (AP-3 vesicle-vacuole fusion) modes in cooperation with the Rab GTPase Ypt7 (PMID:21079247, PMID:19193765). In mammals VPS41 is recruited into HOPS through a RING–RING interaction with VPS18, and its WD40 domain binds the small GTPase Arl8b to tether TGN-derived LAMP1/LAMP2A carriers—including the cholesterol transporter NPC1—to lysosomes, a cargo-tethering activity unique among HOPS subunits (PMID:28931724, PMID:39907656, PMID:41452985). Loss of VPS41/HOPS function delays lysosomal delivery of endocytic and autophagic cargo, redistributes mTORC1 to the cytosol, drives constitutive nuclear TFE3 localization, and blocks autophagic flux (PMID:33851776, PMID:36708709). Independently of HOPS, VPS41 self-assembles into a lattice acting with AP-3 to build large dense-core and insulin secretory granules, and β-cell-specific loss reduces secretory granule number, diverts insulin to lysosomal degradation, and causes diabetes in mice (PMID:24210660, PMID:33168621, PMID:39716868). Patient-derived VPS41 variants that disrupt functional HOPS assembly underlie a human neurological disorder, and the secretory and HOPS functions are genetically separable (PMID:33851776, PMID:33168621).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1997 High

    Established VPS41 as a core post-Golgi sorting factor by showing its deletion disrupts delivery and processing of multiple vacuolar hydrolases.

    Evidence Genetic deletion (vps41Δ) with vacuolar hydrolase processing and iron transport assays in yeast

    PMID:9159129

    Open questions at the time
    • Did not define molecular partners or the fusion machinery involved
    • No mammalian relevance addressed
  2. 1999 High

    Defined a direct molecular role for VPS41 in vesicle formation by demonstrating it binds AP-3 δ-adaptin and is required to generate AP-3 transport vesicles at the late Golgi.

    Evidence Biochemical vesicle isolation, genetic inactivation, and Vps41–AP-3 δ-adaptin binding assay in yeast

    PMID:10559961

    Open questions at the time
    • Did not explain how VPS41 distinguishes endosomal from vacuolar membranes
    • Regulation of the AP-3 interaction unknown
  3. 2008 Medium

    Linked V-ATPase function to VPS41 dynamics by showing the V0 subunit Vma16 is needed to release Vps41 from vacuolar puncta independently of its phosphorylation state.

    Evidence Genetic screen for yck3Δ-mimicking mutants, microscopy, and in vitro vacuole fusion assays in yeast

    PMID:18405665

    Open questions at the time
    • Mechanism of V-ATPase-dependent release not biochemically resolved
    • Relationship to phosphorylation-based switch unclear
  4. 2009 High

    Showed that Yck3 phosphorylation of a specific Vps41 serine controls its localization to fusion sites, and that Ypt7 cooperates with Yck3 to regulate it, framing VPS41 as a phospho-regulated tethering node.

    Evidence Reciprocal phospho-mutant and phosphomimetic alleles, ultrastructural analysis, and Ypt7 overexpression epistasis in yeast

    PMID:19193765

    Open questions at the time
    • Did not establish the membrane feature being sensed
    • Molecular consequence of phosphorylation on partner binding not yet defined
  5. 2010 High

    Resolved the mechanism of the phosphoswitch by identifying an ALPS motif that senses membrane curvature and masks the AP-3 binding site until Yck3 phosphorylation exposes it, unifying VPS41's two trafficking roles.

    Evidence Phosphorylation mapping, liposome curvature-sensing assays, EPR, mutagenesis, and live imaging in yeast

    PMID:21079247

    Open questions at the time
    • Conservation of the ALPS switch in mammals not tested here
    • Quantitative kinetics of switching in vivo unknown
  6. 2012 Medium

    Extended VPS41 function to disease relevance by showing human VPS41 requires both AP-3 and HOPS to protect dopaminergic neurons from α-synuclein toxicity.

    Evidence Domain-deletion mutants, neuron-specific RNAi epistasis in C. elegans, and α-syn inclusion assays in H4 cells

    PMID:22323726

    Open questions at the time
    • Mechanism connecting trafficking to α-syn clearance not resolved
    • SNP effects characterized only functionally
  7. 2012 Medium

    Identified p38α-MAPK phosphorylation of VPS41 (S796) as a signal driving HOPS recruitment to phagosomes, revealing a kinase-controlled checkpoint exploited by pathogens.

    Evidence Phosphomimetic/phospho-null mutants, p38α manipulation, and bacterial infection assays in macrophages

    PMID:23245320

    Open questions at the time
    • Direct phosphorylation of VPS41 by p38α inferred
    • Generalizability beyond phagosome-lysosome fusion unclear
  8. 2012 Low

    Reported a physical interaction between VPS41 and caspase-8 promoting Fas-induced apoptosis, proposing a trafficking-independent pro-apoptotic role.

    Evidence Yeast two-hybrid, co-IP in HEK293T, domain mapping, and caspase-3 cleavage assays

    PMID:23173123

    Open questions at the time
    • Single co-IP/Y2H without mutagenesis validation of the interaction in mammalian cells
    • No independent replication
    • Physiological significance unestablished
  9. 2013 High

    Defined a mammalian-specific function in which VPS41 self-assembles into a lattice to act as a coat with AP-3 in large dense-core vesicle biogenesis along the biosynthetic secretory pathway.

    Evidence Overexpression/knockdown in neuroendocrine cells, EM of LDCVs, self-assembly biochemistry, and cryo-EM lattice visualization

    PMID:24210660

    Open questions at the time
    • Structure of the AP-3–VPS41 coassembly not solved
    • Whether lattice formation is regulated in vivo unknown
  10. 2017 High

    Identified the structural basis for HOPS incorporation in humans, showing VPS41 is recruited via a RING–RING interaction with VPS18 absent in yeast.

    Evidence Biochemical co-purification, in-cell RING integration assay, and domain truncation/mutagenesis

    PMID:28931724

    Open questions at the time
    • Functional consequence of the species-specific RING contact not explored
    • Regulation of HOPS assembly not addressed
  11. 2018 Medium

    Demonstrated conserved tonoplast tethering function in plants, with phosphoinositide-regulated membrane binding and a SNARE (VTI11) requirement for vacuole fusion.

    Evidence Inducible knockdown, confocal imaging, liposome binding with PI inhibition, and genetic epistasis in Arabidopsis

    PMID:30104351

    Open questions at the time
    • Plant ortholog; direct relevance to mammalian VPS41 limited
    • Mechanism of PI-mediated binding inhibition not resolved
  12. 2019 Medium

    Showed in vivo that the Vps8:Vps41 stoichiometry gates HOPS assembly and HOPS-dependent fusion events, identifying competitive regulation of complex formation.

    Evidence Transgenic overexpression, HOPS subunit localization imaging, and trafficking assays in Drosophila

    PMID:31194677

    Open questions at the time
    • Drosophila ortholog; mammalian stoichiometric regulation untested
    • Molecular basis of the competition not defined
  13. 2020 High

    Established VPS41 as required for insulin secretory granule biogenesis in vivo, with a human variant acting independently of HOPS, dissociating secretory and tethering roles.

    Evidence β-cell-specific knockout mice, EM of granules, secretion assays, and human point mutation analysis

    PMID:33168621

    Open questions at the time
    • Molecular mechanism of the HOPS-independent secretory function not fully defined
    • Granule cargo selection mechanism unclear
  14. 2021 High

    Connected VPS41 to a human Mendelian disorder by showing patient variants block functional HOPS assembly, delaying lysosomal cargo delivery and dysregulating mTORC1/TFE3 and autophagy.

    Evidence Patient fibroblasts and VPS41-depleted HeLa cells with HOPS assembly IP, cargo delivery, mTORC1/TFE3 localization, and autophagic flux assays

    PMID:33851776

    Open questions at the time
    • How mTORC1 substrate phosphorylation is preserved despite cytosolic redistribution unexplained
    • Tissue-specific basis of neurological phenotype unresolved
  15. 2023 Medium

    Provided pharmacological evidence that VPS41 mediates autophagosome/late-endosome–lysosome fusion, with inhibition blocking autophagic flux and inducing methuosis in cancer cells.

    Evidence Small-molecule VPS41 inhibitor (DMBP), autophagic flux assays, and live-cell vacuolization imaging in cancer lines

    PMID:36708709

    Open questions at the time
    • Mechanism inferred from a single targeted compound
    • Direct VPS41 engagement specificity not fully validated
  16. 2024 Medium

    Showed acute β-cell VPS41 loss diverts mature insulin to lysosomal degradation and downregulates β-cell identity genes, placing VPS41 upstream of a degradative pathway controlling insulin content.

    Evidence Acute depletion and conditional KO mice with lysosomal inhibitor rescue, TFE3/AP-3 imaging, and qRT-PCR of identity genes

    PMID:39716868

    Open questions at the time
    • Direct link between TFE3 activation and identity gene loss not mechanistically proven
    • Single lab extension of prior KO work
  17. 2025 High

    Defined a unique cargo-tethering activity in which the VPS41 WD40 domain binds Arl8b to recruit newly synthesized TGN-derived LAMP carriers—including NPC1—to lysosomes, with loss causing lysosomal cholesterol accumulation and SREBP activation.

    Evidence Ectopic mitochondrial targeting, RUSH pulse-chase of LAMP/NPC1, VPS41-Arl8b domain-mapping co-IP, proximity labeling, and EM in engineered HeLa cells

    PMID:39907656 PMID:41452985

    Open questions at the time
    • How this biosynthetic tethering coordinates with HOPS-mediated fusion unresolved
    • Selectivity of LAMP carrier cargo recognition not fully defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how VPS41's distinct activities—HOPS-mediated fusion, AP-3 coat assembly for secretory granules, and Arl8b-dependent biosynthetic cargo tethering—are coordinated and differentially regulated within a single cell.
  • No unified structural model of VPS41 in HOPS versus coat versus Arl8b-bound states
  • Regulatory hierarchy among phosphorylation, RING contacts, and stoichiometry unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0008289 lipid binding 2 GO:0005198 structural molecule activity 1 GO:0008092 cytoskeletal protein binding 1
Localization
GO:0005764 lysosome 3 GO:0005768 endosome 3 GO:0005794 Golgi apparatus 2 GO:0031410 cytoplasmic vesicle 2
Pathway
R-HSA-5653656 Vesicle-mediated transport 3 R-HSA-1430728 Metabolism 2 R-HSA-9612973 Autophagy 2 R-HSA-5357801 Programmed Cell Death 1
Partners
AP-3 DELTA-ADAPTIN/AP3D1ARL8BCASPASE-8NPC1VPS18VPS8VTI11
Complex memberships
AP-3HOPS

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 Vps41 is required for formation of AP-3 transport vesicles at the late Golgi in yeast; it binds directly to the AP-3 delta-adaptin subunit (Apl5/δ-adaptin), and inactivation of Vps41 or AP-3 blocks accumulation of 50–130 nm vesicles containing AP-3 adaptors and ALP pathway cargo. Biochemical vesicle isolation, immunocytochemistry, genetic inactivation (vps41 mutant), and binding assay between Vps41 and AP-3 δ-adaptin subunit Nature cell biology High 10559961
1997 Yeast Vps41 (992 aa, hydrophilic, no signal sequence) functions in post-Golgi protein sorting to the vacuole; deletion causes defective high-affinity iron transport due to impaired Fet3p activity and defects in processing/sorting of multiple vacuolar hydrolases, indicating a role in vacuolar protein trafficking. Genetic deletion (vps41Δ), biochemical assays of vacuolar hydrolase processing, iron transport assays, sequence analysis Proceedings of the National Academy of Sciences of the United States of America High 9159129
2010 Vps41 contains an amphipathic lipid-packing sensor (ALPS) motif that inserts into highly curved membranes (endosomes) masking the AP-3 δ-adaptin (Apl5) binding site. At the less curved vacuole, the resident casein kinase Yck3 phosphorylates the ALPS motif, exposing the Apl5-binding site and allowing AP-3 vesicles to dock and fuse. This phosphorylation-based switch enables Vps41 to operate in both endosome-vacuole and AP-3 vesicle-vacuole fusion pathways. Phosphorylation mapping, site-directed mutagenesis, membrane curvature sensing assay (liposomes), EPR spectroscopy, fluorescence microscopy, genetic complementation The Journal of cell biology High 21079247
2009 Yck3-mediated phosphorylation of Vps41 (at a specific serine) controls its localization to endosome-vacuole fusion sites; non-phosphorylatable Vps41-S-A accumulates with other HOPS subunits at endosomal structures proximal to the vacuole, while phosphomimetic Vps41-S-D mislocalizes and causes multilobed vacuoles. Overproduction of the vacuolar Rab GTPase Ypt7 rescues both phenotypes, indicating Ypt7 and Yck3 cooperate to regulate Vps41 at fusion sites. Site-directed mutagenesis (phospho-mutant and phosphomimetic alleles), fluorescence microscopy, ultrastructural analysis, genetic epistasis with class E mutants and Ypt7 overexpression Molecular biology of the cell High 19193765
2013 Mammalian VPS41 promotes large dense-core vesicle (LDCV) formation through a conserved mechanism with AP-3, acting in the biosynthetic pathway. VPS41 self-assembles into a lattice structure, suggesting it functions as a coat protein recruiting AP-3 cargo into the regulated secretory pathway. VPS41 overexpression/knockdown in neuroendocrine cells, electron microscopy of LDCV number/morphology, biochemical self-assembly assay, cryo-EM lattice visualization Developmental cell High 24210660
2017 Human VPS41 is recruited into the HOPS complex via a direct RING–RING domain interaction with VPS18; the VPS18 RING domain is required to recruit VPS41 to the four-subunit HOPS core. This mechanism is not conserved in yeast, where Vps41 lacks a C-terminal zinc-finger motif. Biochemical co-purification, in-cell RING domain integration assay using endogenous HOPS, domain truncation/mutagenesis The Biochemical journal High 28931724
2008 The V0-subunit of the vacuolar V-ATPase (Vma16) is required for release of Vps41 from vacuolar dots; loss of Vma16 causes Vps41 accumulation independently of its phosphorylation status, and fusion between V0-subunit mutant vacuoles is reduced, linking V-ATPase function to Vps41 dynamics and vacuole fusion/fission. Genetic screen for yck3Δ-mimicking mutants, fluorescence microscopy, in vitro vacuole fusion assay FEBS letters Medium 18405665
2012 Human VPS41 requires both a functional AP-3 complex and a functional HOPS complex to protect C. elegans dopaminergic neurons from α-synuclein-induced neurodegeneration; the AP-3 interaction domain and clathrin heavy-chain repeat domain of hVPS41 are each required for neuroprotection and for preventing α-syn inclusion formation in human neuroglioma cells. Two SNPs in the AP-3 interacting domain attenuate neuroprotective function. Domain-deletion mutants, neuron-specific RNAi epistasis in C. elegans, α-syn inclusion assay in H4 cells, SNP functional analysis The Journal of neuroscience Medium 22323726
2012 p38α-MAPK phosphorylates Vps41 (at S796 in the human ortholog) to drive HOPS complex recruitment to phagosomes, directing phagosome–lysosome fusion. Pathogenic Coxiella burnetii LPS antagonizes TLR4 signaling to prevent p38α-MAPK activation and consequent Vps41 phosphorylation, blocking trafficking to phagolysosomes; a phosphomimetic Vps41-S796E mutant overrides this block. Phosphomimetic and phospho-null Vps41 mutant expression, p38α-MAPK inhibition/activation, bacterial infection assays in macrophages, vesicle colocalization by fluorescence microscopy Cell host & microbe Medium 23245320
2021 Patient-derived VPS41 variants (S285P, R662*, splice site) prevent formation of a functional HOPS complex, causing delayed lysosomal delivery of endocytic and autophagic cargo. Loss of VPS41/HOPS function causes cytosolic redistribution of mTORC1, constitutive nuclear localization of TFE3, elevated LC3II, and reduced autophagic response to starvation, while mTORC1 substrate phosphorylation (S6K1, 4EBP1) is unaffected. The VPS41-S285P variant retains the ability to support regulated secretion, dissociating HOPS and secretory functions. Patient fibroblasts and VPS41-depleted HeLa cells, co-immunoprecipitation for HOPS assembly, lysosomal cargo delivery assays, mTORC1 substrate phosphorylation, immunofluorescence for TFE3/mTORC1 localization, autophagic flux measurement EMBO molecular medicine High 33851776
2020 VPS41 is required for insulin secretory granule (SG) biogenesis in pancreatic β-cells; β-cell-specific deletion reduces SG number, alters SG transmembrane protein composition, and impairs regulated exocytosis, causing diabetes in mice. A human point mutation affecting SG formation acts independently of HOPS complex formation. Conditional β-cell VPS41 knockout mice, electron microscopy of SG number, immunofluorescence of SG protein composition, glucose tolerance and insulin secretion assays, human point mutation analysis Diabetes High 33168621
2019 In Drosophila, Vps41/Lt is a HOPS-specific subunit whose late endosomal localization is abolished by Vps8 overexpression, which outcompetes Vps41 and prevents HOPS assembly. The Vps8:Vps41 ratio is critical; excess Vps8 inhibits HOPS-dependent late endosome maturation, autophagosome–lysosome fusion, crinophagy, and lysosome-related organelle formation. Transgenic overexpression in Drosophila, fluorescence microscopy for HOPS subunit localization, autophagy and lysosome-related organelle assays, genetic epistasis eLife Medium 31194677
2025 VPS41's WD40 domain binds the small GTPase Arl8b, and this interaction is required for recruiting TGN-derived LAMP1/LAMP2A-positive carrier vesicles. Ectopically localized (mitochondrial) VPS41 specifically recruits newly synthesized LAMP carriers via Arl8b; other HOPS subunits do not share this activity, defining a unique cargo-tethering function for VPS41 in the biosynthetic lysosomal delivery pathway. Ectopic mitochondrial targeting (ActA-VPS41), RUSH system pulse-chase of newly synthesized LAMP proteins, co-immunoprecipitation mapping of VPS41-Arl8b binding to WD40 domain, electron microscopy The Journal of cell biology High 39907656
2025 NPC1 is a cargo for VPS41-dependent LAMP carriers that travel from the TGN to late endosomes/lysosomes. Loss of VPS41 shifts NPC1 and LAMP1 from late endosomes/lysosomes to biosynthetic LAMP carrier vesicles, causing lysosomal cholesterol accumulation and activation of SREBP signaling despite increased NPC1 abundance. Genome-engineered endogenous NPC1-mNeon HeLa cells, protein proximity-based approaches, VPS41 knockout, immunofluorescence and electron microscopy, VPS41-dependent ectopic recruitment assay Proceedings of the National Academy of Sciences of the United States of America High 41452985
2012 Vps41 physically interacts with caspase-8; the WD40 region and RING-finger motif of Vps41 bind the p18 subunit of caspase-8. Overexpression of Vps41 promotes Fas-induced apoptosis and enhances caspase-3 cleavage downstream of caspase-8. Yeast two-hybrid screen, co-immunoprecipitation in HEK293T cells, co-localization studies, domain-mapping, caspase-3 cleavage assay Acta biochimica Polonica Low 23173123
2024 Acute VPS41 deletion in β-cells causes rapid lysosomal degradation of mature insulin, increased AP-3 complex colocalization with lysosomes, nuclear localization of TFE3, and downregulation of PDX1 and INS mRNA; lysosomal degradation inhibition rescues insulin content, placing VPS41 upstream of a degradative pathway controlling both insulin content and β-cell identity. Acute VPS41 depletion in vitro and conditional KO mice, lysosomal inhibitor rescue, immunofluorescence for AP-3/lysosome colocalization and TFE3 localization, qRT-PCR for β-cell identity genes American journal of physiology. Endocrinology and metabolism Medium 39716868
2023 VPS41 mediates fusion of late endosomes and autophagosomes with lysosomes; inhibiting VPS41 function (via the small molecule DMBP) blocks autophagic flux and induces methuosis (vacuolization) in cancer cells, while VPS41 overexpression reduces autophagic flux impairment. Small molecule VPS41 inhibitor (DMBP) treatment, autophagic flux assays (LC3-II accumulation, p62), live-cell imaging of vacuolization in lung and pancreatic cancer lines Cell chemical biology Medium 36708709
2018 In Arabidopsis, VPS41 (but not VPS33) localizes to the tonoplast via a wortmannin-sensitive (PI3K-dependent) process and to late endosomes. VPS41 and VPS33 bind liposomes, but PtdIns(3)P and PtdIns(3,5)P2 inhibit this binding. Inducible knockdown of VPS41 causes dramatic vacuole fragmentation, and genetic interaction with SNARE VTI11 is required for vacuole fusion. Inducible knockdown, confocal live imaging, liposome binding assays with phosphoinositide inhibition, wortmannin treatment, genetic epistasis with VTI11 Proceedings of the National Academy of Sciences of the United States of America Medium 30104351

Source papers

Stage 0 corpus · 33 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1999 Formation of AP-3 transport intermediates requires Vps41 function. Nature cell biology 113 10559961
2010 Phosphorylation of a membrane curvature-sensing motif switches function of the HOPS subunit Vps41 in membrane tethering. The Journal of cell biology 104 21079247
2020 Loss-of-Function Variants in HOPS Complex Genes VPS16 and VPS41 Cause Early Onset Dystonia Associated with Lysosomal Abnormalities. Annals of neurology 94 32808683
2009 Vps41 phosphorylation and the Rab Ypt7 control the targeting of the HOPS complex to endosome-vacuole fusion sites. Molecular biology of the cell 83 19193765
1997 Characterization of VPS41, a gene required for vacuolar trafficking and high-affinity iron transport in yeast. Proceedings of the National Academy of Sciences of the United States of America 81 9159129
1998 The light gene of Drosophila melanogaster encodes a homologue of VPS41, a yeast gene involved in cellular-protein trafficking. Genome 73 9644832
2012 Functional analysis of VPS41-mediated neuroprotection in Caenorhabditis elegans and mammalian models of Parkinson's disease. The Journal of neuroscience : the official journal of the Society for Neuroscience 72 22323726
2009 VPS41, a protein involved in lysosomal trafficking, is protective in Caenorhabditis elegans and mammalian cellular models of Parkinson's disease. Neurobiology of disease 70 19850127
2013 Self-assembly of VPS41 promotes sorting required for biogenesis of the regulated secretory pathway. Developmental cell 66 24210660
2018 Phosphoinositides control the localization of HOPS subunit VPS41, which together with VPS33 mediates vacuole fusion in plants. Proceedings of the National Academy of Sciences of the United States of America 45 30104351
2021 Neurodegenerative VPS41 variants inhibit HOPS function and mTORC1-dependent TFEB/TFE3 regulation. EMBO molecular medicine 42 33851776
2021 Bi-allelic variants in HOPS complex subunit VPS41 cause cerebellar ataxia and abnormal membrane trafficking. Brain : a journal of neurology 41 33764426
2006 Role of a VPS41 homologue in starvation response, intracellular survival and virulence of Cryptococcus neoformans. Molecular microbiology 40 16879414
2012 Impaired stimulation of p38α-MAPK/Vps41-HOPS by LPS from pathogenic Coxiella burnetii prevents trafficking to microbicidal phagolysosomes. Cell host & microbe 37 23245320
2018 Distinct functional roles of Vps41-mediated neuroprotection in Alzheimer's and Parkinson's disease models of neurodegeneration. Human molecular genetics 31 30508205
2019 Vps8 overexpression inhibits HOPS-dependent trafficking routes by outcompeting Vps41/Lt. eLife 24 31194677
2008 The vacuolar V1/V0-ATPase is involved in the release of the HOPS subunit Vps41 from vacuoles, vacuole fragmentation and fusion. FEBS letters 24 18405665
2023 VPS41-mediated incomplete autophagy aggravates cadmium-induced apoptosis in mouse hepatocytes. Journal of hazardous materials 22 37562348
2022 Nrf2 improves hippocampal synaptic plasticity, learning and memory through the circ-Vps41/miR-26a-5p/CaMKIV regulatory network. Experimental neurology 22 35143833
2017 VPS18 recruits VPS41 to the human HOPS complex via a RING-RING interaction. The Biochemical journal 22 28931724
2023 Targeting VPS41 induces methuosis and inhibits autophagy in cancer cells. Cell chemical biology 15 36708709
2007 Trypanosoma brucei vacuolar protein sorting 41 (VPS41) is required for intracellular iron utilization and maintenance of normal cellular morphology. Parasitology 15 17577424
2022 Circ-Vps41 positively modulates Syp and its overexpression improves memory ability in aging mice. Frontiers in molecular neuroscience 13 36533129
2020 Pancreatic β-Cell-Specific Deletion of VPS41 Causes Diabetes Due to Defects in Insulin Secretion. Diabetes 13 33168621
2024 A condensates-to-VPS41-associated phagic vacuoles conversion pathway controls autophagy degradation in plants. Developmental cell 12 39111309
2025 VPS41 recruits biosynthetic LAMP-positive vesicles through interaction with Arl8b. The Journal of cell biology 7 39907656
2025 EccDNA-Driven VPS41 Amplification Alleviates Genotoxic Stress via Lysosomal KAI1 Degradation. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 6 40271553
2012 Vps41, a protein involved in lysosomal trafficking, interacts with caspase-8. Acta biochimica Polonica 4 23173123
2024 VPS41 deletion triggers progressive loss of insulin stores and downregulation of β-cell identity. American journal of physiology. Endocrinology and metabolism 2 39716868
2023 Making bubbles: Targeting VPS41 induces vacuolization and methuosis. Cell chemical biology 1 36800990
2016 Requirement of the isocitrate lyase gene ICL1 for VPS41-mediated starvation response in Cryptococcus neoformans. Journal of microbiology (Seoul, Korea) 1 27350614
2026 Identification of plasma exosomal VPS41 chr7:38764322A>I editing as a diagnostic biomarker in lung cancer via a pan-cancer screen. Respiratory research 0 42121172
2025 NPC1 trafficking via VPS41-dependent LAMP carriers regulates endosomal cholesterol homeostasis. Proceedings of the National Academy of Sciences of the United States of America 0 41452985

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