Affinage

VPS35

Vacuolar protein sorting-associated protein 35 · UniProt Q96QK1

Length
796 aa
Mass
91.7 kDa
Annotated
2026-04-28
100 papers in source corpus 40 papers cited in narrative 40 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

VPS35 is the central cargo-recognition subunit of the retromer complex, mediating retrograde retrieval of diverse transmembrane cargoes—including sorting receptors (Vps10p, CI-M6PR), BACE1, Lamp2a, EGFR, DRD1, AMPA receptors, RANK, and Trem2—from endosomes to the trans-Golgi network or plasma membrane (PMID:9105038, PMID:22105352, PMID:26203154, PMID:36738481, PMID:27460146, PMID:25416282, PMID:23509071, PMID:27717139). It is recruited to late endosomes through direct interaction with Rab7 at its N-terminal domain and recruits the WASH actin-nucleation complex to endosomes via binding of the FAM21 subunit, thereby promoting actin-dependent membrane tubulation required for cargo sorting; the Parkinson disease-linked D620N mutation selectively reduces FAM21/WASH binding affinity, impairing ATG9A trafficking and autophagy (PMID:25367362, PMID:22070227, PMID:24980502, PMID:24819384). The D620N mutation additionally causes LRRK2 kinase hyperactivation with elevated phosphorylation of Rab8A, Rab10, and Rab12, enhanced VPS35–DLP1 interaction leading to MUL1-dependent MFN2 degradation and mitochondrial fragmentation, and impaired PINK1/Parkin-mediated mitophagy, establishing convergent pathogenic mechanisms in familial Parkinson disease (PMID:29743203, PMID:26618722, PMID:26321632, PMID:34127073). VPS35 also participates in mitochondria-derived vesicle trafficking, mediating transport of MAPL from mitochondria to peroxisomes and selective degradation of damaged mtDNA through endosomal maturation (PMID:20619655, PMID:36344526).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1992 High

    Establishing that VPS35 is a membrane-associated protein required for vacuolar protein sorting resolved a key component of the endosomal sorting machinery, though its precise molecular role was unknown.

    Evidence Gene disruption, subcellular fractionation, and CPY secretion assays in S. cerevisiae

    PMID:1498362

    Open questions at the time
    • Mechanism of VPS35 action on sorting unknown
    • No direct cargo interaction demonstrated
    • Mammalian ortholog function not addressed
  2. 1997 High

    Demonstrating that VPS35 is specifically required for retrograde retrieval of the sorting receptor Vps10p from endosomes to the Golgi established the retromer concept and positioned VPS35 as a cargo-recognition factor rather than a general sorting component.

    Evidence Temperature-conditional VPS35 allele, co-fractionation with Vps10p, genetic epistasis with pep12 in S. cerevisiae

    PMID:9105038

    Open questions at the time
    • Direct physical interaction with cargo not yet proven by binding assay
    • Structural basis unknown
    • Mammalian cargo repertoire undefined
  3. 2006 High

    Structural determination of Vps26A and mapping of its VPS35-binding interface provided the first atomic-level understanding of retromer subcomplex assembly, revealing that a mobile loop in Vps26 is critical for integration into the complex.

    Evidence X-ray crystallography at 2.1 Å, site-directed mutagenesis, endosomal localization assays

    PMID:16732284

    Open questions at the time
    • Full VPS35 structure not solved
    • VPS35-Vps29 interface not mapped
    • Cargo-binding site on VPS35 not identified
  4. 2007 High

    Identification of the conserved PRLYL motif in VPS35's N-terminus as essential for Vps26 binding and retromer integrity, together with evidence for dominant-negative trafficking defects, established that VPS35 serves as a scaffold nucleating retromer assembly.

    Evidence R107W mutagenesis, Co-IP, cross-species dominant-negative expression in yeast and mammalian cells

    PMID:17916227

    Open questions at the time
    • VPS35-Vps29 binding determinants not mapped
    • Full cargo-binding surface unresolved
  5. 2010 High

    Discovery that VPS35 is recruited to mitochondria-derived vesicles and mediates MAPL delivery from mitochondria to peroxisomes expanded retromer function beyond canonical endosome-to-Golgi trafficking to inter-organelle transport.

    Evidence Unbiased protein interaction screen, Co-IP, confocal imaging of VPS35 on MDVs, siRNA knockdown with peroxisomal MAPL quantification

    PMID:20619655

    Open questions at the time
    • Mechanism of VPS35 recruitment to mitochondrial membranes unknown
    • Whether MDV cargo selectivity requires VPS35 directly or through associated factors unclear
  6. 2011 High

    Showing that VPS35 interacts with BACE1 and that haploinsufficiency increases endosomal BACE1 activity and Aβ production in AD mice linked retromer dysfunction to Alzheimer disease pathogenesis through a specific cargo-sorting defect.

    Evidence Co-IP of VPS35-BACE1, hemizygous Vps35 deletion in Tg2576 mice, BACE1 activity assay, behavioral testing

    PMID:22105352

    Open questions at the time
    • Direct BACE1 sorting signal on VPS35 not mapped
    • Whether VPS35 loss affects amyloidogenesis independent of BACE1 not determined
  7. 2012 High

    Identification of FAM21 as the direct bridge between VPS35 and the WASH actin-nucleation complex on endosomes resolved how retromer coordinates membrane remodeling with cargo sorting.

    Evidence Biochemical binding assays, FAM21 tail fragment overexpression, endosomal localization assays

    PMID:22070227

    Open questions at the time
    • Binding site on VPS35 for FAM21 not mapped at residue level
    • Whether WASH recruitment is required for all retromer cargoes unknown
  8. 2014 High

    Biophysical and proteomic characterization of VPS35 D620N revealed that the primary molecular defect is a ~2-fold reduction in FAM21/WASH binding affinity while retromer trimer assembly is unaffected, establishing D620N as a selective WASH-recruitment defect that impairs endosome-to-TGN transport and ATG9A sorting for autophagy.

    Evidence Isothermal calorimetry, SILAC-based quantitative proteomics, ATG9A trafficking assay, patient fibroblasts

    PMID:24152121 PMID:24819384 PMID:24980502

    Open questions at the time
    • Structural basis of D620N-FAM21 affinity loss not resolved
    • Whether all D620N phenotypes are WASH-dependent not tested
  9. 2014 High

    Demonstration that Rab7 recruits retromer to late endosomes via VPS35's N-terminal domain, with allosteric enhancement by Vps26 binding, established the molecular logic of retromer membrane targeting.

    Evidence FRET-based interaction assay in HeLa cells, biophysical binding measurements, mutagenesis of Vps35-Vps26 interface

    PMID:25367362

    Open questions at the time
    • Whether Rab7 GTP/GDP state regulates the interaction quantitatively not fully resolved
    • Role of SNX-BAR dimers in coordinating with Rab7-VPS35 binding unclear
  10. 2014 High

    Showing that VPS35 retrieves Lamp2a from endosomes and that D620N causes accelerated Lamp2a degradation, impairing chaperone-mediated autophagy and leading to α-synuclein accumulation, established a mechanistic link between retromer dysfunction and Parkinson-relevant protein aggregation.

    Evidence Conditional VPS35 KO in DA neurons, Lamp2a trafficking, α-synuclein immunostaining, Lamp2a overexpression rescue

    PMID:26203154

    Open questions at the time
    • Sorting signal on Lamp2a recognized by VPS35 not identified
    • Whether CMA impairment is the dominant pathway for α-synuclein accumulation vs. macroautophagy defects not resolved
  11. 2015 High

    Discovery that D620N enhances VPS35–DLP1 interaction, increasing mitochondrial DLP1 turnover and causing mitochondrial fragmentation, and that VPS35 deficiency elevates MUL1 leading to MFN2 degradation, established a mitochondrial fragmentation axis in PD pathogenesis separable from α-synuclein accumulation.

    Evidence Co-IP of VPS35-DLP1, mitochondrial fission inhibitor rescue, conditional KO with MUL1 epistasis, patient fibroblasts

    PMID:26321632 PMID:26618722

    Open questions at the time
    • Whether enhanced VPS35-DLP1 binding is a direct consequence of WASH loss or an independent D620N effect unclear
    • Structural basis of VPS35-DLP1 interaction resolved only at motif level (FLV)
  12. 2016 High

    Expanding VPS35's cargo repertoire to include Trem2, DRD1, N-Ras, and RANK demonstrated that retromer-mediated receptor recycling controls inflammatory signaling in microglia, dopaminergic signaling, Ras-MAPK signaling, and osteoclast formation.

    Evidence Co-IP, surface recycling assays, inflammatory cytokine measurement, RANK signaling in osteoclasts, farnesyl-dependent N-Ras binding and MAPK readout, hemizygous KO mouse bone phenotype

    PMID:23509071 PMID:27460146 PMID:27502489 PMID:27717139

    Open questions at the time
    • Sorting signals on these diverse cargoes not systematically identified
    • Whether all cargoes require WASH-dependent sorting not tested
  13. 2018 High

    Demonstrating that D620N is a gain-of-function for LRRK2 kinase activity—elevating Rab8A/10/12 phosphorylation in knock-in mice and patient cells—while VPS35 loss suppresses LRRK2-mediated Rab phosphorylation, established VPS35 as an upstream activator of LRRK2 and linked the two major familial PD genes in a common pathway.

    Evidence VPS35 D620N knock-in mice, phospho-Rab Western blot, VPS35 KO/KD, patient neutrophils/monocytes

    PMID:29743203

    Open questions at the time
    • Mechanism by which VPS35 activates LRRK2 kinase not identified (direct binding vs. membrane platform)
    • Whether wild-type VPS35 normally stimulates LRRK2 at physiological levels unclear
  14. 2018 High

    Parkin was shown to ubiquitinate VPS35 at C-terminal lysines via non-degradative poly-ubiquitin chains, and parkin loss reduced WASH complex components and disrupted ATG9A sorting, positioning VPS35 as a Parkin substrate that integrates retromer and mitophagy pathways.

    Evidence Co-IP, ubiquitin chain type and lysine mapping, parkin KO mouse brain analysis, ATG9A trafficking

    PMID:29893854

    Open questions at the time
    • Functional consequence of VPS35 ubiquitination on WASH recruitment not directly tested
    • Whether parkin-mediated ubiquitination regulates VPS35-LRRK2 interplay unknown
  15. 2021 High

    D620N was shown to impair PINK1/Parkin-mediated mitophagy by preventing PINK1 accumulation on depolarized mitochondria, connecting retromer dysfunction to a second mitochondrial quality control pathway beyond fission.

    Evidence CRISPR heterozygous D620N knock-in in SH-SY5Y cells, mitochondrial membrane potential, PINK1/Parkin recruitment imaging

    PMID:34127073

    Open questions at the time
    • Whether the mitophagy defect is secondary to altered mitochondrial membrane potential or a direct VPS35 role in PINK1 stabilization not resolved
  16. 2021 High

    Quantitative lysosomal proteomics in D620N knock-in mice revealed LRRK2-mediated lysosomal recruitment of RILPL1 via TMEM55B binding, identifying a downstream effector pathway of the VPS35-LRRK2 axis that alters lysosomal composition.

    Evidence Lysosomal proteomics (~220 altered proteins), Co-IP of RILPL1-TMEM55B, LRRK2 inhibitor reversal, RILPL1/TMEM55B KO cells

    PMID:38091401

    Open questions at the time
    • Functional consequence of RILPL1 lysosomal recruitment on lysosomal degradation or autophagy not fully defined
    • Whether this pathway operates in human dopaminergic neurons not confirmed
  17. 2022 High

    VPS35 was found to mediate endosomal maturation for selective mtDNA degradation upon mitochondrial DNA damage, with SAMM50 acting as a gatekeeper for nucleoid release, extending VPS35's mitochondrial roles to genome maintenance.

    Evidence Proximity labeling with Twinkle, VPS35 knockdown, ATG5 KO, mouse model with mtDNA alterations

    PMID:36344526

    Open questions at the time
    • Whether this pathway is retromer-dependent or uses VPS35 in a retromer-independent capacity not resolved
    • Mechanism of VPS35 recruitment to damaged nucleoid compartments unknown
  18. 2023 High

    Comparison of D620N knock-in versus haploinsufficient mice confirmed D620N as a gain-of-function for LRRK2 kinase (reversed by inhibitor MLi-2) while haploinsufficiency impairs DAT independently of LRRK2, demonstrating that loss-of-function and gain-of-toxic-function coexist in D620N pathogenesis.

    Evidence VPS35 D620N KI and haploinsufficient mice, phospho-Rab blots, DAT expression/function, LRRK2 inhibitor MLi-2, behavioral testing

    PMID:38110354

    Open questions at the time
    • How D620N simultaneously causes loss of WASH binding and gain of LRRK2 activation structurally unresolved
    • Cell-type-specific contributions of these dual mechanisms in dopaminergic neurons not separated

Open questions

Synthesis pass · forward-looking unresolved questions
  • A high-resolution structure of full-length VPS35 in complex with FAM21, Rab7, and cargo peptides is needed to explain how D620N simultaneously impairs WASH recruitment and hyperactivates LRRK2, and whether these are structurally linked or independent surfaces.
  • No full-length VPS35 structure with bound FAM21 or LRRK2
  • Direct VPS35-LRRK2 binding interface not mapped
  • Cargo-binding specificity determinants on VPS35 for its >10 known cargoes not structurally resolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0038024 cargo receptor activity 5 GO:0060090 molecular adaptor activity 4
Localization
GO:0005768 endosome 6 GO:0005739 mitochondrion 5 GO:0031410 cytoplasmic vesicle 3 GO:0005829 cytosol 1
Pathway
R-HSA-5653656 Vesicle-mediated transport 8 R-HSA-1852241 Organelle biogenesis and maintenance 4 R-HSA-112316 Neuronal System 3 R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-9612973 Autophagy 3
Partners
BACE1DLP1FAM21LRRK2PRKNRAB7AVPS26AVPS29
Complex memberships
Retromer (VPS35-VPS29-VPS26)

Evidence

Reading pass · 40 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 VPS35 (Vps35p) peripherally associates with a membranous particulate cell fraction in yeast and is required for sorting of carboxypeptidase Y (CPY) to the vacuole; null mutants cause selective missorting and secretion of CPY but not other vacuolar hydrolases, indicating alternative sorting pathways exist. Gene disruption (null allele), subcellular fractionation, vacuolar protein sorting assays in S. cerevisiae Molecular biology of the cell High 1498362
1997 Vps35p is required for retrograde retrieval of the vacuolar sorting receptor Vps10p from the prevacuolar endosome back to the Golgi; loss of VPS35 shifts Vps10p to the vacuolar membrane via a Pep12p (endosomal t-SNARE)-dependent route; Vps35p co-fractionates with Vps10p even in vps29 mutants, suggesting direct interaction. Temperature-conditional VPS35 allele, subcellular fractionation, genetic epistasis with sec1 and pep12 mutants, co-fractionation assays in S. cerevisiae The Journal of cell biology High 9105038
2006 Crystal structure of human Vps26A at 2.1-Å resolution reveals an arrestin-fold; the Vps35-binding site maps to a mobile loop (residues 235–246) near the tip of the C-terminal domain; hydrophobic residues and a glycine in this loop are required for Vps26 integration into the retromer complex and endosomal localization. X-ray crystallography (2.1-Å), site-directed mutagenesis of Vps26 loop residues, endosomal localization assays Nature structural & molecular biology High 16732284
2007 A conserved PRLYL motif in the N-terminal domain of Vps35 is essential for retromer subcomplex assembly: the R107W mutation in human VPS35 disrupts co-precipitation with Vps26 and causes dominant-negative trafficking defects when expressed in yeast, shifting VPS35 from endosomes to a juxtanuclear compartment and affecting mannose phosphate receptor and insulin trafficking. Dominant-negative expression in yeast, co-immunoprecipitation, subcellular fractionation, site-directed mutagenesis Traffic (Copenhagen, Denmark) High 17916227
2007 A dominant-negative N-terminal deletion mutant of VPS35 reduces canonical Wnt signaling in HEK-293 cells; GST pulldown identified a possible indirect interaction between the LRP6 intracellular domain and VPS35, linking retromer to Wnt/LRP6 endosomal signaling. Dominant-negative overexpression, GST-fusion pulldown, Wnt reporter assay (Tcf promoter) Neurobiology of disease Low 17239604
2007 Drosophila Vps35 loss impairs scavenger receptor-ligand endocytosis, causes mislocalisation of receptors and endocytic proteins, negatively regulates actin polymerisation, and leads to overproliferation of larval blood cells and upregulation of TGFβ/BMP signaling at the neuromuscular junction. RNAi knockdown in S2 cells and Drosophila, endocytosis assay, genetic interaction analysis Journal of cell science Medium 18057029
2010 VPS35 (retromer) mediates transport of the mitochondrial SUMO E3 ligase MAPL from mitochondria to peroxisomes via mitochondria-derived vesicles (MDVs); Vps35 and Vps26 are found in complex with MAPL by unbiased screen, and Vps35 is recruited to mitochondrial vesicles; silencing Vps35 or Vps26A significantly reduces MAPL delivery to peroxisomes. Unbiased protein interaction screen, Co-immunoprecipitation, confocal imaging of Vps35 on MDVs, siRNA silencing with peroxisomal MAPL quantification Current biology : CB High 20619655
2010 Loss of Vps26b in mice destabilizes the Vps26b-Vps29-Vps35 retromer complex and leads to ~20% increase in sortilin levels, while SorLA is unaffected, implicating this complex in sortilin retrieval from endosomes to the TGN. Vps26b knockout mice, Co-immunoprecipitation, Western blot Biochemical and biophysical research communications Medium 21040701
2011 VPS35 interacts with BACE1 and is required for BACE1 endosome-to-Golgi retrieval; VPS35 haploinsufficiency in Tg2576 AD mice increases BACE1 activity in endosomes, elevates Aβ levels, and causes earlier-onset AD-like phenotypes including cognitive deficits and impaired LTP. Co-immunoprecipitation (VPS35-BACE1), hemizygous Vps35 deletion in Tg2576 mice, BACE1 activity assay, immunofluorescence localization, behavioral testing The Journal of cell biology High 22105352
2012 The WASH complex is recruited to endosomes through direct binding of its FAM21 subunit's unstructured tail domain to VPS35; this interaction is necessary and sufficient for WASH complex endosomal targeting; elevated FAM21-tail expression inhibits WASH-retromer association and causes cell-spreading defects. Biochemical binding assays, overexpression of FAM21 tail fragments, endosomal localization assays, cell spreading phenotype The Biochemical journal High 22070227
2012 VPS35 is required for BACE1 retrograde trafficking in developing hippocampal neurons; Vps35 depletion impairs retrograde BACE1 transport and alters BACE1 distribution, leading to shortened apical dendrites, reduced dendritic spines, and swollen commissural axons; BACE1 suppression partially rescues these deficits. In utero electroporation of microRNA against Vps35, immunofluorescence, genetic epistasis with BACE1 knockdown Biology open Medium 23259059
2013 VPS35 D620N mutant redistributes retromer-positive endosomes to a perinuclear localization and enlarges endosomes; D620N is correctly folded and binds Vps29 and Vps26A with normal affinity; D620N interacts with CI-M6PR but disrupts cathepsin D trafficking, which is responsible for α-synuclein degradation. Subcellular localization imaging, binding affinity measurements, cathepsin D trafficking assay, patient fibroblast analysis Traffic (Copenhagen, Denmark) High 24152121
2013 VPS35 loss of function alters RANK distribution upon RANKL stimulation, enhances RANKL sensitivity, sustains RANKL signaling, and increases hyperresorptive osteoclast formation; hemizygous Vps35 deletion in mice causes osteoporosis with decreased trabecular bone volume. VPS35 siRNA knockdown, hemizygous Vps35 knockout mice, RANKL signaling assays, bone histomorphometry The Journal of cell biology High 23509071
2014 VPS35 D620N mutation impairs WASH complex association with retromer and reduces WASH recruitment to endosomes; autophagy is impaired in D620N-expressing cells or WASH-depleted cells due to abnormal trafficking of ATG9A; retromer is required for endosomal WASH complex recruitment. Co-immunoprecipitation, endosomal recruitment assay, ATG9A trafficking assay, autophagy flux measurement Nature communications High 24819384
2014 The primary molecular defect of VPS35 D620N mutation is a 2.2-fold decrease in binding affinity for the WASH complex component FAM21, measured by isothermal calorimetry; SILAC-based interactome comparison confirms reduced WASH complex association; D620N perturbs endosome-to-TGN transport but not endosome-to-plasma membrane recycling. SILAC-based quantitative proteomics, isothermal calorimetry, retromer cargo trafficking assays, patient-derived cells Current biology : CB High 24980502
2014 Rab7 recruits retromer to late endosomes via direct interactions with N-terminal conserved regions in Vps35; association of Vps26 with Vps35 allosterically enhances high-affinity Rab7 binding to the Vps sub-complex; disrupting the Vps35-Vps26 interaction perturbs Rab7-mediated retromer recruitment. FRET-based interaction assay in HeLa cells, biophysical binding measurements, site-directed mutagenesis of Vps35-Vps26 interface Traffic (Copenhagen, Denmark) High 25367362
2014 VPS35 D620N acts as a loss-of-function mutation for synaptic function: it localizes to dendritic spines and normally regulates AMPA receptor (AMPAR) trafficking; D620N expression impairs excitatory synaptic transmission and AMPAR surface expression and synaptic recycling in mouse cortical neurons and iPSC-derived dopamine neurons from human D620N carriers. Electrophysiology, AMPAR surface expression assay, synaptic recycling assay, iPSC-derived neurons from patients Human molecular genetics High 25416282
2014 VPS35 is required for endosome-to-Golgi retrieval of Lamp2a; VPS35-deficient or D620N-mutant DA neurons exhibit accelerated Lamp2a degradation, impairing chaperone-mediated autophagy and leading to α-synuclein accumulation; Lamp2a overexpression in VPS35-deficient neurons reduces α-synuclein. Conditional VPS35 knockout in dopamine neurons, Lamp2a trafficking assay, α-synuclein immunostaining, epistasis rescue with Lamp2a overexpression The Journal of neuroscience : the official journal of the Society for Neuroscience High 26203154
2014 VPS35 dysfunction impairs retromer-mediated retrieval of the mannose 6-phosphate receptor, reducing lysosomal turnover of M6PR and affecting cathepsin D (CTSD) maturation and trafficking; VPS35 knockdown in Drosophila accumulates detergent-insoluble α-synuclein and exacerbates locomotor impairment. VPS35 RNAi knockdown in Drosophila, CTSD maturation assay, α-synuclein fractionation, behavioral assay Neurobiology of disease Medium 25107340
2015 PD-associated VPS35 mutations (especially D620N) cause mitochondrial fragmentation and cell death through enhanced interaction with dynamin-like protein DLP1, which increases turnover of mitochondrial DLP1 complexes via mitochondria-derived vesicle trafficking to lysosomes; inhibition of mitochondrial fission prevents VPS35-induced mitochondrial deficits; oxidative stress increases the VPS35-DLP1 interaction. Co-immunoprecipitation (VPS35-DLP1), mitochondrial fission inhibition rescue, MDV tracking, patient fibroblast and in vivo mouse substantia nigra analysis Nature medicine High 26618722
2015 VPS35 deficiency or D620N mutation increases mitochondrial E3 ubiquitin ligase MUL1 levels, leading to MFN2 (mitofusin 2) ubiquitin-dependent degradation and mitochondrial fragmentation; MUL1 suppression rescues MFN2 reduction and DA neuron loss but not α-synuclein accumulation. Conditional VPS35 KO in DA neurons, MUL1/MFN2 Western blot, MUL1 knockdown epistasis rescue, TH+ neuron counting Cell reports High 26321632
2015 VPS35 interacts with AMPA receptor subunits GluA1 and GluA2; VPS35 deficiency impairs dendritic spine maturation and decreases surface AMPA receptor levels; GluA2 overexpression partially rescues spine maturation deficits in VPS35-deficient neurons. Co-immunoprecipitation (VPS35-GluA1/GluA2), surface receptor biotinylation, GluA2 rescue epistasis, spine morphology imaging Molecular brain Medium 26521016
2015 VPS29-VPS35 form a biologically stable intermediate sub-complex in vivo; deficiency of VPS35 or VPS29 causes degradation of other retromer subunits, while VPS26 deficiency does not affect VPS29/VPS35 levels; VPS26-VPS35 is more susceptible to ubiquitin-proteasome degradation than VPS29-VPS35. siRNA knockdown of individual subunits, in vitro sub-complex reconstitution, ubiquitin-proteasome pathway inhibitor treatment FEBS letters Medium 25937119
2016 Parkinson disease-associated Vps35 variant R524W, but not P316S, is a loss-of-function mutation: R524W reduces association with the retromer regulatory network and dysregulates endosomal receptor (CI-M6PR) sorting; R524W expression causes accumulation of intracellular α-synuclein-positive aggregates; this phenotype is partially rescued by retromer-stabilizing compound R55. Co-immunoprecipitation, CI-M6PR trafficking assay, α-synuclein aggregation imaging, pharmacological rescue with R55 The Journal of biological chemistry High 27385586
2016 VPS35 interacts with and recycles dopamine receptor D1 (DRD1) from endosomes to the cell surface; VPS35 overexpression increases surface DRD1 and CREB/ERK phosphorylation downstream of dopamine; D620N mutant fails to recycle DRD1 or restore CREB/ERK signaling. Co-immunoprecipitation, surface receptor recycling assay, Western blot of CREB/ERK phosphorylation, VPS35 knockdown/overexpression Neurobiology of aging Medium 27460146
2016 VPS35 binds farnesylated (but not palmitoylated or GTP-loaded) N-Ras in the cytosol within a high-molecular-weight complex; silencing VPS35 increases N-Ras association with cytoplasmic vesicles, diminishes Ras GTP loading, and inhibits MAPK signaling and growth of N-Ras-dependent melanoma cells. Affinity purification of cytosolic Ras + mass spectrometry, Co-IP with farnesyl-dependence test, VPS35 siRNA + Ras GTP loading assay + MAPK signaling The Journal of cell biology High 27502489
2017 VPS35 D620N mutation causes mitochondrial fragmentation through the VPS35-DLP1 interaction via a conserved FLV motif in the C-terminus of DLP1; a decoy peptide based on this FLV motif blocks VPS35-DLP1 interaction and rescues D620N-induced mitochondrial fragmentation and respiratory deficits. Site-directed mutagenesis of DLP1 FLV motif, decoy peptide inhibitor, Co-IP, mitochondrial morphology and respiration assays in M17 cells and patient fibroblasts Human molecular genetics High 28040727
2017 VPS35 regulates lysosomal degradation of parkin substrate AIMP2; VPS35 co-immunoprecipitates with AIMP2 and Lamp2a; D620N mutation disrupts this association; VPS35 overexpression prevents AIMP2-induced PARP1-dependent cell death; VPS35 knockdown causes AIMP2-dependent PARP1 activation and cell death. Co-immunoprecipitation (VPS35-AIMP2-Lamp2a), VPS35 overexpression/knockdown, PARP1 activation assay, epistasis with AIMP2 knockdown Cell death & disease Medium 28383562
2017 Drosophila Vps35 loss affects synaptic vesicle recycling and dopaminergic synaptic release; dLRRK together with Rab5 and Rab11 is also involved; manipulation of LRRK/Rab5/Rab11 activities improves Vps35 synaptic phenotypes, placing Vps35 and LRRK2 in the same synaptic vesicle recycling pathway. Drosophila vps35 null mutants, genetic interaction with LRRK/Rab5/Rab11 transgenes, dopamine release measurement, behavioral assay Human molecular genetics Medium 28482024
2018 VPS35 D620N knock-in mutation strikingly elevates LRRK2-mediated phosphorylation of Rab8A, Rab10, and Rab12 in mouse embryonic fibroblasts and mouse tissues; VPS35 D620N increases LRRK2 kinase activity; knockout or knockdown of VPS35 suppresses LRRK2-mediated Rab phosphorylation, indicating VPS35 controls LRRK2 activity; D620N mutation is a gain-of-function for LRRK2 hyperactivation. VPS35 D620N knock-in mice, phospho-Rab8A/10/12 Western blot, VPS35 KO/KD in multiple cell types, patient neutrophil/monocyte analysis The Biochemical journal High 29743203
2018 Parkin interacts with VPS35 and mediates its poly-ubiquitination at three C-terminal lysine residues via an atypical poly-ubiquitin chain that does not promote proteasomal degradation; parkin KO mice show markedly decreased WASH complex components in brain; parkin silencing in neurons disrupts ATG9A vesicular sorting (a WASH-dependent retromer cargo). Co-immunoprecipitation, ubiquitination assay with lysine mutants, parkin KO mouse brain analysis, ATG9A trafficking assay Human molecular genetics High 29893854
2016 Trem2 undergoes clathrin-dependent endocytosis and is recycled to the plasma membrane via VPS35/retromer; VPS35 knockdown causes Trem2 accumulation in lysosomes; VPS35 deficiency leads to excessive LPS-induced iNOS and IL-6 production in microglia that is reversed by Trem2 overexpression; AD-associated R47H Trem2 mutant fails to interact with Vps35 and becomes unstable. Co-immunoprecipitation (VPS35-Trem2), VPS35 knockdown, lysosome trafficking assay, inflammatory cytokine measurement, rescue with Trem2 overexpression Traffic (Copenhagen, Denmark) Medium 27717139
2019 VPS35 regulates tau phosphorylation through cathepsin D availability: VPS35 overexpression reduces pathological tau, while VPS35 silencing increases tau accumulation; cathepsin D mediates this effect; VPS35 downregulation in a tauopathy mouse model exacerbates motor and learning impairments and tau accumulation. VPS35 overexpression/silencing in neuronal cells, cathepsin D activity assay, tauopathy transgenic mouse model with VPS35 downregulation Molecular psychiatry Medium 31289348
2020 VPS35 deficiency impairs Cdk5/p35 lysosomal degradation; loss of VPS35 increases p35 levels and Cdk5 activity, leading to tau hyperphosphorylation and retinal ganglion cell degeneration; Cdk5 inhibitor roscovitine reduces hyperphosphorylated tau caused by VPS35 deficiency; p35 is identified as a VPS35 cargo. VPS35 downregulation/overexpression in RGCs, Co-immunoprecipitation (Vps35-p35), Cdk5 activity assay, roscovitine rescue, in vivo retinal glutamate excitotoxicity model Investigative ophthalmology & visual science Medium 31995153
2021 VPS35 D620N mutation reduces mitochondrial membrane potential and impairs PINK1/Parkin-mediated mitophagy: D620N cells are desensitized to CCCP-induced mitochondrial potential collapse, show altered fragmentation, cannot accumulate PINK1 at the mitochondrial surface, and consequently fail to recruit Parkin for mitophagy initiation. CRISPR-Cas9 heterozygous D620N knock-in in SH-SY5Y cells, mitochondrial membrane potential assay, PINK1/Parkin recruitment imaging, CCCP treatment Translational neurodegeneration High 34127073
2022 Upon mtDNA damage, VPS35 mediates maturation of early endosomes to late autophagy vesicles for selective mtDNA degradation; SAMM50 acts as a gatekeeper controlling nucleoid release and transfer to endosomes; the ATAD3-SAMM50 axis is disrupted by mtDNA damage, facilitating endosomal recruitment near nucleoid sub-compartments. Proximity labeling (Twinkle as nucleoid marker), VPS35 knockdown, lysosomal function assays, ATG5 KO, mouse model of mtDNA alterations treated with rapamycin Nature communications High 36344526
2021 VPS35 D620N mutation promotes LRRK2-mediated lysosomal recruitment of RILPL1 and its binding to the lysosomal membrane protein TMEM55B; VPS35 D620N reduces RILPL1 levels in mouse tissues in a manner reversed by LRRK2 inhibition and proteasome inhibitors; RILPL1 KO enhances Rab substrate phosphorylation; TMEM55B KO increases RILPL1 levels. Quantitative lysosomal proteomics (~220 proteins altered), Co-IP of RILPL1-TMEM55B, VPS35 D620N knock-in mouse tissues, LRRK2 inhibitor treatment, RILPL1/TMEM55B knockout cells Science advances High 38091401
2023 VPS35 selectively binds endocytosed EGFR in early endosomes and recycles it to the cell surface, activating downstream ERK1/2 signaling; high VPS35 expression increases sensitivity to EGFR inhibitors in gastric cancer xenograft and organoid models. Co-immunoprecipitation (VPS35-EGFR), biotin surface assay, patient-derived xenografts and organoids, EGFR inhibitor response assay EBioMedicine Medium 36738481
2021 VPS35 promotes hepatoma cell proliferation via the PI3K/AKT signaling pathway; VPS35 knockout reduces membrane FGFR3 distribution, demonstrating VPS35's role in sorting and trafficking of transmembrane receptor FGFR3 in hepatoma cells. VPS35 knockout in hepatoma cells, FGFR3 membrane localization assay, PI3K/AKT signaling assay, in vivo xenograft Oncogene Medium 32071398
2023 VPS35 D620N significantly elevates LRRK2-mediated phosphorylation of Rab10, Rab12, and Rab29 in knock-in mice; LRRK2 kinase inhibitor MLi-2 normalizes striatal dopamine transporter (DAT) expression and function and abolishes increased amphetamine-induced hyperlocomotion in VKI mice; VPS35 haploinsufficiency reduces Rab12 phosphorylation and impairs DAT similarly but is not reversed by MLi-2, confirming D620N is a gain-of-function for LRRK2 kinase. VPS35 D620N knock-in and haploinsufficient mice, phospho-Rab Western blot, DAT expression/function assay, LRRK2 inhibitor MLi-2 treatment, behavioral testing NPJ Parkinson's disease High 38110354

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 A mutation in VPS35, encoding a subunit of the retromer complex, causes late-onset Parkinson disease. American journal of human genetics 696 21763483
2011 VPS35 mutations in Parkinson disease. American journal of human genetics 677 21763482
2014 Mutation in VPS35 associated with Parkinson's disease impairs WASH complex association and inhibits autophagy. Nature communications 364 24819384
1997 Endosome to Golgi retrieval of the vacuolar protein sorting receptor, Vps10p, requires the function of the VPS29, VPS30, and VPS35 gene products. The Journal of cell biology 353 9105038
2015 Parkinson's disease-associated mutant VPS35 causes mitochondrial dysfunction by recycling DLP1 complexes. Nature medicine 263 26618722
2010 Vps35 mediates vesicle transport between the mitochondria and peroxisomes. Current biology : CB 241 20619655
2011 VPS35 haploinsufficiency increases Alzheimer's disease neuropathology. The Journal of cell biology 217 22105352
2015 VPS35 in Dopamine Neurons Is Required for Endosome-to-Golgi Retrieval of Lamp2a, a Receptor of Chaperone-Mediated Autophagy That Is Critical for α-Synuclein Degradation and Prevention of Pathogenesis of Parkinson's Disease. The Journal of neuroscience : the official journal of the Society for Neuroscience 209 26203154
2015 VPS35 Deficiency or Mutation Causes Dopaminergic Neuronal Loss by Impairing Mitochondrial Fusion and Function. Cell reports 207 26321632
2012 Recruitment of the endosomal WASH complex is mediated by the extended 'tail' of Fam21 binding to the retromer protein Vps35. The Biochemical journal 189 22070227
2013 The Vps35 D620N mutation linked to Parkinson's disease disrupts the cargo sorting function of retromer. Traffic (Copenhagen, Denmark) 178 24152121
2018 The Parkinson's disease VPS35[D620N] mutation enhances LRRK2-mediated Rab protein phosphorylation in mouse and human. The Biochemical journal 163 29743203
2014 VPS35 dysfunction impairs lysosomal degradation of α-synuclein and exacerbates neurotoxicity in a Drosophila model of Parkinson's disease. Neurobiology of disease 156 25107340
2018 Genotype-phenotype relations for the Parkinson's disease genes SNCA, LRRK2, VPS35: MDSGene systematic review. Movement disorders : official journal of the Movement Disorder Society 153 30357936
2014 Retromer binding to FAM21 and the WASH complex is perturbed by the Parkinson disease-linked VPS35(D620N) mutation. Current biology : CB 149 24980502
2018 Phospholipase PLA2G6, a Parkinsonism-Associated Gene, Affects Vps26 and Vps35, Retromer Function, and Ceramide Levels, Similar to α-Synuclein Gain. Cell metabolism 144 29909971
2006 The retromer subunit Vps26 has an arrestin fold and binds Vps35 through its C-terminal domain. Nature structural & molecular biology 142 16732284
2014 Parkinson's disease genes VPS35 and EIF4G1 interact genetically and converge on α-synuclein. Neuron 141 25533483
2017 VPS35, the Retromer Complex and Parkinson's Disease. Journal of Parkinson's disease 140 28222538
2014 Parkinson's disease-linked mutations in VPS35 induce dopaminergic neurodegeneration. Human molecular genetics 126 24740878
2014 Retromer-dependent neurotransmitter receptor trafficking to synapses is altered by the Parkinson's disease VPS35 mutation p.D620N. Human molecular genetics 115 25416282
2008 Arabidopsis VPS35, a retromer component, is required for vacuolar protein sorting and involved in plant growth and leaf senescence. Plant & cell physiology 101 18222962
1992 Alternative pathways for the sorting of soluble vacuolar proteins in yeast: a vps35 null mutant missorts and secretes only a subset of vacuolar hydrolases. Molecular biology of the cell 97 1498362
2017 Vps35 in cooperation with LRRK2 regulates synaptic vesicle endocytosis through the endosomal pathway in Drosophila. Human molecular genetics 92 28482024
2019 Parkinson's disease-linked D620N VPS35 knockin mice manifest tau neuropathology and dopaminergic neurodegeneration. Proceedings of the National Academy of Sciences of the United States of America 86 30842285
2014 Vacuolar protein sorting 35 (Vps35) rescues locomotor deficits and shortened lifespan in Drosophila expressing a Parkinson's disease mutant of Leucine-Rich Repeat Kinase 2 (LRRK2). Molecular neurodegeneration 79 24915984
2012 A multi-centre clinico-genetic analysis of the VPS35 gene in Parkinson disease indicates reduced penetrance for disease-associated variants. Journal of medical genetics 79 23125461
2007 Drosophila Vps35 function is necessary for normal endocytic trafficking and actin cytoskeleton organisation. Journal of cell science 75 18057029
2013 The VPS35 gene and Parkinson's disease. Movement disorders : official journal of the Movement Disorder Society 73 23536430
2016 Parkinson Disease-linked Vps35 R524W Mutation Impairs the Endosomal Association of Retromer and Induces α-Synuclein Aggregation. The Journal of biological chemistry 71 27385586
2012 Frequency of the D620N mutation in VPS35 in Parkinson disease. Archives of neurology 71 22801713
2012 VPS35 mutation in Japanese patients with typical Parkinson's disease. Movement disorders : official journal of the Movement Disorder Society 70 22991136
2014 Molecular insights into Rab7-mediated endosomal recruitment of core retromer: deciphering the role of Vps26 and Vps35. Traffic (Copenhagen, Denmark) 68 25367362
2022 Mitochondrial membrane proteins and VPS35 orchestrate selective removal of mtDNA. Nature communications 67 36344526
2015 VPS35-deficiency results in an impaired AMPA receptor trafficking and decreased dendritic spine maturation. Molecular brain 66 26521016
2018 Increased Microglial Activity, Impaired Adult Hippocampal Neurogenesis, and Depressive-like Behavior in Microglial VPS35-Depleted Mice. The Journal of neuroscience : the official journal of the Society for Neuroscience 64 29853629
2018 Altered dopamine release and monoamine transporters in Vps35 p.D620N knock-in mice. NPJ Parkinson's disease 62 30155515
2016 Vps35-dependent recycling of Trem2 regulates microglial function. Traffic (Copenhagen, Denmark) 61 27717139
2015 VPS35 pathogenic mutations confer no dominant toxicity but partial loss of function in Drosophila and genetically interact with parkin. Human molecular genetics 61 26251041
2012 VPS35 regulates developing mouse hippocampal neuronal morphogenesis by promoting retrograde trafficking of BACE1. Biology open 61 23259059
2018 A Golgi-targeting fluorescent probe for labile Fe(ii) to reveal an abnormal cellular iron distribution induced by dysfunction of VPS35. Chemical science 59 30809369
2016 Impaired striatal dopamine release in homozygous Vps35 D620N knock-in mice. Human molecular genetics 57 28173004
2018 Parkin mediates the ubiquitination of VPS35 and modulates retromer-dependent endosomal sorting. Human molecular genetics 55 29893854
2013 Whole exome sequencing of rare variants in EIF4G1 and VPS35 in Parkinson disease. Neurology 53 23408866
2011 Screening for VPS35 mutations in Parkinson's disease. Neurobiology of aging 50 22154191
2010 Implication of mouse Vps26b-Vps29-Vps35 retromer complex in sortilin trafficking. Biochemical and biophysical research communications 50 21040701
2020 The Role of VPS35 in the Pathobiology of Parkinson's Disease. Cellular and molecular neurobiology 47 32323152
2016 VPS35 binds farnesylated N-Ras in the cytosol to regulate N-Ras trafficking. The Journal of cell biology 46 27502489
2021 Parkinson's disease-associated VPS35 mutant reduces mitochondrial membrane potential and impairs PINK1/Parkin-mediated mitophagy. Translational neurodegeneration 45 34127073
2017 Parkinson's disease-associated pathogenic VPS35 mutation causes complex I deficits. Biochimica et biophysica acta. Molecular basis of disease 43 28765075
2020 Vps35 Deficiency Impairs Cdk5/p35 Degradation and Promotes the Hyperphosphorylation of Tau Protein in Retinal Ganglion Cells. Investigative ophthalmology & visual science 42 31995153
2020 Mitochondrial and Clearance Impairment in p.D620N VPS35 Patient-Derived Neurons. Movement disorders : official journal of the Movement Disorder Society 41 33142012
2014 VPS35 Parkinson's disease phenotype resembles the sporadic disease. Journal of neural transmission (Vienna, Austria : 1996) 41 24557499
2013 Vps35 loss promotes hyperresorptive osteoclastogenesis and osteoporosis via sustained RANKL signaling. The Journal of cell biology 41 23509071
2019 Contributions of VPS35 Mutations to Parkinson's Disease. Neuroscience 40 30660673
2016 VPS35 regulates cell surface recycling and signaling of dopamine receptor D1. Neurobiology of aging 39 27460146
2020 (D620N) VPS35 causes the impairment of Wnt/β-catenin signaling cascade and mitochondrial dysfunction in a PARK17 knockin mouse model. Cell death & disease 38 33257649
2020 Coupling of terminal differentiation deficit with neurodegenerative pathology in Vps35-deficient pyramidal neurons. Cell death and differentiation 37 31907392
2017 A conserved retromer sorting motif is essential for mitochondrial DLP1 recycling by VPS35 in Parkinson's disease model. Human molecular genetics 37 28040727
2019 VPS35 regulates tau phosphorylation and neuropathology in tauopathy. Molecular psychiatry 36 31289348
2022 Microglial VPS35 deficiency impairs Aβ phagocytosis and Aβ-induced disease-associated microglia, and enhances Aβ associated pathology. Journal of neuroinflammation 34 35236374
2020 DNA and RNA sequencing identified a novel oncogene VPS35 in liver hepatocellular carcinoma. Oncogene 34 32071398
2014 In vivo evidence of pathogenicity of VPS35 mutations in the Drosophila. Molecular brain 33 25288323
2022 Understanding the contributions of VPS35 and the retromer in neurodegenerative disease. Neurobiology of disease 32 35588987
2021 KLF7/VPS35 axis contributes to hepatocellular carcinoma progression through CCDC85C-activated β-catenin pathway. Cell & bioscience 32 33858520
2023 VPS35 promotes cell proliferation via EGFR recycling and enhances EGFR inhibitors response in gastric cancer. EBioMedicine 30 36738481
2023 Parkinson's VPS35[D620N] mutation induces LRRK2-mediated lysosomal association of RILPL1 and TMEM55B. Science advances 30 38091401
2021 VPS35 D620N knockin mice recapitulate cardinal features of Parkinson's disease. Aging cell 30 33745227
2013 Pathogenic mutation in VPS35 impairs its protection against MPP(+) cytotoxicity. International journal of biological sciences 30 23411763
2007 The vacuolar-ATPase inhibitor bafilomycin and mutant VPS35 inhibit canonical Wnt signaling. Neurobiology of disease 30 17239604
2020 VPS35 and the mitochondria: Connecting the dots in Parkinson's disease pathophysiology. Neurobiology of disease 29 32853677
2015 VPS29-VPS35 intermediate of retromer is stable and may be involved in the retromer complex assembly process. FEBS letters 29 25937119
2007 Dominant-negative behavior of mammalian Vps35 in yeast requires a conserved PRLYL motif involved in retromer assembly. Traffic (Copenhagen, Denmark) 29 17916227
2019 Interaction between VPS35 and RABG3f is necessary as a checkpoint to control fusion of late compartments with the vacuole. Proceedings of the National Academy of Sciences of the United States of America 28 31570580
2023 VPS35 promotes gastric cancer progression through integrin/FAK/SRC signalling-mediated IL-6/STAT3 pathway activation in a YAP-dependent manner. Oncogene 26 37950040
2014 VPS35 and DNAJC13 disease-causing variants in essential tremor. European journal of human genetics : EJHG 26 25118025
2012 VPS35 Asp620Asn and EIF4G1 Arg1205His mutations are rare in Parkinson disease from southwest China. Neurobiology of aging 25 23261770
2020 Ependymal Vps35 Promotes Ependymal Cell Differentiation and Survival, Suppresses Microglial Activation, and Prevents Neonatal Hydrocephalus. The Journal of neuroscience : the official journal of the Society for Neuroscience 24 32291328
2016 Role of the VPS35 D620N mutation in Parkinson's disease. Parkinsonism & related disorders 24 27964832
2013 EIF4G1 R1205H and VPS35 D620N mutations are rare in Parkinson's disease from South Africa. Neurobiology of aging 24 24080171
2023 Elevated urine BMP phospholipids in LRRK2 and VPS35 mutation carriers with and without Parkinson's disease. NPJ Parkinson's disease 23 37015928
2021 Formation of retromer transport carriers is disrupted by the Parkinson disease-linked Vps35 D620N variant. Traffic (Copenhagen, Denmark) 23 33347683
2017 Identification of VPS35 p.D620N mutation-related Parkinson's disease in a Taiwanese family with successful bilateral subthalamic nucleus deep brain stimulation: a case report and literature review. BMC neurology 23 28985717
2019 VPS35-Based Approach: A Potential Innovative Treatment in Parkinson's Disease. Frontiers in neurology 22 31920908
2017 VPS35 regulates parkin substrate AIMP2 toxicity by facilitating lysosomal clearance of AIMP2. Cell death & disease 22 28383562
2019 Microglial VPS35 deficiency regulates microglial polarization and decreases ischemic stroke-induced damage in the cortex. Journal of neuroinflammation 21 31771656
2014 Vps35 haploinsufficiency results in degenerative-like deficit in mouse retinal ganglion neurons and impairment of optic nerve injury-induced gliosis. Molecular brain 21 24512632
2013 VPS35 and EIF4G1 mutations are rare in Parkinson's disease among Indians. Neurobiology of aging 21 23726718
2021 Neuronal VPS35 deletion induces spinal cord motor neuron degeneration and early post-natal lethality. Brain communications 20 34704029
2020 Endosomal dysfunction in iPSC-derived neural cells from Parkinson's disease patients with VPS35 D620N. Molecular brain 20 33032646
2012 Contribution of VPS35 genetic variability to LBD in the Flanders-Belgian population. Neurobiology of aging 20 22336192
2021 Impaired neurogenesis in the hippocampus of an adult VPS35 mutant mouse model of Parkinson's disease through interaction with APP. Neurobiology of disease 19 33636388
1996 Genetic mapping and embryonic expression of a novel, maternally transcribed gene Mem3. Mammalian genome : official journal of the International Mammalian Genome Society 19 8678978
2023 Inhibition of LRRK2 kinase activity rescues deficits in striatal dopamine physiology in VPS35 p.D620N knock-in mice. NPJ Parkinson's disease 18 38110354
2020 Altered striatal dopamine levels in Parkinson's disease VPS35 D620N mutant transgenic aged mice. Molecular brain 17 33261640
2018 VPS35 depletion does not impair presynaptic structure and function. Scientific reports 17 29445238
2016 Autosomal dominant Parkinson's disease: Incidence of mutations in LRRK2, SNCA, VPS35 and GBA genes in Brazil. Neuroscience letters 17 27777137
2020 Depletion of VPS35 attenuates metastasis of hepatocellular carcinoma by restraining the Wnt/PCP signaling pathway. Genes & diseases 16 33997170
2024 Intermittent hypoxia training enhances Aβ endocytosis by plaque associated microglia via VPS35-dependent TREM2 recycling in murine Alzheimer's disease. Alzheimer's research & therapy 15 38831312
2021 Mechanisms of VPS35-Mediated Neurodegeneration in Parkinson's Disease. International review of movement disorders 15 35497708