Affinage

DNAJC13

DnaJ homolog subfamily C member 13 · UniProt O75165

Length
2243 aa
Mass
254.4 kDa
Annotated
2026-06-09
29 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

DNAJC13 (RME-8) is an endosome-associated DnaJ/Hsc70 co-chaperone that governs the balance between cargo recycling and degradation at the endosomal membrane (PMID:11451999, PMID:19763082). It is recruited as a peripheral membrane protein to early endosomes through its N-terminal PH-like domain, which binds PI(3)P; this localization is held in check by autoinhibitory contacts involving the J-domain HPD triad and a conserved C-terminal YLT motif, and efficient membrane binding requires oligomerization, with derepressing mutations enhancing PI(3)P binding and endosomal clustering at the cost of cargo recycling (PMID:40737286). At the membrane it engages Hsc70 through its DnaJ domain to drive clathrin uncoating dynamics (PMID:15051737, PMID:16179350), working together with the retromer-associated sorting nexin SNX1 and the WASH-complex subunit FAM21 to control SNX1 membrane tubulation and the sorting of cargo away from degradation (PMID:19763082, PMID:24643499). DNAJC13 and SNX1 oppose the assembly of ESCRT-0 (HRS/HGRS-1) degradative microdomains, thereby favoring retrograde and recycling itineraries over lysosomal delivery, a conserved antagonism that determines the fate of cargoes including Wntless, EGFR, Notch, and multiple GPCRs (PMID:19763082, PMID:28053230, PMID:26169355, PMID:39223388). Beyond classical endosomal sorting, DNAJC13 is a positive modulator of autophagy: it supports ATG9A trafficking from the recycling endosome and maintains clathrin at autolysosomal membranes to enable autophagic lysosome reformation (PMID:32322926, PMID:37942902). The p.Asn855Ser substitution segregates with autosomal-dominant Parkinson's disease, acting as a combined loss-of-function and dominant-negative variant that destabilizes the protein, increases SNX1 tubulation, impairs cargo trafficking, promotes α-synuclein accumulation, and reduces autophagy (PMID:24218364, PMID:29309590, PMID:31082451, PMID:40717240).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2001 High

    Established that the gene product is required for endocytosis and acts at endosomes before the lysosome, defining its compartment and stage of action.

    Evidence Loss-of-function genetics and endocytic marker uptake in C. elegans coelomocytes with live localization

    PMID:11451999

    Open questions at the time
    • No molecular partners or biochemical mechanism identified
    • Mammalian relevance not yet tested
  2. 2004 High

    Identified Hsc70 as a functional partner acting through the J-domain, placing the protein in a chaperone-dependent endocytic pathway.

    Evidence Drosophila genetic screen, biochemical pulldown, and genetic epistasis with Hsc70-4

    PMID:15051737

    Open questions at the time
    • Substrate of the Hsc70 co-chaperone activity not defined
    • Endosomal clathrin role not yet shown
  3. 2005 High

    Showed the mammalian protein is a clathrin-coated-vesicle/endosome component binding Hsc70 and selectively required for EGF and lysosomal-enzyme receptor trafficking but not transferrin endocytosis.

    Evidence CCV proteomics, affinity selection, fractionation, and siRNA knockdown with multiple cargo readouts in mammalian cells

    PMID:16179350

    Open questions at the time
    • Mechanism distinguishing affected vs unaffected cargo unknown
    • Membrane recruitment determinants undefined
  4. 2008 High

    Localized the human protein specifically to early (not late) endosomes via its N-terminal region and linked it to recycling and degradative cargo flux.

    Evidence Immuno-EM, Rab co-localization, and truncation-mutant trafficking assays in human cells

    PMID:18256511 PMID:18307993

    Open questions at the time
    • Lipid/protein basis of N-terminal membrane binding not resolved
    • EGFR sorting mechanism inferred from steady-state levels
  5. 2009 High

    Defined a retromer-linked mechanism in which the protein, SNX1, and Hsc70 control endosomal clathrin dynamics to route cargo to the Golgi rather than the lysosome.

    Evidence Reciprocal co-IP, genetic epistasis, live clathrin imaging, and Wntless missorting assays in C. elegans

    PMID:19763082

    Open questions at the time
    • Direct biochemistry of clathrin uncoating not reconstituted
    • Whether SNX1 binding is direct unresolved
  6. 2015 High

    Placed the protein upstream of and in opposition to retromer and ESCRT-0 in deciding receptor recycling versus degradation, using Notch as a readout.

    Evidence Drosophila double-knockdown genetic epistasis with Vps26 and Hrs/Stam plus Notch signaling assays

    PMID:26169355

    Open questions at the time
    • Molecular basis of the antagonism not defined
    • Mammalian Notch relevance not tested here
  7. 2014 High

    Linked the protein physically to the WASH complex (FAM21) and SNX1, showing it restrains branched endosomal tubulation and coordinates WASH activity with sorting-nexin tubulation.

    Evidence Reciprocal co-IP, siRNA knockdown, live tubule imaging, and cargo localization

    PMID:24643499

    Open questions at the time
    • Direct vs indirect FAM21 interaction not dissected
    • How it limits tubulation mechanistically unclear
  8. 2017 High

    Demonstrated that the protein with SNX1 directly opposes ESCRT-0 degradative microdomain assembly with defined directionality, conserved from worm to human.

    Evidence C. elegans microdomain imaging with retromer-component specificity, membrane fractionation, and HeLa knockdown

    PMID:28053230

    Open questions at the time
    • Biochemical mechanism limiting HGRS-1 membrane binding unknown
    • How specificity for ESCRT-0 vs retromer is achieved unresolved
  9. 2022 Medium

    Resolved the domain logic of conformational autoinhibition, showing IWN domains and SNX-1 gate productive exposure of the DnaJ domain for uncoating activity.

    Evidence Mutagenesis with in vivo microdomain imaging and AlphaFold modeling in C. elegans

    PMID:36279308

    Open questions at the time
    • Structure is computational, not experimental
    • Conformational model not validated biochemically in mammals
  10. 2025 High

    Defined PI(3)P binding by the PH-like domain as the membrane-recruitment mechanism, regulated by autoinhibitory J-domain and YLT motifs and dependent on oligomerization.

    Evidence In vitro PI(3)P binding with mutagenesis, quantitative imaging, and overexpression cargo-recycling assays

    PMID:40737286

    Open questions at the time
    • Oligomerization stoichiometry and trigger not defined
    • How autoinhibition is relieved on the membrane unclear
  11. 2020 Medium

    Extended function to autophagy, showing the protein promotes autophagic flux by enabling ATG9A trafficking from the recycling endosome.

    Evidence Knockdown/overexpression in human cells and C. elegans RNAi with ATG9A localization and LC3B flux assays

    PMID:32322926

    Open questions at the time
    • Direct role in ATG9A vesicle formation vs sorting unclear
    • Connection to clathrin/Hsc70 activity not tested
  12. 2023 High

    Showed the protein maintains clathrin at autolysosomes to drive autophagic lysosome reformation, integrating its clathrin-uncoating role with late autophagy.

    Evidence C. elegans and mouse cortical neuron imaging, autophagic flux assays, and epistasis with ALR regulators

    PMID:37942902

    Open questions at the time
    • Whether Hsc70 co-chaperone activity drives ALR clathrin dynamics untested
    • Substrate at autolysosome undefined
  13. 2024 High

    Generalized the cargo-sorting role to GPCR trafficking and endosomal proteome homeostasis via an unbiased genome-wide screen.

    Evidence Genome-wide CRISPRi screen with GPCR trafficking biosensors and endosomal proteomics in human cells

    PMID:39223388

    Open questions at the time
    • Whether GPCR effects are direct or via global endosomal disruption unresolved
    • Specific sorting step for each GPCR undefined
  14. 2013 Medium

    Connected the gene to autosomal-dominant Parkinson's disease through the p.N855S variant, with disease-relevant trafficking impairment and Lewy-body immunoreactivity.

    Evidence Exome/Sanger sequencing, case-control genotyping, cellular functional analysis, and immunohistochemistry

    PMID:24218364

    Open questions at the time
    • Whether variant is gain- or loss-of-function not resolved here
    • Mechanistic basis of trafficking defect unclear
  15. 2018 Medium

    Linked the N855S variant mechanistically to α-synuclein endosomal accumulation and dopaminergic neurodegeneration in vivo.

    Evidence Cell trafficking assays and α-synuclein transgenic Drosophila with behavioral and pathological readouts

    PMID:29309590

    Open questions at the time
    • α-synuclein accumulation inferred from trafficking defect, not direct biochemistry
    • Relationship to neuronal autophagy not tested here
  16. 2019 Medium

    Showed in a physiological knock-in neuron model that N855S acts as a dominant-negative on SNX1 tubulation without disrupting WASH-retromer assembly.

    Evidence Knock-in mouse primary cortical neurons with quantitative SNX1 tubule morphometry

    PMID:31082451

    Open questions at the time
    • Single lab, limited mechanistic detail
    • Link from tubulation defect to neurodegeneration not established
  17. 2025 Medium

    Clarified the dual nature of N855S as both destabilizing/loss-of-function and dominant-negative across autophagy and cargo-distribution phenotypes.

    Evidence Stable knockdown rescue, mutant stability assays, M6PR co-localization, cathepsin D activity, and autophagy gene expression in human cells

    PMID:40717240

    Open questions at the time
    • Dominant-negative mechanism inferred from co-localization, not reconstituted
    • Cause of accelerated degradation undefined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How autoinhibition is relieved on the membrane to productively expose the DnaJ domain and direct Hsc70-driven clathrin uncoating toward specific substrates remains unresolved.
  • No experimental high-resolution structure of the full-length protein or its membrane-bound conformation
  • Direct uncoating substrates at endosomes vs autolysosomes not biochemically defined
  • Quantitative link between specific trafficking defects and Parkinson's pathogenesis incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 4 GO:0098772 molecular function regulator activity 3 GO:0008289 lipid binding 1
Localization
GO:0005768 endosome 4 GO:0005886 plasma membrane 2 GO:0005764 lysosome 1
Pathway
R-HSA-5653656 Vesicle-mediated transport 5 R-HSA-1643685 Disease 3 R-HSA-9609507 Protein localization 3 R-HSA-9612973 Autophagy 2
Partners
FAM21HSPA8SNX1

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 RME-8 (DNAJC13 ortholog in C. elegans) is required for receptor-mediated and fluid-phase endocytosis; it localizes to the limiting membrane of large endosomes and functions in endosomal trafficking prior to the lysosome, as demonstrated by loss-of-function mutants that fail to accumulate endocytosis markers in coelomocytes. Genetic analysis of C. elegans mutants, fluorescence localization, endocytosis marker uptake assays Molecular biology of the cell High 11451999
2004 Drosophila Rme-8 interacts specifically with Hsc70-4 via its J-domain (biochemical and genetic interaction), and is required for clathrin-dependent endocytosis; rme-8 mutants phenocopy Hsc70-4 mutants, placing them in a common pathway. Drosophila genetic screen (dominant-negative dynamin interaction), biochemical pulldown, genetic epistasis, endocytosis tracer uptake assays The Journal of cell biology High 15051737
2005 Mammalian RME-8 (DNAJC13) was identified in clathrin-coated vesicle proteomics from rat liver; affinity selection assays identify Hsc70 as its major binding partner via the DnaJ domain; RME-8 is tightly associated with microsomal membranes and co-localizes with endosomal markers. siRNA knockdown does not affect transferrin endocytosis but reduces EGF internalization and disrupts trafficking of cation-independent mannose 6-phosphate receptor and cathepsin D sorting. Proteomic analysis of clathrin-coated vesicles, affinity selection (pulldown), subcellular fractionation, co-localization, siRNA knockdown with cargo trafficking readouts The Journal of biological chemistry High 16179350
2008 Human RME-8 (DNAJC13) is a peripheral membrane protein associated via its N-terminal region, localizing primarily to early endosomes (co-localizes with early endosomal markers, confirmed by immunoelectron microscopy). Expression of C-terminally truncated mutants perturbs transferrin recycling and EGF degradation through early endosomes. It does not co-localize with late endosomal markers. Cloning and biochemical characterization, immunoelectron microscopy, dominant-active Rab co-localization, truncation mutant overexpression, endocytic pathway assays Cell structure and function High 18256511
2008 RME-8 depletion leads to increased EGFR degradation (decreased steady-state EGFR levels at both surface and intracellular pools), implicating DNAJC13 in sorting decisions at endosomes that protect EGFR from degradation; transferrin receptor levels are unaffected. siRNA knockdown, receptor level quantification, degradation rate assays FEBS letters Medium 18307993
2009 C. elegans RME-8 associates with retromer component SNX-1; loss of SNX-1, RME-8, or the clathrin chaperone Hsc70/HSP-1 leads to over-accumulation of endosomal clathrin, reduced clathrin dynamics, and missorting of MIG-14/Wntless to the lysosome instead of the Golgi. This defines a mechanism whereby retromer regulates endosomal clathrin dynamics through RME-8 and Hsc70. Co-immunoprecipitation, genetic epistasis in C. elegans, live fluorescence imaging of clathrin dynamics, cargo missorting assays The EMBO journal High 19763082
2013 The DNAJC13 p.Asn855Ser mutation segregates with autosomal dominant Parkinson's disease; cellular analysis shows this mutation confers a toxic gain-of-function and impairs endosomal transport. DNAJC13 immunoreactivity was detected within Lewy body inclusions. Exome sequencing, Sanger sequencing, case-control genotyping, cellular functional analysis, immunohistochemistry Human molecular genetics Medium 24218364
2014 RME-8 (DNAJC13) interacts with FAM21 (a subunit of the WASH complex) and with SNX1; loss of RME-8 causes altered kinetics of SNX1 membrane association and a pronounced increase in highly branched endosomal tubules containing WASH-complex-dependent cargo, indicating that RME-8 coordinates WASH complex activity with the membrane-tubulating function of sorting nexins. Co-immunoprecipitation, siRNA knockdown, live fluorescence imaging of endosomal tubules, cargo localization assays Journal of cell science High 24643499
2015 In Drosophila, Rme-8 depletion causes Notch receptor accumulation in enlarged tubulated Rab4-positive endosomes and impairs Notch signaling. Simultaneous depletion of retromer component Vps26 or ESCRT-0 components Hrs/Stam with Rme-8 causes ectopic Notch activation, placing Rme-8 upstream and in opposition to these complexes in regulating Notch recycling versus degradation. Drosophila genetic epistasis (double knockdown/mutants), live and fixed fluorescence imaging, Notch signaling readouts The Journal of cell biology High 26169355
2017 SNX-1 and RME-8 together oppose the assembly of ESCRT-0/HGRS-1 degradative microdomains on endosomes; loss of snx-1 or rme-8 (but not other retromer components snx-3 or vps-35) increases endosomal coverage and intensity of HGRS-1-labeled microdomains and increases membrane-bound HGRS-1. Loss of hgrs-1 has little to no effect on SNX-1/RME-8 microdomains, indicating directionality of the interaction. The antagonism between recycling (RME-8/SNX-1) and degradative (ESCRT-0) microdomains is conserved in human HeLa cells. C. elegans genetics with in vivo fluorescence imaging of endosomal microdomains, siRNA knockdown in HeLa cells, membrane fractionation Proceedings of the National Academy of Sciences of the United States of America High 28053230
2018 The PD-linked N855S mutant DNAJC13 causes α-synuclein accumulation in the endosomal compartment due to defective cargo trafficking from early to late/recycling endosomes. In human αSYN transgenic Drosophila, mutant DNAJC13 increases insoluble αSYN, induces dopaminergic neurodegeneration, rough eye phenotype, and age-dependent locomotor impairment. Cell-based trafficking assays, Drosophila in vivo model with behavioral and pathological readouts, biochemical fractionation Human molecular genetics Medium 29309590
2019 The DNAJC13 p.Asn855Ser knock-in mutation in primary cortical neurons (from a mouse knock-in model) significantly increases SNX1-enriched endosomal tubule formation without affecting SNX1 puncta density or WASH-retromer assembly, indicating a dominant-negative gain-of-function that disrupts SNX1 membrane-tubulation dynamics. Knock-in mouse model, primary cortical neuron cultures, fluorescence imaging of SNX1 tubules, quantitative morphometry Neuroscience letters Medium 31082451
2020 DNAJC13 acts as a positive modulator of autophagy; knockdown reduces autophagic flux in C. elegans and human cell lines and impairs ATG9A trafficking from the recycling endosome, reducing ATG9A co-localization at LC3B-positive autophagic puncta. The PD-associated N855S mutant fails to enhance autophagy upon overexpression. siRNA knockdown and overexpression in human cells, C. elegans RNAi, ATG9A localization by fluorescence microscopy, autophagic flux assays (LC3B puncta, autophagy markers) Cellular and molecular life sciences : CMLS Medium 32322926
2022 Structure-function analysis of C. elegans RME-8 identified that: (1) the C-terminus is important for microdomain localization and substrate binding; (2) N-terminal sequences beyond the PH-like domain are important for endosome recruitment; (3) IWN4 and IWN3 domains are important for autoinhibitory DNAJ domain binding, with IWN3 playing a critical role in HRS/HGRS-1 uncoating activity. AlphaFold structural modeling combined with in vivo mutation analysis supports a model whereby SNX-1 and IWN domains control RME-8 conformation and productive exposure of its DNAJ domain, with SNX-1 acting as an activator and target of RME-8 uncoating activity. Random and site-directed mutagenesis, AlphaFold structural modeling, in vivo C. elegans fluorescence imaging of endosomal microdomains, phylogenetic analysis PLoS genetics Medium 36279308
2023 Loss of RME-8/DNAJC13 in C. elegans mechanosensory neurons and primary mouse cortical neurons causes accumulation of grossly elongated autolysosomal tubules, indicating a role in autophagic lysosome reformation (ALR). In C. elegans, this phenotype is shared with bec-1/beclin, vps-15/PIK3R4, and dyn-1/dynamin mutants (known ALR regulators). Loss of RME-8 causes severe depletion of clathrin from neuronal autolysosomes, phenocopying bec-1 and vps-15 mutants. Loss of RME-8/DNAJC13 also reduces autophagic flux in both systems. C. elegans genetics and live fluorescence imaging, primary mouse cortical neuron culture, autophagic flux assays, clathrin localization Autophagy High 37942902
2024 Genome-wide CRISPR interference screen identified DNAJC13 as a regulator of δ-opioid receptor (DOR) trafficking through the endosomal-lysosomal pathway; DNAJC13 controls trafficking of multiple GPCRs and regulates the composition of the endosomal proteome and endosomal homeostasis. Genome-wide CRISPRi screen using GPCR-APEX2/AUR trafficking biosensor, validation by loss-of-function with multiple GPCR trafficking readouts, quantitative proteomics of endosomal compartment Nature chemical biology High 39223388
2025 DNAJC13 localizes to endosomes through its N-terminal PH-like domain binding to PI(3)P; the J domain (HPD catalytic triad) and a conserved YLT motif in the disordered C-terminus act as negative regulators of this localization. Mutation of either motif enhances endosomal localization and PI(3)P binding in vitro. The PH-like domain binds PI(3)P weakly in isolation and requires oligomerization for efficient PI(3)P binding and endosomal localization. Overexpression of derepressed mutants causes endosomal clustering and loss of membrane protein cargo recycling. Structure-function mutagenesis, PI(3)P binding assays in vitro, quantitative cell imaging, overexpression phenotypic analysis, quantitative proteomics Molecular biology of the cell High 40737286
2025 The DNAJC13 N855S variant is less stable than wild-type protein and shows accelerated degradation. It fails to rescue impaired autophagy in DNAJC13 knockdown cells (loss-of-function), exerts a dominant-negative effect on cation-independent mannose-6-phosphate receptor distribution (without affecting overall cathepsin D levels or activity), and chronic DNAJC13 knockdown reduces expression of autophagy induction and biogenesis genes. Stable knockdown cell lines, transient N855S mutant expression, biochemical stability assays, co-localization by fluorescence microscopy, cathepsin D activity assays, gene expression analysis Journal of cellular physiology Medium 40717240

Source papers

Stage 0 corpus · 29 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 DNAJC13 mutations in Parkinson disease. Human molecular genetics 238 24218364
2001 RME-8, a conserved J-domain protein, is required for endocytosis in Caenorhabditis elegans. Molecular biology of the cell 143 11451999
2009 Regulation of endosomal clathrin and retromer-mediated endosome to Golgi retrograde transport by the J-domain protein RME-8. The EMBO journal 134 19763082
2005 The DnaJ-domain protein RME-8 functions in endosomal trafficking. The Journal of biological chemistry 99 16179350
2014 RME-8 coordinates the activity of the WASH complex with the function of the retromer SNX dimer to control endosomal tubulation. Journal of cell science 92 24643499
2004 The J-domain protein Rme-8 interacts with Hsc70 to control clathrin-dependent endocytosis in Drosophila. The Journal of cell biology 84 15051737
2017 SNX-1 and RME-8 oppose the assembly of HGRS-1/ESCRT-0 degradative microdomains on endosomes. Proceedings of the National Academy of Sciences of the United States of America 74 28053230
2008 Human RME-8 is involved in membrane trafficking through early endosomes. Cell structure and function 51 18256511
2018 Parkinson's disease-linked DNAJC13 mutation aggravates alpha-synuclein-induced neurotoxicity through perturbation of endosomal trafficking. Human molecular genetics 43 29309590
2014 DNAJC13 genetic variants in parkinsonism. Movement disorders : official journal of the Movement Disorder Society 37 25393719
2015 Rme-8 depletion perturbs Notch recycling and predisposes to pathogenic signaling. The Journal of cell biology 30 26169355
2014 Tumor suppressive microRNA-193b promotes breast cancer progression via targeting DNAJC13 and RAB22A. International journal of clinical and experimental pathology 30 25550792
2008 RME-8 regulates trafficking of the epidermal growth factor receptor. FEBS letters 27 18307993
2014 VPS35 and DNAJC13 disease-causing variants in essential tremor. European journal of human genetics : EJHG 26 25118025
2020 Receptor-mediated endocytosis 8 (RME-8)/DNAJC13 is a novel positive modulator of autophagy and stabilizes cellular protein homeostasis. Cellular and molecular life sciences : CMLS 25 32322926
2015 DNAJC13 p.Asn855Ser mutation screening in Parkinson's disease and pathologically confirmed Lewy body disease patients. European journal of neurology 22 26278106
2018 DNAJC13 mutation screening in patients with Parkinson's disease from South Italy. Parkinsonism & related disorders 17 29887357
2014 Clinical, positron emission tomography, and pathological studies of DNAJC13 p.N855S Parkinsonism. Movement disorders : official journal of the Movement Disorder Society 16 25186792
2022 Mutagenesis and structural modeling implicate RME-8 IWN domains as conformational control points. PLoS genetics 11 36279308
2024 An engineered trafficking biosensor reveals a role for DNAJC13 in DOR downregulation. Nature chemical biology 9 39223388
2023 A conserved requirement for RME-8/DNAJC13 in neuronal autophagic lysosome reformation. Autophagy 9 37942902
2019 DNAJC13 p.Asn855Ser, implicated in familial parkinsonism, alters membrane dynamics of sorting nexin 1. Neuroscience letters 9 31082451
2024 DNAJC13 influences responses of the extended reward system to conditioned stimuli: a genome-wide association study. European archives of psychiatry and clinical neuroscience 3 39417891
2012 Analysis of the MRPL3, DNAJC13 and OFCC1 variants in Chinese Han patients with TS-CTD. Neuroscience letters 3 22507240
2002 Candidate gene analysis of KIAA0678 encoding a DnaJ-like protein for adolescent nephronophthisis and Senior-Løken syndrome type 3. Cytogenetic and genome research 3 12438707
2025 The Parkinson Disease-Associated Mutant DNAJC13(N855S) Leads to Its Accelerated Degradation and Negatively Affects Macroautophagy and Retromer Complex-Mediated Dynamics. Journal of cellular physiology 2 40717240
2023 A Conserved Requirement for RME-8/DNAJC13 in Neuronal Autolysosome Reformation. bioRxiv : the preprint server for biology 2 36909501
2025 DNAJC13 localization to endosomes is opposed by its J domain and its disordered C-terminus. Molecular biology of the cell 1 40737286
2024 DNAJC13 localization to endosomes is opposed by its J domain and its disordered C-terminal tail. bioRxiv : the preprint server for biology 0 39763938

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