Affinage

DNAJC10

Endoplasmic reticulum disulfide reductase DNAJC10 · UniProt Q8IXB1

Length
793 aa
Mass
91.1 kDa
Annotated
2026-06-09
29 papers in source corpus 24 papers cited in narrative 24 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

DNAJC10 (ERdj5) is an ER-resident protein disulfide reductase and BiP co-chaperone that couples disulfide reduction to ER quality control, secretory homeostasis, and Ca2+ regulation (PMID:18653895, PMID:19788412). It is organized as an N-terminal J domain that binds BiP in an ATP-dependent manner followed by six tandem thioredoxin domains arranged into N- and C-terminal clusters, with the C-terminal cluster forming a highly reducing platform that engages EDEM1 and reduces EDEM1-recruited misfolded substrates (PMID:12411443, PMID:21329881). Through this activity ERdj5 acts within a supramolecular ERAD complex with EDEM, BiP, and the Hrd1 component Sel1L, cleaving non-native disulfide bonds in misfolded glycoproteins and accelerating their retrotranslocation from the calnexin cycle to the dislocation channel (PMID:18653895, PMID:21329881, PMID:23363602). Its physiological role is reduction rather than isomerization of non-native disulfides, providing the reductive pathway that lets alternative PDIs compensate when ERp57 is absent (PMID:36655611). Beyond ERAD, ERdj5 reduces non-native disulfides during productive folding of clients including the LDL receptor and P23H rod opsin, and activates the SERCA2b calcium pump by reducing its luminal disulfide bond, with this activity switched off at high luminal Ca2+ through BiP-regulated oligomerization to provide feedback control of ER Ca2+ homeostasis (PMID:23769672, PMID:25055872, PMID:27694578). Conformational dynamics of the thioredoxin clusters around a flexible linker are required for efficient substrate reduction and for stepwise disaggregation of disulfide-linked oligomers in cooperation with BiP (PMID:28479060, PMID:37739037). Loss of ERdj5 disrupts Ca2+ balance and triggers Drp1-mediated mitochondrial fragmentation and senescence, sensitizes cells to PERK-dependent ER stress, and in mice causes salivary gland ER stress and a Sjögren's syndrome-like autoimmune phenotype (PMID:19788412, PMID:30967862, PMID:34728782, PMID:37496439). ERdj5 also reduces disulfide bonds of SV40 and facilitates retrotranslocation of cholera toxin CTA1, linking it to viral infection and toxin-driven immune activation (PMID:26085143, PMID:31275300).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2002 Medium

    Established that ERdj5 is an ER luminal protein and a bona fide BiP co-chaperone, defining its domain architecture and placing it in the Hsp70 chaperone cycle.

    Evidence In vitro DnaJ domain-BiP binding assay plus immunofluorescence/fractionation in cells

    PMID:12411443

    Open questions at the time
    • Enzymatic activity of the thioredoxin domains undefined
    • No substrate identified
    • BiP interaction shown in vitro only
  2. 2007 Medium

    First functional context: ERdj5 protects cells against ER stress-induced apoptosis, linking it to cell survival under proteostatic stress.

    Evidence siRNA knockdown with apoptosis readout after fenretinide in neuroectodermal tumour cells

    PMID:17353921

    Open questions at the time
    • Molecular mechanism of protection not defined
    • Single cell type
    • Does not connect to disulfide chemistry
  3. 2008 High

    Defined ERdj5's core biochemical activity as a disulfide reductase acting within an EDEM-BiP ERAD complex to accelerate retrotranslocation of misfolded substrates.

    Evidence In vitro reductase assay, reciprocal Co-IP (EDEM, BiP), siRNA with ERAD degradation readout; parallel SP-C/p97 study with HPD-motif mutant rescue

    PMID:18400946 PMID:18653895

    Open questions at the time
    • Structural basis of substrate selection unknown
    • How reduction is coordinated with dislocation channel unclear
  4. 2009 High

    Established physiological requirement in vivo and a dose-dependent influence on the UPR: reductase activity is needed for ER quality control in secretory cells, while overexpression compromises PERK/eIF2α-mediated stress signaling.

    Evidence ERdj5 knockout mice (salivary gland ER stress, mutant rescue) and overexpression studies with eIF2α phosphorylation and ER-targeted Bcl-2 rescue

    PMID:19122239 PMID:19788412

    Open questions at the time
    • Tissue specificity of salivary gland phenotype unexplained
    • Mechanistic link between ERdj5 levels and PERK not resolved
  5. 2011 High

    Solved the full-length structure and ordered the ERAD pathway, showing the C-terminal thioredoxin cluster as the reducing platform receiving EDEM1-recruited substrates en route from calnexin to BiP-mediated retrotranslocation.

    Evidence X-ray crystallography, reductase/binding assays, pulse-chase substrate tracking

    PMID:21329881

    Open questions at the time
    • Conformational behavior in solution not addressed
    • Dynamics of substrate handoff not captured by static structure
  6. 2013 Medium

    Broadened ERdj5 function beyond ERAD to productive folding and connected it to the Hrd1 complex and toxin retrotranslocation, while in-vivo trapping mapped endogenous disulfide partners.

    Evidence Mixed-disulfide trapping with LDLR folding assays; Sel1L Co-IP with CTA1 retrotranslocation; tissue disulfide-partner capture with MS validation

    PMID:23363602 PMID:23769672 PMID:24055038

    Open questions at the time
    • Full client repertoire still incomplete
    • How ERdj5 distinguishes folding from degradative reduction unclear
  7. 2013 Medium

    Demonstrated conserved cytoprotective function of the ERdj5 ortholog and an early link to mitochondrial integrity and proteotoxicity.

    Evidence RNAi in C. elegans dnj-27 disease models with aggregation, motility, and mitochondrial morphology readouts

    PMID:23641861

    Open questions at the time
    • Mechanism of mitochondrial fragmentation not defined in this model
    • Ortholog findings not yet mapped to mammalian biochemistry
  8. 2014 Medium

    Showed ERdj5 controls biogenesis of a disease-relevant client (P23H rod opsin) requiring both reductase and co-chaperone activities, with domain mutants acting as dominant negatives.

    Evidence Overexpression/shRNA with FRAP, aggregation, ER retention, and domain-mutant analysis

    PMID:25055872

    Open questions at the time
    • Single cell system
    • Whether effect translates in vivo not addressed here
  9. 2015 Medium

    Extended ERdj5 reductase activity to non-self substrates, reducing SV40 disulfides to enable ER-to-cytosol penetration and viral infection.

    Evidence siRNA, infection assays, negative-stain EM of ER-localized SV40, SV40-BAP31 Co-IP

    PMID:26085143

    Open questions at the time
    • Generality across other viruses limited
    • Cooperation with PDI not fully reconstituted
  10. 2016 High

    Defined a non-folding role in Ca2+ homeostasis: ERdj5 activates SERCA2b by reducing its luminal disulfide, with BiP- and Ca2+-dependent oligomerization providing feedback regulation.

    Evidence In vitro reductase and SERCA2b activity assays, Co-IP, Ca2+ measurement, oligomerization analysis

    PMID:27694578

    Open questions at the time
    • Structure of the oligomeric inactive state not solved
    • Quantitative thresholds in living cells not established
  11. 2017 High

    Established that conformational dynamics of the thioredoxin clusters, not a static arrangement, drive efficient reduction and substrate transfer.

    Evidence Second crystal structure, high-speed AFM single-molecule imaging, fixed-cluster mutant ERAD assays

    PMID:28479060

    Open questions at the time
    • Energetics of cluster motion unquantified
    • Coupling of dynamics to BiP cycle not mapped
  12. 2019 Medium

    Connected ERdj5 loss to organ-level pathology and immune function: knockout causes Sjögren's-like salivary autoimmunity, and ERdj5 in dendritic cells is required for cholera toxin-driven immune activation via CTA1 retrotranslocation.

    Evidence Knockout mice with histopathology/serology/saliva measurements; DC activation, immunization, and cytokine assays

    PMID:30967862 PMID:31275300

    Open questions at the time
    • Causal client(s) driving autoimmunity unidentified
    • Single-lab phenotypes
  13. 2020 Medium

    Provided in vivo proof-of-concept that restoring ERdj5 is protective, preserving photoreceptors in a P23H rhodopsin retinal degeneration model.

    Evidence AAV subretinal ERdj5 overexpression with ERG, OCT, morphometry, and rhodopsin localization

    PMID:32196553

    Open questions at the time
    • Durability and dosing not optimized
    • Mechanism inferred from earlier cell work
  14. 2021 Medium

    Mechanistically linked ERdj5 loss to mitochondrial dysfunction, showing Ca2+ imbalance activates Drp1-driven fission and senescence.

    Evidence Knockout cells with Ca2+ measurement, Drp1 activation, mitochondrial morphology, and senescence markers

    PMID:34728782

    Open questions at the time
    • Whether SERCA2b is the sole upstream node untested
    • Reversibility of senescence not addressed
  15. 2023 High

    Refined ERdj5's essential cellular role as a dedicated reductase and reconstituted its disaggregase-like cooperation with BiP on disulfide-linked oligomers.

    Evidence ERdj5/ERp57 knockout cells distinguishing reduction vs isomerization; in vitro reconstitution and single-molecule AFM of stepwise J-chain oligomer reduction with mutagenesis

    PMID:36655611 PMID:37739037

    Open questions at the time
    • In vivo relevance of disaggregation activity not established
    • Substrate specificity rules for oligomer reduction incomplete
  16. 2024 Medium

    Positioned DNAJC10 upstream of PERK in disease cells, where its loss selectively triggers PERK-eIF2α-ATF4 driven apoptosis of leukemia stem cells.

    Evidence shRNA/CRISPR in AML lines and LSCs, MLL-AF9 model in knockout mice, PERK inhibitor epistasis rescue

    PMID:37496439

    Open questions at the time
    • Why LSCs are selectively dependent unclear
    • Direct ER substrate driving PERK activation unknown
  17. 2025 Medium

    Linked DNAJC10 to UPR-controlled transcription, showing it suppresses EGFR in glioblastoma by inhibiting the IRE1α-XBP-1s axis and downstream SET7/9-mediated promoter methylation.

    Evidence Overexpression/knockdown with XBP-1s rescue, ChIP for XBP-1s and H3K4 marks, histone methylation inhibition, xenograft assays

    PMID:41191192

    Open questions at the time
    • How an ER reductase modulates IRE1α activity mechanistically unresolved
    • Single-lab, single tumor context

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ERdj5 redox state, BiP-regulated oligomerization, and conformational dynamics are integrated to differentially route a given client toward productive folding, ERAD, or Ca2+ pump activation — and which clients drive its disease phenotypes — remains unresolved.
  • Decision logic between folding vs degradation reduction unknown
  • Endogenous clients driving autoimmunity and UPR phenotypes unidentified
  • No structure of active SERCA2b-engaged or oligomeric inactive states

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016491 oxidoreductase activity 4 GO:0044183 protein folding chaperone 3 GO:0140096 catalytic activity, acting on a protein 3 GO:0098772 molecular function regulator activity 1
Localization
GO:0005783 endoplasmic reticulum 3
Pathway
R-HSA-392499 Metabolism of proteins 3 R-HSA-8953897 Cellular responses to stimuli 3 R-HSA-382551 Transport of small molecules 1
Partners
ATP2A2EDEM1ERO1HSPA5LDLRSEL1L
Complex memberships
EDEM1-BiP-ERdj5 ERAD complexHrd1/Sel1L ERAD complex

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 ERdj5 (DNAJC10) interacts with BiP via its DnaJ domain in an ATP-dependent manner, and localizes to the ER lumen; it contains DnaJ, protein-disulfide isomerase, and thioredoxin domains. In vitro binding assay (DnaJ domain-BiP interaction), immunofluorescence/subcellular fractionation for ER localization The Journal of biological chemistry Medium 12411443
2008 ERdj5 functions as a disulfide reductase that cleaves disulfide bonds of misfolded proteins in the ER, physically associates with EDEM and BiP as part of a supramolecular ERAD complex, and accelerates retrotranslocation of ERAD substrates. In vitro reductase assay, co-immunoprecipitation (ERdj5-EDEM and ERdj5-BiP), siRNA knockdown with ERAD substrate degradation readout Science (New York, N.Y.) High 18653895
2008 ERdj5 and ERdj4 associate with misfolded surfactant protein C (SP-C) and coprecipitate with p97/VCP, remaining associated until substrate dislocation to the cytosol; HPD motif mutations abolishing BiP ATPase stimulation prevent ERdj5-mediated ERAD of misfolded SP-C. Co-immunoprecipitation, siRNA knockdown with ERAD readout, dominant-negative HPD mutant rescue experiment in XBP1−/− MEFs Molecular biology of the cell High 18400946
2011 Crystal structure of full-length ERdj5 revealed an N-terminal J domain followed by six tandem thioredoxin domains organized into N- and C-terminal clusters; the C-terminal cluster forms the highly reducing platform that interacts with EDEM1 and reduces EDEM1-recruited ERAD substrates; pulse-chase experiments showed sequential substrate movement from calnexin → EDEM1-ERdj5 complex → retrotranslocation channel via BiP. X-ray crystallography, systematic biochemical analyses (reductase activity, binding assays), pulse-chase experiment Molecular cell High 21329881
2007 Knockdown of ERdj5 by RNA interference in neuroectodermal tumour cells increased the apoptotic response to fenretinide, indicating ERdj5 normally protects against ER stress-induced apoptosis in these cells. siRNA knockdown with apoptosis readout (cell viability, apoptosis assays) following fenretinide treatment British journal of cancer Medium 17353921
2009 ERdj5 overexpression sensitizes neuroblastoma cells to ER stress-induced apoptosis by abolishing eIF2α phosphorylation and inactivating PERK, thereby compromising the integrated stress response; ER-targeted Bcl-2 prevented this apoptosis, confirming ER-stress-regulated apoptosis pathway. Overexpression with ER stress inducers, phosphorylation assays (eIF2α), ER-targeted Bcl-2 rescue experiment The Journal of biological chemistry Medium 19122239
2009 ERdj5 knockout mice show activated ER stress responses specifically in salivary glands; re-expression of ERdj5 (but not thioredoxin-like motif mutants) mitigated ER stress caused by overproduction of alpha-amylase, demonstrating that ERdj5's reductase activity is required for ER quality control in secretory cells in vivo. ERdj5 knockout mouse generation and analysis, ER stress markers (qPCR/western), rescue with wild-type vs thioredoxin-motif mutant ERdj5 The Biochemical journal High 19788412
2013 ERdj5 forms mixed disulfides with multiple endogenous ER client proteins including the LDL receptor (LDLR); for LDLR, ERdj5 reduces non-native disulfides formed during productive folding (not only for ERAD), and this function requires ERdj5's interaction with BiP. Trapping of mixed disulfides (substrate trapping mutant), co-immunoprecipitation, LDLR folding assay, BiP interaction analysis Molecular cell High 23769672
2013 ERdj5 interacts directly with the Sel1L N-terminal lumenal domain, linking it to the Hrd1 ERAD complex; ERdj5 promotes CTA1 retrotranslocation partly via its J domain by regulating BiP-CTA interaction proximal to the Hrd1 complex. Co-immunoprecipitation (ERdj5-Sel1L interaction), loss-of-function and gain-of-function approaches, retrotranslocation assay Molecular biology of the cell Medium 23363602
2013 Redox partners of ERdj5 were identified from mouse epididymis tissue by combining acid quenching and thiol-alkylation to capture disulfide-linked complexes; two identified proteins were confirmed to interact with ERdj5 via intermolecular disulfide bonds in vivo. Acid quenching, thiol-alkylation, affinity purification followed by mass spectrometry, validation by western blot of disulfide-linked complexes Biochemical and biophysical research communications Medium 24055038
2013 In C. elegans, dnj-27/ERdj5 ortholog is an ER luminal protein whose expression is induced by ER stress via IRE-1/XBP-1; its knockdown increases aggregation and pathological phenotypes of Aβ, α-synuclein, and polyQ proteins, and causes mitochondrial fragmentation. RNAi knockdown in C. elegans disease models, fluorescence microscopy of protein aggregation, motility/paralysis assays, mitochondrial morphology analysis Antioxidants & redox signaling Medium 23641861
2014 ERdj5 (DNAJC10) regulates P23H rod opsin biogenesis; overexpression promoted degradation and prevented aggregation of P23H rod opsin, while shRNA knockdown delayed degradation and promoted aggregation; both reductase and co-chaperone activities of ERdj5 were required, and mutations in these domains acted as dominant negatives affecting wild-type rod opsin biogenesis. Overexpression and shRNA knockdown with fluorescence microscopy (FRAP, aggregation), domain mutant analysis including dominant negative effects, ER retention assays Human molecular genetics Medium 25055872
2015 ERdj5 reduces disulfide bonds of SV40 virus in the ER lumen, a reaction required for ER membrane transport and infection; ERdj5 cooperates with PDI to induce structural rearrangements in SV40 enabling engagement of BAP31 for membrane penetration; ERdj5 also mediates BK PyV infection. Loss-of-function (siRNA), infection assays, negative-stain electron microscopy of ER-localized SV40, co-immunoprecipitation (SV40-BAP31) Journal of virology Medium 26085143
2016 ERdj5 activates SERCA2b calcium pump function by reducing its luminal disulfide bond; at lower ER luminal Ca2+ concentrations ERdj5 is active, while higher Ca2+ induces ERdj5 oligomerization preventing SERCA2b interaction; BiP binding to the J domain of ERdj5 regulates this oligomerization, providing Ca2+-dependent feedback regulation of ER Ca2+ homeostasis. In vitro reductase activity assay, SERCA2b activity assay, co-immunoprecipitation, Ca2+ measurement, oligomerization analysis Proceedings of the National Academy of Sciences of the United States of America High 27694578
2017 A new crystal structure of ERdj5 revealed a largely different cluster arrangement relative to the original structure; high-speed atomic force microscopy showed rapid cluster movement around the flexible linker loop; ERdj5 mutants with fixed-cluster orientation compromised ERAD enhancement activity, indicating that conformational dynamics are required for efficient reduction of aberrantly formed disulfide bonds and substrate transfer. X-ray crystallography, high-speed atomic force microscopy (single-molecule observation), ERAD activity assays with fixed-cluster mutants Structure (London, England : 1993) High 28479060
2019 ERdj5 ablation in mice produces a Sjögren's syndrome-like phenotype including spontaneous inflammation in salivary glands with T and B lymphocyte infiltration, reduced saliva flow, production of anti-SSA/Ro and anti-SSB/La autoantibodies, and a distinct cytokine signature, demonstrating ERdj5 is required for salivary gland homeostasis and prevention of autoimmune inflammatory responses. ERdj5 knockout mouse model, histopathology, serological assays (ANA, cytokine profiling), saliva flow rate measurement Frontiers in immunology Medium 30967862
2019 ERdj5 in innate immune cells (particularly dendritic cells) is required for full immune activation by cholera toxin; ERdj5-knockout DCs show decreased costimulatory molecule expression (MHC II, CD80, CD86) and reduced pro-inflammatory cytokine secretion (IL-1β, TNF-α, IL-6), and ERdj5 KO mice show impaired antigen-specific IgG/IgA responses after CT immunization, specifically through CTA1 retro-translocation. ERdj5 knockout mouse model, DC activation assays (flow cytometry, ELISA), intranasal immunization with CT, cytokine profiling Frontiers in immunology Medium 31275300
2020 AAV-mediated overexpression of ERdj5 in P23H-3 rats reduced visual function loss and preserved photoreceptor cells, correlating with reduced rhodopsin retention in the outer nuclear layer, demonstrating in vivo therapeutic benefit of ERdj5 overexpression for P23H rhodopsin-mediated retinal degeneration. AAV subretinal injection, electroretinogram (ERG), optical coherence tomography, outer nuclear layer morphometry, rhodopsin immunolocalization Human molecular genetics Medium 32196553
2021 ERdj5 deletion causes intracellular Ca2+ imbalance, which activates Drp1 (a cytosolic GTPase involved in mitochondrial fission), leading to aberrant mitochondrial fragmentation and a cellular senescence phenotype, demonstrating that ERdj5-mediated Ca2+ regulation is essential for mitochondrial homeostasis. ERdj5 knockout cell lines, Ca2+ measurement, Drp1 activation assays (phosphorylation), mitochondrial morphology (fluorescence microscopy), senescence markers Scientific reports Medium 34728782
2022 ERdj5 (Dnajc10) loss in mice exacerbates alcohol-induced liver injury and promotes oxidative stress; mechanistically, ERdj5 deficiency reduces nuclear Nrf2 and downstream antioxidant gene expression, and decreases hepatic glutathione content, placing ERdj5 upstream of the Nrf2 antioxidant pathway. Dnajc10 knockout mouse (chronic-binge ethanol model), H2O2 measurement, Nrf2 nuclear fractionation/western blot, antioxidant gene expression (qRT-PCR), glutathione assay Free radical biology & medicine Medium 35390453
2023 ERdj5 and BiP cooperate in a reconstituted in vitro system to reduce disulfide-linked J-chain oligomers in a stepwise manner (large oligomers → trimers → dimers → monomers); BiP synergistically enhances ERdj5-mediated reduction in an ATP-dependent manner; single-molecule AFM showed stochastic release of small oligomers through repeated ERdj5 actions on peripheral/flexible regions of aggregates; systematic mutagenesis dissected the molecular requirements. In vitro reconstitution with purified proteins, biochemical reduction assays, high-speed atomic force microscopy (single-molecule), systematic mutagenesis The Journal of biological chemistry High 37739037
2023 ERdj5 (DNAJC10) functions specifically as a reductase (not isomerase) in ER disulfide bond processing; ERp57 is required for isomerisation of non-native disulfides in glycoproteins; ERdj5 is required to provide the reductive pathway that enables alternative PDIs to compensate for absence of ERp57, indicating ERdj5's essential cellular function is reduction of non-native disulfides. Knockout cell lines (ERdj5 and ERp57), disulfide bond formation/isomerization assays, metabolic labeling, substrate folding analysis Journal of cell science High 36655611
2024 DNAJC10 deficiency in AML specifically induces ER stress and activates the PERK-EIF2α-ATF4 branch of the UPR, leading to apoptosis of leukemia stem cells; blocking PERK (with GSK2606414 or shRNA) rescued the DNAJC10 loss-of-function phenotype both in vitro and in vivo, placing DNAJC10 upstream of PERK in the UPR. shRNA knockdown and CRISPR knockout in human AML lines and LSC-enriched populations, MLL-AF9 murine leukemia model in Dnajc10 knockout mice, PERK inhibitor rescue (GSK2606414), apoptosis assays, UPR pathway analysis Haematologica Medium 37496439
2025 DNAJC10 overexpression suppresses EGFR transcription in glioblastoma by inhibiting the IRE1α-XBP-1s axis of the UPR; XBP-1s binds the EGFR promoter and recruits SET7/9 methyltransferase, promoting H3K4me3 and H3K4me1 marks; XBP-1s overexpression reverses DNAJC10-mediated EGFR downregulation; pharmacological histone methylation inhibition attenuates XBP-1s-induced EGFR transcription. Overexpression and knockdown of DNAJC10, XBP-1s overexpression rescue, ChIP (XBP-1s binding to EGFR promoter, H3K4me3/me1), pharmacological inhibition of histone methylation, in vitro and xenograft invasion assays Molecular biomedicine Medium 41191192

Source papers

Stage 0 corpus · 29 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 ERdj5 is required as a disulfide reductase for degradation of misfolded proteins in the ER. Science (New York, N.Y.) 319 18653895
2002 ERdj5, an endoplasmic reticulum (ER)-resident protein containing DnaJ and thioredoxin domains, is expressed in secretory cells or following ER stress. The Journal of biological chemistry 155 12411443
2008 ERdj4 and ERdj5 are required for endoplasmic reticulum-associated protein degradation of misfolded surfactant protein C. Molecular biology of the cell 132 18400946
2011 Structural basis of an ERAD pathway mediated by the ER-resident protein disulfide reductase ERdj5. Molecular cell 117 21329881
2013 ERdj5 is the ER reductase that catalyzes the removal of non-native disulfides and correct folding of the LDL receptor. Molecular cell 110 23769672
2007 Targeting homeostatic mechanisms of endoplasmic reticulum stress to increase susceptibility of cancer cells to fenretinide-induced apoptosis: the role of stress proteins ERdj5 and ERp57. British journal of cancer 104 17353921
2016 Redox-assisted regulation of Ca2+ homeostasis in the endoplasmic reticulum by disulfide reductase ERdj5. Proceedings of the National Academy of Sciences of the United States of America 86 27694578
2013 Protective role of DNJ-27/ERdj5 in Caenorhabditis elegans models of human neurodegenerative diseases. Antioxidants & redox signaling 50 23641861
2015 ERdj5 Reductase Cooperates with Protein Disulfide Isomerase To Promote Simian Virus 40 Endoplasmic Reticulum Membrane Translocation. Journal of virology 40 26085143
2009 Positive contribution of ERdj5/JPDI to endoplasmic reticulum protein quality control in the salivary gland. The Biochemical journal 39 19788412
2013 The ERdj5-Sel1L complex facilitates cholera toxin retrotranslocation. Molecular biology of the cell 36 23363602
2009 ERdj5 sensitizes neuroblastoma cells to endoplasmic reticulum stress-induced apoptosis. The Journal of biological chemistry 34 19122239
2017 The Highly Dynamic Nature of ERdj5 Is Key to Efficient Elimination of Aberrant Protein Oligomers through ER-Associated Degradation. Structure (London, England : 1993) 25 28479060
2014 The co-chaperone and reductase ERdj5 facilitates rod opsin biogenesis and quality control. Human molecular genetics 25 25055872
2019 Ablation of the Chaperone Protein ERdj5 Results in a Sjögren's Syndrome-Like Phenotype in Mice, Consistent With an Upregulated Unfolded Protein Response in Human Patients. Frontiers in immunology 18 30967862
2019 Upregulation of JHDM1D-AS1 protects PDLSCs from H2O2-induced apoptosis by decreasing DNAJC10 via phosphorylation of eIF2α. Biochimie 18 31276733
2013 Identification of the redox partners of ERdj5/JPDI, a PDI family member, from an animal tissue. Biochemical and biophysical research communications 13 24055038
2022 Loss of ERdj5 exacerbates oxidative stress in mice with alcoholic liver disease via suppressing Nrf2. Free radical biology & medicine 12 35390453
2017 A genome-wide association analysis identifies PDE1A|DNAJC10 locus on chromosome 2 associated with idiopathic pulmonary arterial hypertension in a Japanese population. Oncotarget 11 29088834
2024 DNAJC10 maintains survival and self-renewal of leukemia stem cells through PERK branch of the unfolded protein response. Haematologica 10 37496439
2020 AAV-mediated ERdj5 overexpression protects against P23H rhodopsin toxicity. Human molecular genetics 10 32196553
2023 Distinct role of ERp57 and ERdj5 as a disulfide isomerase and reductase during ER protein folding. Journal of cell science 9 36655611
2023 ERdj5 protects goblet cells from endoplasmic reticulum stress-mediated apoptosis under inflammatory conditions. Experimental & molecular medicine 9 36759578
2023 Mechanistic characterization of disulfide bond reduction of an ERAD substrate mediated by cooperation between ERdj5 and BiP. The Journal of biological chemistry 9 37739037
2021 Deregulation of the Kallikrein Protease Family in the Salivary Glands of the Sjögren's Syndrome ERdj5 Knockout Mouse Model. Frontiers in immunology 9 34305928
2019 ERdj5 in Innate Immune Cells Is a Crucial Factor for the Mucosal Adjuvanticity of Cholera Toxin. Frontiers in immunology 7 31275300
2021 Ca2+ imbalance caused by ERdj5 deletion affects mitochondrial fragmentation. Scientific reports 6 34728782
2024 MCM8 promotes lung cancer progression through upregulating DNAJC10. Journal of cellular and molecular medicine 1 39031896
2025 Endoplasmic reticulum-resident protein DNAJC10 inhibits glioblastoma metastasis by suppressing XBP-1s-driven EGFR transcription. Molecular biomedicine 0 41191192

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