Affinage

DNAJB4

DnaJ homolog subfamily B member 4 · UniProt Q9UDY4

Length
337 aa
Mass
37.8 kDa
Annotated
2026-06-09
36 papers in source corpus 25 papers cited in narrative 25 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

DNAJB4 (HLJ1) is an HSP40/DNAJ-family co-chaperone whose J-domain-dependent chaperone activity governs client-protein triage across proteostasis, tissue homeostasis, and tumor suppression (PMID:36264506, PMID:39468638). Its central biochemical function is to distinguish folded from misfolded clients: it stabilizes correctly folded proteins while routing aberrant species toward proteasomal clearance, exemplified by its direct binding to E-cadherin, where it preserves wild-type protein at the plasma membrane but drives ERAD of misfolded HDGC mutant E-cadherin (PMID:24293545). This client-triage activity depends on an intact J-domain, since loss-of-function J-domain variants produce stable proteins that fail to disaggregate TDP-43 and fail to complement DNAJB4 in yeast (PMID:39468638), and operates in concert with the HSP70 chaperone system to limit ER stress (PMID:42065820). In skeletal muscle DNAJB4 localizes to the Z-disc and is essential for myofibrillar proteostasis; loss-of-function and dominant variants cause myopathy with accumulation of Z-disc and chaperone proteins and selective fiber degeneration, establishing a direct Mendelian disease link (PMID:36264506, PMID:36512060). As a chaperone DNAJB4 also remodels the oligomeric/assembly state of partner proteins—maintaining bioactive IL-12p70 heterodimers in LPS-stimulated macrophages to amplify NK-cell IFN-γ and sepsis severity (PMID:35983991), and forming heterodimers with NPM1 that recruit AP-2alpha to repress MMP-2 and STAT3 (PMID:20145123). Across epithelial cancers DNAJB4 acts as a tumor suppressor, directly binding and inhibiting Src kinase through its Y172 and P301/P304 motifs to dismantle EGFR/FAK/STAT3 oncogenic signaling and block EMT and metastasis (PMID:27065329), and suppressing the peritumoral IL-6/STAT3 axis (PMID:39738726). Its expression is controlled by YY1 at the promoter acting synergistically with AP-1 factors (FosB, JunB, JunD) and p300 at an upstream enhancer (PMID:15782117, PMID:17510411).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2006 Medium

    Established DNAJB4/HLJ1 as a functional tumor suppressor, answering whether this chaperone has a direct role in cancer cell behavior rather than being a passive marker.

    Evidence overexpression/knockdown in CL1-5 lung cancer cells with in vivo tumorigenesis and a defined STAT1/p21 pathway readout

    PMID:16788156

    Open questions at the time
    • Molecular mechanism linking DNAJB4 chaperone activity to STAT1/p21 not defined
    • p53/interferon-independence shown but upstream trigger unknown
  2. 2005 High

    Identified the transcriptional driver of DNAJB4, showing YY1 directly activates its promoter and that this circuit controls E-cadherin and invasion.

    Evidence luciferase reporters, promoter deletion, EMSA and site-directed mutagenesis with HLJ1 siRNA epistasis

    PMID:15782117

    Open questions at the time
    • Did not address enhancer-level regulation
    • Mechanism by which DNAJB4 raises E-cadherin not resolved
  3. 2007 High

    Resolved the full regulatory architecture, showing an upstream enhancer with an AP-1 site cooperates with the YY1 promoter via p300 to amplify DNAJB4 expression.

    Evidence ChIP for in vivo FosB/JunB/JunD binding, promoter/enhancer deletion mapping and TF overexpression

    PMID:17510411

    Open questions at the time
    • Physiological signals engaging this enhancer not defined here
    • DNA-bending/synergy model not structurally confirmed
  4. 2010 Medium

    Defined a chaperone-based transcriptional control mechanism whereby DNAJB4 heterodimerizes with NPM1 to repress MMP-2 and STAT3.

    Evidence Co-IP, siRNA/overexpression and MMP-2 promoter reporter assays mapping AP-2alpha recruitment

    PMID:20145123

    Open questions at the time
    • Direct vs indirect AP-2alpha recruitment not fully resolved
    • Stoichiometry of HLJ1-NPM1 heterodimer not determined
  5. 2010 Medium

    Showed DNAJB4 is itself regulated post-translationally, being a caspase-3 substrate that promotes UV-induced apoptosis.

    Evidence caspase inhibitor rescue, mutagenesis of a non-canonical MEID cleavage site, enforced expression

    PMID:20494979

    Open questions at the time
    • Functional consequence of cleaved fragments unknown
    • Link between cleavage and chaperone activity not tested
  6. 2013 High

    Established the core client-triage chaperone function: DNAJB4 distinguishes folded from misfolded E-cadherin and mediates ERAD of mutant client.

    Evidence Drosophila genetic screen, direct Co-IP binding, proteasome inhibition and CAM tumor assay

    PMID:24293545

    Open questions at the time
    • Recognition determinants for misfolded client not defined
    • HSP70 cooperation not addressed in this study
  7. 2016 High

    Defined the direct molecular basis of DNAJB4 tumor suppression: it binds and inhibits Src kinase through specific residues, collapsing downstream oncogenic signaling.

    Evidence reciprocal Co-IP, Y172 and P301/P304 mutagenesis, KO mouse and patient specimens

    PMID:27065329

    Open questions at the time
    • Whether Src inhibition requires chaperone/J-domain activity not resolved
    • Relationship to NPM1/STAT3 axis not integrated
  8. 2022 High

    Generalized the chaperone assembly-control function to immunity, showing DNAJB4 converts misfolded IL-12p35 to enable bioactive IL-12p70 and drive IFN-γ in sepsis.

    Evidence KO mice, adoptive macrophage transfer, CLP model, scRNA-seq and chaperone assays

    PMID:35983991

    Open questions at the time
    • Structural basis of p35 remodeling not determined
    • Whether the same mechanism operates in human macrophages not shown
  9. 2022 High

    Established DNAJB4 as a Mendelian disease gene, localizing it to the muscle Z-disc and showing loss-of-function and dominant variants cause myopathy through proteostatic failure.

    Evidence exome sequencing, patient biopsies, KO and knockin mouse models, yeast complementation and disaggregation assays

    PMID:36264506 PMID:36512060

    Open questions at the time
    • Specific endogenous muscle clients of DNAJB4 not identified
    • Why type 1 fibers are selectively vulnerable unexplained
  10. 2024 Medium

    Mapped the chaperone activity to the J-domain, showing disease variants there preserve protein stability but abolish client disaggregation.

    Evidence yeast complementation and TDP-43 disaggregation assays with J-domain missense variants

    PMID:39468638

    Open questions at the time
    • HSP70 ATPase coupling by the J-domain not directly measured
    • TDP-43 used as proxy client; native clients not tested
  11. 2024 Medium

    Linked DNAJB4 to ER-stress control via HSP70, showing its loss exacerbates drug-induced liver injury through unresolved ER stress.

    Evidence Dnajb4-/- mice, Co-IP and AlphaFold-Multimer modeling of HSP70 interaction, ER-stress marker profiling

    PMID:42065820

    Open questions at the time
    • Direct HSP70 binding interface not experimentally resolved
    • Whether ER-stress effect is cell-autonomous unclear
  12. 2024 Medium

    Extended tumor suppression to the microenvironment, showing HLJ1 restrains IL-6/STAT3 signaling in peritumoral tissue.

    Evidence KO mice, DEN carcinogenesis, transcriptomics and syngeneic transplantation

    PMID:39738726

    Open questions at the time
    • Cell type mediating peritumoral STAT3 suppression not pinpointed
    • Direct DNAJB4-STAT3 molecular link not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • How DNAJB4 mechanistically reconciles its dual roles—tumor suppressor in epithelial cancers versus EMT/metastasis promoter in some breast and mesenchymal contexts—remains unresolved.
  • Context-dependent client repertoire not defined
  • No unifying structural or regulatory model for opposing phenotypes
  • Whether HSP70 partnering differs across tissues unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0044183 protein folding chaperone 4 GO:0098772 molecular function regulator activity 2 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005783 endoplasmic reticulum 2 GO:0005730 nucleolus 1 GO:0005829 cytosol 1 GO:0005856 cytoskeleton 1
Pathway
R-HSA-392499 Metabolism of proteins 3 R-HSA-1643685 Disease 2 R-HSA-162582 Signal Transduction 1 R-HSA-168256 Immune System 1 R-HSA-8953897 Cellular responses to stimuli 1
Partners
ACTBAHSA1CDH1HSPA1ANPM1OPRM1SDIM1SRC

Evidence

Reading pass · 25 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2016 HLJ1/DNAJB4 directly binds to the catalytic and protein-binding domains of Src kinase through its amino acid Y172 and the P301/P304 motif, suppressing Src catalytic activity. Src-induced phosphorylation of HLJ1 at Y172 elevates the HLJ1-Src interaction, resulting in Src inhibition. HLJ1 also downregulates formation of oncogenic complexes involving EGFR, FAK, and STAT3 signaling pathways, thereby inhibiting epithelial-mesenchymal transition and lung cancer metastasis. shRNA silencing, ectopic expression, co-immunoprecipitation, site-directed mutagenesis (Y172, P301/P304), HLJ1-knockout mouse specimens, lung cancer patient specimens Oncogene High 27065329
2013 DNAJB4 directly interacts with both wild-type (WT) and mutant E-cadherin (Ecad). Increased DNAJB4 expression stabilizes WT Ecad at the plasma membrane while inducing premature proteasomal degradation of unfolded HDGC-associated mutant Ecad (e.g., E757K), acting as a molecular mediator of endoplasmic reticulum-associated degradation (ERAD). The interaction is enhanced in the context of the unfolded mutant when proteasome degradation is inhibited. Drosophila genetic screen (DnaJ-1/Ecad interaction in vivo), co-immunoprecipitation (direct interaction), overexpression/knockdown in cells, proteasome inhibition, chick embryo chorioallantoic membrane assay Human molecular genetics High 24293545
2010 HLJ1 specifically interacts with nucleophosmin (NPM1), forming a multiprotein complex that alters the nucleolar distribution and oligomerization state of NPM1. HLJ1 prevents NPM1 oligomerization by forming HLJ1-NPM1 heterodimers, and this complex recruits the transcriptional corepressor AP-2alpha to the MMP-2 promoter, suppressing MMP-2 expression and STAT3 activity. Silencing HLJ1 accelerates NPM1 oligomerization and increases MMP-2 and STAT3 activities. Co-immunoprecipitation, overexpression, siRNA knockdown, promoter reporter assay, western blotting Cancer research Medium 20145123
2010 Under acidic extracellular pH (pHe 6.4), HLJ1 undergoes tyrosine phosphorylation, and this tyrosine-phosphorylated form of HLJ1 markedly enhances interaction with beta-actin. The association between HLJ1 and beta-actin is tyrosine phosphorylation-dependent and is linked to impaired cell migration under acidic stress. Acidic culture conditions, co-immunoprecipitation, subcellular fractionation, phosphorylation site identification, migration assay Experimental cell research Medium 20615403
2010 HLJ1 is a substrate of caspase-3 during UV-induced apoptosis, cleaved at a non-typical caspase-3 cleavage site (MEID) at amino acids 125–128. HLJ1 overexpression promotes UV-induced apoptosis by enhancing JNK and caspase-3 activation. Caspase inhibitors (zVAD-fmk, DEVD-fmk) prevent UV-induced HLJ1 degradation. Flow cytometry, caspase-specific inhibitors, site identification by mutagenesis, enforced HLJ1 expression, western blotting Nucleic acids research Medium 20494979
2006 HLJ1 inhibits lung cancer cell proliferation, anchorage-independent growth, tumorigenesis, cell motility, and invasion, and slows cell cycle progression through a STAT1/P21(WAF1) pathway that is independent of P53 and interferon. HLJ1 overexpression and knockdown in CL1-5 cells, DNA microarray, pathway analysis, western blotting, in vivo tumorigenesis assay, cell cycle analysis Journal of the National Cancer Institute Medium 16788156
2005 Transcription factor YY1 directly upregulates HLJ1 basal promoter activity by binding to YY1-binding sites within the HLJ1 promoter region (-232 to +176). YY1-driven HLJ1 upregulation increases E-cadherin expression and suppresses cancer cell invasion; these effects are reversed by HLJ1 siRNA. Luciferase reporter assay, serial promoter deletion, site-directed mutagenesis, EMSA, co-transfection, YY1 overexpression, siRNA knockdown, invasion assay Oncogene High 15782117
2007 An enhancer segment (-2125 to -1039 bp upstream of transcription start site) controls HLJ1 expression. A minimal 50-bp element (-1492 to -1443 bp) contains an AP-1 site (-1457 to -1451 bp) that binds transcription factors FosB, JunB, and JunD in vivo. YY1 at the promoter and AP-1 at the enhancer act synergistically via DNA bending and multiprotein complex formation with coactivator p300 to upregulate HLJ1 expression >5-fold and inhibit cancer cell invasion. Luciferase reporter assay, chromatin immunoprecipitation (ChIP), overexpression experiments, promoter deletion analysis, co-transfection Cancer research High 17510411
2008 Curcumin transcriptionally upregulates HLJ1 through an AP-1 site within the HLJ1 enhancer, via the JNK/JunD signaling pathway. JNK phosphorylation by curcumin leads to JunD upregulation, which drives HLJ1 expression. HLJ1 induction then upregulates E-cadherin and suppresses lung cancer cell invasion and metastasis. JNK inhibitor SP-600125 attenuates curcumin-induced JunD and HLJ1 expression. Luciferase reporter assay, siRNA knockdown, JNK inhibitor treatment, in vitro invasion assay, in vivo metastasis assay, western blotting Cancer research Medium 18794131
2022 HLJ1/DNAJB4 acts as a molecular chaperone that converts misfolded IL-12p35 homodimers to monomers in LPS-stimulated macrophages, thereby maintaining bioactive IL-12p70 heterodimerization and secretion. This promotes IFN-γ production by NK cells and amplifies sepsis severity. HLJ1-deleted macrophages adoptively transferred into LPS-treated mice reduce IL-12 and IFN-γ levels and protect from IFN-γ-dependent mortality. HLJ1 knockout mice, adoptive macrophage transfer, CLP sepsis model, single-cell RNA sequencing, IL-12 and IFN-γ measurement, functional chaperone assays eLife High 35983991
2022 DNAJB4 normally localizes to the Z-disc in skeletal muscle. Loss-of-function variants (stop gain p.Lys286Ter, missense p.Leu262Ser causing rapid degradation; missense p.Arg25Gln which is stable but functionally null) cause myopathy with early respiratory failure. DNAJB4 knockout mice develop muscle weakness, fiber atrophy, myofibrillar disorganization, and accumulation of Z-disc proteins and protein chaperones, establishing DNAJB4 as essential for skeletal muscle proteostasis. Exome sequencing, patient muscle biopsy, immunofluorescence localization, DNAJB4 KO mouse model, yeast complementation assay, protein disaggregation assay, heat shock protection assay Acta neuropathologica High 36264506
2022 A dominant heterozygous DNAJB4 variant (p.F90L) causes a distal myopathy with cytoplasmic inclusions and accumulation of desmin, p62, HSP70, and DNAJB4 predominantly in type 1 muscle fibers. Both Dnajb4(F90L) knockin and Dnajb4 knockout mice develop muscle weakness and recapitulate the muscle pathology in soleus muscle, indicating defective chaperone function leads to selective muscle degeneration. Whole-exome sequencing, patient muscle biopsy, knockin mouse model, knockout mouse model, immunofluorescence, muscle function testing Acta neuropathologica High 36512060
2006 The carboxyl-terminal portion of HLJ1 directly binds the carboxyl tail of the human mu opioid receptor (but not the third cytoplasmic loop), as demonstrated by yeast two-hybrid, in vitro overlay (His-fusion HLJ1 + GST-fusion receptor tail), and co-immunoprecipitation in HEK cell lysates. Confocal microscopy shows co-localization of HLJ1 and the mu opioid receptor at the cell membrane. Yeast two-hybrid screen, overlay assay (in vitro direct binding), co-immunoprecipitation, confocal immunofluorescence Brain research Medium 16542645
2011 SDIM1, a novel neuronal membrane protein, physically interacts with DNAJB4 (both in vitro and in vivo by yeast two-hybrid and co-immunoprecipitation). Co-overexpression of SDIM1 attenuates cell death caused by DNAJB4 overexpression in neuro-progenitor cells, suggesting SDIM1 sequesters DNAJB4 to increase cell viability. Yeast two-hybrid, co-immunoprecipitation, overexpression in neuro-progenitor cells, cell viability assay Molecular neurodegeneration Medium 21255413
2018 DNAJB4 is down-regulated in metastatic melanoma cells compared to primary melanoma cells. Overexpression of DNAJB4 suppresses invasion of melanoma cells through diminished expression and activities of MMP-2 and MMP-9. Targeted LC-MS/MS proteomics (parallel-reaction monitoring), cell invasion assay, MMP-2/MMP-9 activity assay Analytical chemistry Low 29722524
2019 DNAJB4 expression increases during epithelial-mesenchymal transition (EMT) in human mammary epithelial cells. Suppression of DNAJB4 in mesenchymal breast cancer cells decreases cell migration in vitro and reduces primary tumor growth, extravasation, and lung metastasis in vivo. Quantitative mass spectrometry proteomics, DNAJB4 knockdown, in vitro migration assay, in vivo xenograft and metastasis model Molecular & cellular proteomics : MCP Medium 31221721
2011 Hepatitis B virus (HBV) protein upregulates HLJ1 expression through the transcription factor YY1 sites within the HLJ1 promoter. YY1 expression is upregulated by HBV in a concentration-dependent manner, and knockdown of YY1 partially reduces HBV-induced HLJ1 activation. Transient and stable HBV expression in HepG2 cells, HLJ1 promoter activity assay, YY1 siRNA knockdown, western blotting Virus research Low 21345358
2024 DNAJB4/HLJ1 physically interacts with HSP70 (validated by AlphaFold-Multimer modeling and co-immunoprecipitation) and attenuates ER stress in APAP-induced liver injury. DNAJB4-deficient mice show exacerbated hepatic necrosis, elevated liver enzymes, enhanced c-jun/JNK activation, altered APAP metabolism with GSH depletion, and upregulated ER stress markers (ATF6, XBP1, CHOP). Restoration of DNAJB4 expression attenuates ER stress and liver injury. DNAJB4 KO mouse model (Dnajb4-/-), co-immunoprecipitation, AlphaFold-Multimer structural modeling, transcriptomic analysis, pharmacological ER stress inhibition, metabolic profiling Cell biology and toxicology Medium 42065820
2026 AHSA1 binds to DNAJB4 (confirmed by co-immunoprecipitation) and promotes DNAJB4 protein production. The AHSA1-DNAJB4 complex suppresses ERAD pathway activity (reducing XBP-1s, ATF4, CHOP, GADD34 expression) and promotes endometrial cancer cell colony formation and survival. Knockdown of DNAJB4 negates the pro-tumorigenic effects of AHSA1 overexpression, placing DNAJB4 downstream of AHSA1 in this ERAD regulatory axis. Co-immunoprecipitation, DNAJB4 knockdown, AHSA1 overexpression, colony formation assay, flow cytometry apoptosis assay, western blot for ERAD proteins Journal of reproductive immunology Medium 41990440
2024 DNAJB4 loss-of-function missense variants in the J-domain (p.K35N, p.R61G) produce stable proteins that fail to complement DNAJB4 function in yeast and fail to disaggregate TDP-43 client proteins, establishing the J-domain as essential for chaperone client-protein processing activity. Yeast complementation assay, TDP-43 disaggregation assay, protein stability assessment, whole-exome sequencing, patient clinical data Acta neuropathologica communications Medium 39468638
2013 Andrographolide upregulates HLJ1 via JunB activation; HLJ1 induction then modulates AP-2alpha binding at the MMP-2 promoter to repress MMP-2 expression. Silencing of HLJ1 partially reverses the inhibition of cancer cell invasion by andrographolide. Drug screening using HLJ1 promoter-enhancer reporter, siRNA knockdown, MMP-2 promoter reporter, in vitro invasion assay, in vivo tumorigenesis Carcinogenesis Low 23306212
2024 HLJ1 deficiency in mice leads to altered gene signatures enriched in IL-6/STAT3 signaling, and DEN-induced STAT3 and H2AX phosphorylation is amplified. Long-term DEN treatment in HLJ1 KO mice enhances tumor proliferation with pronounced STAT3 phosphorylation in peritumoral normal tissues. Transplantation of HLJ1-wildtype cancer cells into HLJ1-deficient mice augments tumorigenesis, confirming a tumor-suppressive role for HLJ1 in the peritumoral microenvironment via STAT3 pathway suppression. HLJ1 KO mice, DEN carcinogenesis model, whole-genome transcriptomics, syngeneic transplantation assay, phospho-STAT3 and phospho-H2AX immunostaining Cell biology and toxicology Medium 39738726
2023 DNAJB4 overexpression activates the Hippo signaling pathway in triple-negative breast cancer (TNBC) cells, promoting apoptosis. DNAJB4 knockdown suppresses Hippo pathway activity and inhibits TNBC cell apoptosis. Gain- and loss-of-function in vitro and in vivo assays, western blot for Hippo pathway components, flow cytometry apoptosis assay, xenograft model Discover oncology Low 37012515
2008 HLJ1 protein localizes to the cytoplasm of human embryonic liver cells, as determined by immunohistochemistry with validated monoclonal antibodies. Immunohistochemistry with anti-HLJ1 monoclonal antibodies on human embryonic liver tissue Sheng wu gong cheng xue bao = Chinese journal of biotechnology Low 18837411
2022 Genetic deletion of HLJ1 does not alter blood loss, activity of extrinsic and intrinsic coagulation pathways, or blood clot formation in mice, despite HLJ1 being detectable in plasma and co-localizing with CD41 (platelet/megakaryocyte marker) in bone marrow. This is a negative result establishing no role for HLJ1 in blood coagulation under normal physiological conditions. HLJ1 KO mouse (HLJ1-/-), tail bleeding assay, coagulation pathway activity tests, thromboelastography, western blot, immunohistochemistry International journal of molecular sciences Medium 35216179

Source papers

Stage 0 corpus · 36 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 Curcumin inhibits lung cancer cell invasion and metastasis through the tumor suppressor HLJ1. Cancer research 179 18794131
2006 A new tumor suppressor DnaJ-like heat shock protein, HLJ1, and survival of patients with non-small-cell lung carcinoma. Journal of the National Cancer Institute 104 16788156
2005 The transcriptional factor YY1 upregulates the novel invasion suppressor HLJ1 expression and inhibits cancer cell invasion. Oncogene 76 15782117
2007 Synergistic activation of the tumor suppressor, HLJ1, by the transcription factors YY1 and activator protein 1. Cancer research 51 17510411
2013 The HLJ1-targeting drug screening identified Chinese herb andrographolide that can suppress tumour growth and invasion in non-small-cell lung cancer. Carcinogenesis 39 23306212
2019 Systems-level Analysis Reveals Multiple Modulators of Epithelial-mesenchymal Transition and Identifies DNAJB4 and CD81 as Novel Metastasis Inducers in Breast Cancer. Molecular & cellular proteomics : MCP 38 31221721
2012 Dimethyl sulfoxide promotes the multiple functions of the tumor suppressor HLJ1 through activator protein-1 activation in NSCLC cells. PloS one 31 22529897
2018 A Targeted Proteomic Approach for Heat Shock Proteins Reveals DNAJB4 as a Suppressor for Melanoma Metastasis. Analytical chemistry 30 29722524
2011 Hepatitis B virus protein up-regulated HLJ1 expression via the transcription factor YY1 in human hepatocarcinoma cells. Virus research 30 21345358
2022 Loss of function variants in DNAJB4 cause a myopathy with early respiratory failure. Acta neuropathologica 27 36264506
2016 HLJ1 is an endogenous Src inhibitor suppressing cancer progression through dual mechanisms. Oncogene 27 27065329
2013 DNAJB4 molecular chaperone distinguishes WT from mutant E-cadherin, determining their fate in vitro and in vivo. Human molecular genetics 27 24293545
2010 HLJ1 is a novel caspase-3 substrate and its expression enhances UV-induced apoptosis in non-small cell lung carcinoma. Nucleic acids research 26 20494979
2014 Tumour suppressor HLJ1: A potential diagnostic, preventive and therapeutic target in non-small cell lung cancer. World journal of clinical oncology 22 25493224
2014 HLJ1 is a novel biomarker for colorectal carcinoma progression and overall patient survival. International journal of clinical and experimental pathology 21 24696714
2017 HLJ1 (DNAJB4) Gene Is a Novel Biomarker Candidate in Breast Cancer. Omics : a journal of integrative biology 20 28481734
2010 Tumor suppressor HLJ1 binds and functionally alters nucleophosmin via activating enhancer binding protein 2alpha complex formation. Cancer research 20 20145123
2022 HLJ1 amplifies endotoxin-induced sepsis severity by promoting IL-12 heterodimerization in macrophages. eLife 16 35983991
2022 Distinctive chaperonopathy in skeletal muscle associated with the dominant variant in DNAJB4. Acta neuropathologica 15 36512060
2010 Acidic stress facilitates tyrosine phosphorylation of HLJ1 to associate with actin cytoskeleton in lung cancer cells. Experimental cell research 13 20615403
2022 CircRNA 0009043 suppresses non-small-cell lung cancer development via targeting the miR-148a-3p/DNAJB4 axis. Biomarker research 11 35974419
2006 A member of the heat shock protein 40 family, hlj1, binds to the carboxyl tail of the human mu opioid receptor. Brain research 11 16542645
2011 A novel neuron-enriched protein SDIM1 is down regulated in Alzheimer's brains and attenuates cell death induced by DNAJB4 over-expression in neuro-progenitor cells. Molecular neurodegeneration 10 21255413
2023 DNAJB4 promotes triple-negative breast cancer cell apoptosis via activation of the Hippo signaling pathway. Discover oncology 9 37012515
2023 Human Endogenous Retrovirus-H-Derived miR-4454 Inhibits the Expression of DNAJB4 and SASH1 in Non-Muscle-Invasive Bladder Cancer. Genes 8 37510314
2023 DNAJB4 suppresses breast cancer progression and promotes tumor immunity by regulating the Hippo signaling pathway. Discover oncology 8 37548821
2024 Genotype‒phenotype correlation in recessive DNAJB4 myopathy. Acta neuropathologica communications 7 39468638
2024 Sodium Butyrate Inhibits the Malignant Proliferation of Colon Cancer Cells via the miR-183/DNAJB4 Axis. Biochemical genetics 5 38244156
2022 A pleiotropic variant in DNAJB4 is associated with multiple myeloma risk. International journal of cancer 2 36082445
2025 Homozygous DNAJB4 deletion revealing myopathy with acute respiratory failure. Revue neurologique 1 40769870
2024 Genotype-phenotype correlation in recessive DNAJB4 myopathy. Research square 1 39483874
2024 DNAJB4/HLJ1 deficiency sensitizes diethylnitrosamine-induced hepatocarcinogenesis with peritumoral STAT3 activation. Cell biology and toxicology 1 39738726
2026 AHSA1-DNAJB4 axis: A regulatory mechanism that initiates the ERAD pathway to facilitate endometrial cancer progression. Journal of reproductive immunology 0 41990440
2026 DNAJB4/HLJ1 protects against acetaminophen-induced liver injury by attenuating ER stress via HSP70. Cell biology and toxicology 0 42065820
2022 Genetic Deletion of HLJ1 Does Not Affect Blood Coagulation in Mice. International journal of molecular sciences 0 35216179
2008 [Preparation of the anti-HLJ1 monoclonal antibodies and establishment of method for detection of the antigen]. Sheng wu gong cheng xue bao = Chinese journal of biotechnology 0 18837411

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