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RNF19A

E3 ubiquitin-protein ligase RNF19A · UniProt Q9NV58

Length
838 aa
Mass
90.7 kDa
Annotated
2026-06-10
22 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RNF19A (Dorfin) is an RBR-type (RING-IBR-RING) E3 ubiquitin ligase that catalyzes substrate ubiquitination—predominantly K48-linked chains targeting substrates for proteasomal degradation—across neuronal protein quality control, innate immune signaling, DNA repair, and cancer pathways (PMID:11237715, PMID:12145308, PMID:29215004). Its catalytic core comprises two RING-finger motifs and an IBR domain that bind the ubiquitin-conjugating enzymes UbcH7 and UbcH8, and deletion of this region abolishes both E2 binding and ligase activity (PMID:11237715). RNF19A activity toward substrates such as mutant SOD1 requires direct association with the AAA-ATPase VCP/p97, which forms a large endogenous complex with RNF19A and whose ATPase activity is needed for ligase function (PMID:15456787). In neurodegeneration, RNF19A selectively binds and ubiquitylates familial ALS mutant SOD1 (but not wild-type), enhancing its clearance, reducing mitochondrial mutant SOD1, cytochrome c release, and caspase activation, and protecting motor neurons in cell and transgenic mouse models (PMID:12145308, PMID:15030390, PMID:19610091); it localizes to centrosomes and to ubiquitylated inclusion bodies across ALS, Parkinson's disease, and related disorders (PMID:11237715, PMID:12875980). RNF19A also binds the postsynaptic scaffold PSD-95, and its loss in mice alters hippocampal plasticity, neurogenesis, and contextual fear memory with a reduced brain ubiquitinome (PMID:26553645). In innate immunity, RNF19A is recruited by NLRP11 to drive K48-linked ubiquitination and degradation of TRAF6, dampening TLR-induced NF-κB/MAPK signaling (PMID:29215004), and it negatively regulates antiviral responses by degrading TBK1 and RIG-I (PMID:34990937, PMID:37480121). Across cancers, RNF19A degrades distinct substrates to opposing functional ends: it ubiquitylates BARD1 to dissociate the BRCA1-BARD1 dimer and suppress homologous recombination (PMID:34789768), degrades TRIP13 within an AR/HIF1A-driven axis (PMID:36623445), and degrades ILK, MST1, and MKP-1 to modulate AKT/mTOR, Hippo/YAP, and MAPK signaling respectively (PMID:39508245, PMID:40293542, PMID:41506118).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2001 High

    Established RNF19A as a bona fide E3 ubiquitin ligase by defining its catalytic architecture and E2 partners, answering whether the RING/IBR domains support ubiquitin transfer.

    Evidence Co-IP, domain-deletion mutagenesis, proteasome inhibition, and immunofluorescence localization

    PMID:11237715

    Open questions at the time
    • No physiological substrate identified at this stage
    • Chain-linkage specificity not defined
    • Functional consequence of centrosomal localization unknown
  2. 2002 High

    Identified mutant SOD1 as a disease-relevant substrate, showing RNF19A selectively clears misfolded proteins and rescues neuronal toxicity.

    Evidence Co-IP, in vitro ubiquitination, toxicity rescue in neural cells, and ALS tissue immunohistochemistry

    PMID:12145308

    Open questions at the time
    • Mechanism of mutant-versus-wild-type discrimination not resolved
    • In vivo relevance not yet tested at this stage
  3. 2003 Medium

    Mapped RNF19A to ubiquitylated inclusions across multiple neurodegenerative diseases, while ruling out alpha-synuclein as a direct binding partner.

    Evidence Affinity-purified antibody immunohistochemistry, double immunofluorescence, and filter trap assay

    PMID:12875980

    Open questions at the time
    • Inclusion localization is correlative, not causal
    • Substrate(s) within inclusions other than SOD1 undefined
  4. 2004 High

    Defined VCP/p97 as an obligate cofactor whose ATPase activity is required for RNF19A E3 activity, revealing the ligase operates within a large multiprotein complex.

    Evidence Mass spectrometry, glycerol gradient, direct binding, and dominant-negative VCP(K524A) functional assay

    PMID:15456787

    Open questions at the time
    • How VCP ATPase mechanistically couples to ubiquitin transfer not resolved
    • Whether VCP is required for all substrates or only SOD1 unknown
  5. 2004 Medium

    Connected substrate clearance to an organelle-level rescue, showing RNF19A reduces mitochondrial mutant SOD1 and blocks the apoptotic cascade.

    Evidence Neuronal overexpression with subcellular fractionation, cytochrome c release, and caspase activation assays

    PMID:15030390

    Open questions at the time
    • Single-lab functional readout
    • Direct mitochondrial targeting mechanism unclear
  6. 2006 High

    Extended substrate range beyond aggregation-prone proteins to a membrane receptor, showing RNF19A drives ER-associated degradation of the calcium-sensing receptor.

    Evidence Yeast two-hybrid, Co-IP, lysine mutagenesis, dominant-negative, and glycosidase/ER assays

    PMID:16513638

    Open questions at the time
    • Physiological context of CaR regulation by RNF19A not established in vivo
  7. 2006 Medium

    Demonstrated that RNF19A's substrate-binding module can be re-engineered with a more stable catalytic domain to improve mutant SOD1 clearance, mapping function to modular domains.

    Evidence Dorfin-CHIP chimeric proteins with ubiquitination, stability, aggresome, and viability readouts

    PMID:17157513

    Open questions at the time
    • Engineered tool, not endogenous mechanism
    • Single-lab cell-based assays
  8. 2009 Medium

    Linked RNF19A to the proteasome machinery and tissue-specific developmental function via interaction with Psmc3 during spermiogenesis.

    Evidence Co-IP and dynamic immunofluorescence co-localization across spermatid development

    PMID:19517565

    Open questions at the time
    • No substrate identified in acrosome biogenesis
    • Functional requirement not tested by loss-of-function
  9. 2010 Medium

    Provided in vivo proof that RNF19A overexpression mitigates ALS pathology, validating it as a therapeutic modifier of mutant SOD1 disease.

    Evidence G93A SOD1 transgenic mouse overexpression with immunoblot, phenotype scoring, and motor neuron histology

    PMID:19610091

    Open questions at the time
    • Single-lab transgenic model
    • Endogenous RNF19A loss-of-function effect on ALS not tested
  10. 2015 High

    Defined a synaptic and behavioral role through PSD-95 interaction and knockout phenotyping, establishing RNF19A as a regulator of the brain ubiquitinome and plasticity.

    Evidence Reciprocal Co-IP, knockout electrophysiology, behavior, and proteomic ubiquitinome analysis

    PMID:26553645

    Open questions at the time
    • Synaptic substrates degraded via PSD-95 association not identified
    • Mechanism linking ubiquitination to LTP/neurogenesis changes unresolved
  11. 2017 High

    Revealed RNF19A as an effector E3 in innate immunity, recruited by NLRP11 to degrade TRAF6 and restrain TLR-induced inflammation.

    Evidence Reciprocal Co-IP, K48-linkage-specific ubiquitination, dual loss-of-function, and NF-κB/MAPK/cytokine readouts

    PMID:29215004

    Open questions at the time
    • How NLRP11 directs RNF19A substrate selectivity not fully resolved
  12. 2021 High

    Uncovered a non-degradative-localization mechanism in DNA repair, where RNF19A ubiquitylation of BARD1 dissociates BRCA1-BARD1 and exports BARD1 to suppress homologous recombination.

    Evidence Co-IP, ubiquitination assay, NES mapping, fractionation, HR assay, and PARP inhibitor sensitivity

    PMID:34789768

    Open questions at the time
    • Upstream regulation of RNF19A in the DNA damage response unknown
  13. 2022 Medium

    Showed RNF19A negatively regulates RIG-I signaling by K48-linked degradation of TBK1, dampening type I interferon and antiviral responses.

    Evidence Co-IP, K48-linkage ubiquitination, siRNA knockdown, viral replication, and IFN measurements

    PMID:34990937

    Open questions at the time
    • Single-lab study
    • In vivo antiviral relevance not established here
  14. 2023 Medium

    Extended antiviral negative regulation to RIG-I itself and embedded RNF19A in an epigenetic circuit, with EZH2-mediated H3K27me3 silencing of Rnf19a relieving RIG-I suppression during JEV infection.

    Evidence ChIP-seq, EZH2 perturbation, RIG-I ubiquitination, Co-IP, and in vitro/in vivo JEV models

    PMID:37480121

    Open questions at the time
    • Direct EZH2 recruitment mechanism to the locus not detailed
    • Single-lab study
  15. 2023 Medium

    Placed RNF19A in a cancer signaling axis, identifying TRIP13 as a degradation substrate downstream of AR/HIF1A transcriptional activation in prostate cancer.

    Evidence CRISPR screen of E3 ligases, ubiquitination/quantitative proteomics, transcriptomics, and Co-IP

    PMID:36623445

    Open questions at the time
    • Direct AR/HIF1A binding to the RNF19A promoter not fully dissected
    • Single-lab study
  16. 2024 Medium

    Demonstrated tumor-suppressive function in bladder cancer through K48-linked degradation of ILK and consequent AKT/mTOR pathway inactivation.

    Evidence Co-IP, ubiquitination assay, cycloheximide chase, rescue experiments, and phospho-AKT/mTOR/S6K1 blots

    PMID:39508245

    Open questions at the time
    • Single-lab study
    • Context dependence of tumor-suppressive versus oncogenic roles unresolved
  17. 2025 Medium

    Identified MKP-1 (DUSP1) as a substrate within a ZBTB20-driven positive feedback loop activating MAPK signaling and promoting methotrexate resistance in rheumatoid arthritis synoviocytes.

    Evidence Co-IP, ubiquitination assay, fractionation, ChIP/reporter for ZBTB20, and in vivo validation

    PMID:40293542

    Open questions at the time
    • Single-lab study
    • Generalizability of the feedback loop to other tissues unknown
  18. 2026 Medium

    Showed an oncogenic role in gastric cancer via MST1 (STK4) degradation, inhibiting Hippo/YAP signaling and increasing nuclear YAP to drive growth and metastasis.

    Evidence Co-IP, in vivo ubiquitylation, half-life assay, fractionation, immunofluorescence, xenograft/metastasis models, and MST1 rescue

    PMID:41506118

    Open questions at the time
    • Single-lab study
    • Reconciliation of pro- and anti-tumor roles across cancer types unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How RNF19A achieves substrate selectivity across such diverse contexts—and what determines whether its ubiquitination drives degradation versus relocalization—remains unresolved.
  • No structural model of the RNF19A RBR catalytic mechanism in the corpus
  • Determinants of context-specific substrate engagement (adaptors like NLRP11/VCP versus direct binding) not unified
  • No reconciliation of opposing tumor-suppressive and oncogenic roles

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 6 GO:0016874 ligase activity 5
Localization
GO:0005783 endoplasmic reticulum 1 GO:0005815 microtubule organizing center 1 GO:0005886 plasma membrane 1
Pathway
R-HSA-392499 Metabolism of proteins 4 R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3 R-HSA-112316 Neuronal System 2 R-HSA-73894 DNA Repair 1
Partners
BARD1DLG4ILKNLRP11PSMC3UBE2L3UBE2L6VCP
Complex memberships
RNF19A-VCP/p97 complex

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 Dorfin/RNF19A contains two RING-finger motifs and an IBR motif at its N-terminus, binds specifically to ubiquitin-conjugating enzymes UbcH7 and UbcH8 through the RING-finger/IBR domain, and mediates ubiquitin ligase (E3) activity; partial deletion of the RING-finger/IBR domain eliminated these interactions and ubiquitination activity. Dorfin is a short-lived protein that accumulates upon proteasome inhibition. It is localized to the centrosome. Co-immunoprecipitation, domain deletion mutagenesis, proteasome inhibitor treatment (MG132), subcellular localization by immunofluorescence Biochemical and biophysical research communications High 11237715
2002 Dorfin/RNF19A physically binds and ubiquitylates mutant SOD1 proteins (from familial ALS patients) but not wild-type SOD1, enhancing their proteasomal degradation; overexpression of Dorfin protects neural cells from mutant SOD1 toxicity and reduces SOD1 inclusion bodies. Dorfin localizes to inclusion bodies in familial and sporadic ALS motor neurons. Co-immunoprecipitation, in vitro ubiquitination assay, overexpression with toxicity rescue assay, immunohistochemistry/immunofluorescence localization The Journal of biological chemistry High 12145308
2003 Dorfin/RNF19A localizes to ubiquitylated inclusions (Lewy bodies, glial cell inclusions, hyaline inclusions) in Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, and ALS, showing a distribution pattern parallel to ubiquitin. However, direct binding of alpha-synuclein to Dorfin was not detected (negative result). Immunohistochemistry with affinity-purified antibody, double immunofluorescence, filter trap assay The American journal of pathology Medium 12875980
2004 Valosin-containing protein (VCP/p97) directly binds to Dorfin/RNF19A through the C-terminal region of Dorfin, forms an endogenous ~400–600 kDa complex with Dorfin, and VCP ATPase activity is required for the E3 ubiquitin ligase activity of Dorfin toward mutant SOD1; a dominant-negative VCP(K524A) reduced Dorfin E3 activity but had no effect on Parkin autoubiquitylation. Both proteins co-localize in aggresomes and ubiquitylated inclusions in ALS and PD neurons. Mass spectrometry identification, glycerol gradient centrifugation, co-immunoprecipitation, in vitro direct binding, dominant-negative VCP functional assay, immunofluorescence co-localization The Journal of biological chemistry High 15456787
2004 Dorfin/RNF19A significantly reduces mutant SOD1 levels in mitochondria, thereby decreasing cytochrome c release and caspase cascade activation, and preventing neuronal cell death in a neuronal cell model of familial ALS. Overexpression in neuronal cell model, subcellular fractionation (mitochondrial fraction), cytochrome c release assay, caspase activation assay Journal of neurochemistry Medium 15030390
2006 Dorfin/RNF19A binds the intracellular carboxyl terminus of the calcium-sensing receptor (CaR) (identified by yeast two-hybrid and confirmed by co-immunoprecipitation), ubiquitinates CaR, and promotes its proteasomal degradation from the endoplasmic reticulum; mutation of all putative intracellular lysine residues abolished CaR ubiquitination. VCP/p97 associates with both CaR and Dorfin. A dominant-negative Dorfin fragment had opposite (stabilizing) effects on CaR. Yeast two-hybrid, co-immunoprecipitation, ubiquitination assay, dominant-negative construct, lysine mutagenesis, tunicamycin/MG132 treatment, endoglycosidase assay The Journal of biological chemistry High 16513638
2006 Dorfin-CHIP chimeric proteins containing the substrate-binding domain of Dorfin and the U-box domain of CHIP are more stable in cells than wild-type Dorfin, more effectively ubiquitylate mutant SOD1 in vivo, degrade mutant SOD1 more rapidly, reduce aggresome formation, and rescue neuronal cells from mutant SOD1 toxicity better than wild-type Dorfin. Chimeric protein engineering, in vivo ubiquitination assay, cell viability assay, aggresome quantification, pulse-chase/protein stability assay Neurobiology of disease Medium 17157513
2009 Rnf19a interacts with Psmc3, a component of the 19S regulatory cap of the 26S proteasome, in rat spermatids; during spermatid development, Rnf19a and Psmc3 are found in Golgi-derived proacrosomal vesicles, along acrosomal membranes, the acroplaxome, the marginal ring, and in the developing head-tail coupling apparatus, implicating the ubiquitin-proteasome system in acrosome biogenesis and spermatid head shaping. Co-immunoprecipitation, immunofluorescence co-localization during spermatogenesis, cDNA cloning and sequence analysis Developmental dynamics Medium 19517565
2010 Overexpression of human Dorfin/RNF19A in G93A mutant SOD1 transgenic mice decreased mutant SOD1 protein levels in spinal cord, ameliorated neurological phenotypes, and reduced motor neuron degeneration in vivo. Transgenic mouse overexpression, immunoblotting of spinal cord proteins, neurological phenotype scoring, motor neuron histology Journal of neuroscience research Medium 19610091
2015 Dorfin/RNF19A is a novel binding partner of the excitatory postsynaptic scaffolding protein PSD-95. Dorfin-knockout mice show reduced adult neurogenesis and enhanced long-term potentiation in the hippocampal dentate gyrus but normal LTP in CA1, impaired contextual fear conditioning, and decreased ubiquitination of multiple brain proteins identified by proteomics. Co-immunoprecipitation (PSD-95 interaction), knockout mouse phenotyping, electrophysiology (LTP), behavioral testing, proteomic ubiquitinome analysis Scientific reports High 26553645
2017 RNF19A is recruited by NLRP11 to catalyze K48-linked ubiquitination of TRAF6 at multiple sites, leading to proteasomal degradation of TRAF6 and attenuation of TLR signaling; deficiency of either NLRP11 or RNF19A abrogates K48-linked ubiquitination and degradation of TRAF6, promoting NF-κB and MAPK activation and increased proinflammatory cytokine production. Co-immunoprecipitation, ubiquitination assay (K48-linkage specific), siRNA/shRNA knockdown, overexpression, NF-κB/MAPK pathway readouts, cytokine measurement Nature communications High 29215004
2021 RNF19A ubiquitinates BARD1, causing dissociation of the BRCA1-BARD1 heterodimer and exposing a nuclear export sequence in BARD1 that is otherwise masked by BRCA1, resulting in cytoplasmic export of BARD1. This suppresses homologous recombination and increases cancer cell sensitivity to PARP inhibitors. Co-immunoprecipitation, ubiquitination assay, nuclear export sequence mapping, cellular fractionation, HR assay, PARP inhibitor sensitivity assay, overexpression and knockdown Nature communications High 34789768
2022 RNF19A mediates K48-linked ubiquitination and proteasomal degradation of TBK1; silencing of RNF19A enhanced type I interferon production and suppressed RNA viral replication, indicating that RNF19A acts as a negative regulator of the RIG-I signaling pathway. Co-immunoprecipitation, K48-linked ubiquitination assay, siRNA knockdown, viral replication assay, IFN production measurement Molecular immunology Medium 34990937
2023 RNF19A ubiquitinates RIG-I (DDX58), mediating its degradation and negatively regulating neuroinflammation during Japanese encephalitis virus infection; H3K27me3 modification of the Rnf19a locus (mediated by EZH2) increases upon JEV infection, downregulating Rnf19a expression and thereby relieving suppression of RIG-I. ChIP-sequencing (H3K27me3), EZH2 knockdown/inhibitor treatment, ubiquitination assay (RIG-I as substrate), co-immunoprecipitation, cytokine measurements, in vitro and in vivo JEV infection model Journal of neuroinflammation Medium 37480121
2023 RNF19A ubiquitylates TRIP13, promoting its degradation; RNF19A is transcriptionally activated by androgen receptor (AR) and HIF1A in prostate cancer cells, establishing an AR/HIF1A–RNF19A–TRIP13 signaling axis. CRISPR screening (656 E3 ligases), ubiquitination proteomic analysis, quantitative proteomics, transcriptomics, co-immunoprecipitation Drug resistance updates Medium 36623445
2024 RNF19A directly interacts with ILK (integrin-linked kinase) and promotes its K48-linked ubiquitination and proteasomal degradation, thereby inactivating the AKT/mTOR signaling pathway and suppressing bladder cancer cell proliferation, migration, and invasion. Co-immunoprecipitation, ubiquitination assay, cycloheximide chase, rescue experiments (ILK overexpression/knockdown), western blot for p-AKT/p-mTOR/p-S6K1 Biology direct Medium 39508245
2025 RNF19A promotes K48-linked ubiquitination and degradation of MKP-1 (DUSP1) in fibroblast-like synoviocytes, activating the MAPK signaling pathway; this facilitates nuclear translocation of the transcription factor ZBTB20, which in turn transcriptionally upregulates RNF19A, forming a positive feedback loop contributing to methotrexate resistance in rheumatoid arthritis. Co-immunoprecipitation, ubiquitination assay, overexpression/knockdown, western blot for MAPK pathway, nuclear/cytoplasmic fractionation, ChIP/reporter assay for ZBTB20 regulation, in vivo validation Cellular and molecular life sciences Medium 40293542
2026 RNF19A interacts with MST1 (STK4), mediates K48-linked ubiquitination of MST1 leading to its degradation, inhibiting the Hippo/YAP pathway by reducing YAP phosphorylation and increasing nuclear YAP levels, thereby promoting gastric cancer cell growth and metastasis. Co-immunoprecipitation, in vivo ubiquitylation assay, protein half-life assay, nuclear/cytoplasmic fractionation, immunofluorescence, xenograft and metastasis models, rescue by MST1 knockdown International immunopharmacology Medium 41506118

Source papers

Stage 0 corpus · 22 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Dorfin ubiquitylates mutant SOD1 and prevents mutant SOD1-mediated neurotoxicity. The Journal of biological chemistry 164 12145308
2017 NLRP11 attenuates Toll-like receptor signalling by targeting TRAF6 for degradation via the ubiquitin ligase RNF19A. Nature communications 72 29215004
2001 A novel centrosomal ring-finger protein, dorfin, mediates ubiquitin ligase activity. Biochemical and biophysical research communications 69 11237715
2004 Physical and functional interaction between Dorfin and Valosin-containing protein that are colocalized in ubiquitylated inclusions in neurodegenerative disorders. The Journal of biological chemistry 65 15456787
2006 Calcium-sensing receptor ubiquitination and degradation mediated by the E3 ubiquitin ligase dorfin. The Journal of biological chemistry 64 16513638
2009 Rnf19a, a ubiquitin protein ligase, and Psmc3, a component of the 26S proteasome, tether to the acrosome membranes and the head-tail coupling apparatus during rat spermatid development. Developmental dynamics : an official publication of the American Association of Anatomists 47 19517565
2003 Dorfin localizes to the ubiquitylated inclusions in Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, and amyotrophic lateral sclerosis. The American journal of pathology 43 12875980
2006 Dorfin-CHIP chimeric proteins potently ubiquitylate and degrade familial ALS-related mutant SOD1 proteins and reduce their cellular toxicity. Neurobiology of disease 35 17157513
2021 RNF19A-mediated ubiquitination of BARD1 prevents BRCA1/BARD1-dependent homologous recombination. Nature communications 23 34789768
2015 Mice lacking the PSD-95-interacting E3 ligase, Dorfin/Rnf19a, display reduced adult neurogenesis, enhanced long-term potentiation, and impaired contextual fear conditioning. Scientific reports 23 26553645
2004 Dorfin prevents cell death by reducing mitochondrial localizing mutant superoxide dismutase 1 in a neuronal cell model of familial amyotrophic lateral sclerosis. Journal of neurochemistry 20 15030390
2010 Dorfin ameliorates phenotypes in a transgenic mouse model of amyotrophic lateral sclerosis. Journal of neuroscience research 18 19610091
2023 CRISPR screening reveals gleason score and castration resistance related oncodriver ring finger protein 19 A (RNF19A) in prostate cancer. Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy 14 36623445
2008 Cooperative exonization of MaLR and AluJo elements contributed an alternative promoter and novel splice variants of RNF19. Gene 11 18721867
2023 LncRNA KCNQ10T1 shuttled by bone marrow mesenchymal stem cell-derived exosome inhibits sepsis via regulation of miR-154-3p/RNF19A axis. Cell and tissue research 8 37326687
2022 RNF19a inhibits antiviral immune response to RNA viruses through degradation of TBK1. Molecular immunology 7 34990937
2023 H3K27me3 of Rnf19a promotes neuroinflammatory response during Japanese encephalitis virus infection. Journal of neuroinflammation 6 37480121
2024 RNF19A inhibits bladder cancer progression by regulating ILK ubiquitination and inactivating the AKT/mTOR signalling pathway. Biology direct 3 39508245
2012 Porcine dorfin: molecular cloning of the RNF19 gene, sequence comparison, mapping and expression analysis. Molecular biology reports 3 22760261
2025 Single-cell multi-dimensional data analysis decodes RNF19A-mediated drug resistance in rheumatoid arthritis fibroblast-like synoviocytes: mechanisms and biological insights. Cellular and molecular life sciences : CMLS 1 40293542
2026 RNF19A facilitates gastric cancer progression by regulating the Hippo/YAP axis. International immunopharmacology 0 41506118
2026 RNF19A::PLAG1-rearranged uterine mesenchymal tumor with myofibroblastic features and focal adipocytic differentiation: broadening the histologic and molecular genetic spectrum of PLAG1-rearranged uterine mesenchymal neoplasms. Virchows Archiv : an international journal of pathology 0 42178368

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