Affinage

PRPF19

Pre-mRNA-processing factor 19 · UniProt Q9UMS4

Length
504 aa
Mass
55.2 kDa
Annotated
2026-04-28
50 papers in source corpus 20 papers cited in narrative 20 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PRPF19 is a U-box E3 ubiquitin ligase that functions as a homotetrameric core of the nineteen complex (NTC), linking pre-mRNA splicing to DNA damage repair and targeted protein degradation. As a spliceosomal factor, PRPF19 oligomerization is essential for spliceosome assembly and catalytic activity; its autoinhibited E3 ligase is allosterically activated by stepwise incorporation of SPF27, CDC5L, and PLRG1, and it promotes tri-snRNP integrity by facilitating PRPF3–PRPF8 interaction, thereby controlling alternative splicing events such as the MDM4 exon 6 inclusion that restrains p53 activation (PMID:29547724, PMID:34144037, PMID:16332694). In DNA damage responses, PRPF19 binds double-stranded DNA, recruits ATRIP to RPA-coated ssDNA to activate ATR–CHK1 signaling, cooperates with WRN helicase for interstrand cross-link repair, and promotes homologous recombination, with ATM-dependent phosphorylation at S149 conferring resistance to oxidative stress-induced apoptosis (PMID:12960389, PMID:24443570, PMID:16223718, PMID:22529335, PMID:24675077). Beyond its NTC roles, PRPF19 acts as a substrate recognition receptor for CRL4B complexes and independently ubiquitinates diverse targets—including SARS-CoV-2 ORF6, VDR, MYL9, and ATXN3-polyQ—directing them to proteasomal or autophagic degradation (PMID:38265236, PMID:40414879, PMID:37031206, PMID:33542212).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1996 High

    Establishing that PSO4 and PRP19 are the same gene resolved the paradox of how a spliceosome factor could also confer sensitivity to DNA cross-linking agents, placing PRPF19 at the intersection of splicing and repair.

    Evidence Genetic complementation and gene disruption in S. cerevisiae with multiple phenotypic readouts

    PMID:8918805

    Open questions at the time
    • Mechanism linking splicing to DNA repair not determined
    • No biochemical activity assigned
  2. 2003 High

    Demonstrating that human PRPF19 directly binds dsDNA and that its depletion causes DSB accumulation established a direct mammalian DNA repair function independent of splicing.

    Evidence Purified protein DNA-binding assay, siRNA knockdown, comet assay in human cells

    PMID:12960389

    Open questions at the time
    • Repair pathway(s) involved not specified
    • Enzymatic mechanism of repair contribution unknown
  3. 2005 High

    Three concurrent studies defined the PRPF19 complex composition (Cdc5L, Plrg1, Spf27), established its requirement for interstrand cross-link processing via WRN helicase, demonstrated that homo-oligomerization is essential for spliceosome assembly, and identified E3 ubiquitin ligase activity with proteasome association.

    Evidence In vitro ICL processing reconstitution with WRN mutagenesis; immunodepletion/splicing assay with domain mapping; Co-IP of PSMB4 with in vitro E3 ligase assay

    PMID:15660529 PMID:16223718 PMID:16332694

    Open questions at the time
    • Substrates of E3 ligase activity unidentified
    • Whether E3 activity is required for splicing or repair not resolved
    • Structural basis of autoinhibition unknown
  4. 2007 Medium

    Finding that DNA damage induces a ubiquitylated oligomeric form of PRPF19 that dissociates from CDC5L/PLRG1 suggested damage-triggered remodeling of the NTC, linking E3 activity to the DNA damage response.

    Evidence Non-reducing SDS-PAGE, chromatin fractionation, Co-IP after genotoxic stress in human cells

    PMID:17276391

    Open questions at the time
    • Thiolester linkage between Ub and Cys not confirmed by mutagenesis
    • Functional consequence of NTC remodeling not established
    • Single lab observation
  5. 2008 High

    Identification of PRPF19 as the DNA-binding and recruitment platform for Metnase at DSB sites established a mechanism by which PRPF19 facilitates DNA end joining.

    Evidence Co-IP, siRNA knockdown abolishing Metnase localization and end-joining activity, immunofluorescence after IR

    PMID:18263876

    Open questions at the time
    • Whether Metnase interaction is relevant outside NHEJ not tested
    • Stoichiometry of the complex on chromatin unknown
  6. 2012 Medium

    Identification of ATM-dependent S149 phosphorylation provided the first post-translational modification linking PRPF19 to the canonical DNA damage kinase cascade and explaining its anti-apoptotic function under oxidative stress.

    Evidence Mass spectrometry site identification, ATM inhibitor, phospho-dead mutant overexpression with apoptosis and lifespan assays

    PMID:22529335

    Open questions at the time
    • Downstream effectors of pS149 unknown
    • Whether S149 phosphorylation affects E3 ligase or splicing activity not tested
  7. 2014 High

    Two studies established PRPF19's role in ATR–CHK1 checkpoint signaling—via RPA interaction and ATRIP recruitment requiring its E3 activity—and in homologous recombination, resolving how it contributes to both damage sensing and repair.

    Evidence Co-IP with RPA, siRNA KD impairing CHK1/RPA2 phosphorylation and ATRIP foci; HR reporter assay, PARP inhibitor sensitivity, cell cycle analysis

    PMID:24443570 PMID:24675077

    Open questions at the time
    • Direct ubiquitination substrate at damage sites not identified
    • Whether splicing defects contribute to observed DDR phenotypes not fully excluded
  8. 2018 High

    Structural determination of the autoinhibited PRPF19 tetramer and its stepwise activation by SPF27→CDC5L→PLRG1 resolved the molecular mechanism of NTC assembly and E3 ligase regulation, revealing that PLRG1 binding is the final allosteric trigger.

    Evidence Crystal structure, cryo-EM/SAXS, crosslinking mass spectrometry, mutagenesis, in vitro ubiquitin ligation reconstitution

    PMID:29547724

    Open questions at the time
    • Physiological substrates ubiquitinated by the fully assembled NTC not identified
    • Structural basis of how E3 activity contributes to spliceosome catalysis unknown
  9. 2021 High

    Demonstrating that PRPF19 controls MDM4 alternative splicing by promoting PRPF3–PRPF8 interaction connected its spliceosomal role to a specific p53-regulatory circuit, while parallel work identified mutant ATXN3-polyQ as a direct ubiquitination substrate modulated by Exo70.

    Evidence siRNA KD with RNA-seq and RT-PCR for MDM4 splicing; Co-IP of PRPF3–PRPF8; ubiquitination assay for ATXN3-polyQ in mammalian and Drosophila models

    PMID:33542212 PMID:34144037

    Open questions at the time
    • Full spectrum of PRPF19-dependent alternative splicing events not catalogued
    • Mechanism by which Exo70 antagonizes E3 activity structurally undefined
  10. 2022 Medium

    Discovery that PRPF19 recruits the E3 ligase MARCH8 to PEDV nucleocapsid for ubiquitination and NDP52-mediated selective autophagy revealed a non-NTC antiviral mechanism operating through autophagy rather than the proteasome.

    Evidence Co-IP, ubiquitination assay, autophagy flux assay, siRNA knockdown in PEDV-infected cells

    PMID:36541804

    Open questions at the time
    • Whether PRPF19 recruits MARCH8 to other viral substrates unknown
    • Direct binding between PRPF19 and MARCH8 not structurally characterized
  11. 2023 Medium

    Identification of MYL9 as a K63-linked ubiquitination substrate of PRPF19 that activates Src–YAP1 signaling established a non-degradative ubiquitin-signaling role promoting cancer cell invasion.

    Evidence K63-specific ubiquitination assay, gain/loss-of-function, migration/invasion assays in colorectal cancer cells

    PMID:37031206

    Open questions at the time
    • Whether K63 ubiquitination of MYL9 is direct or requires NTC cofactors not resolved
    • In vivo tumor model validation absent
  12. 2024 Medium

    Demonstrating that PRPF19 serves as a substrate receptor for a CRL4B complex targeting SARS-CoV-2 ORF6 for degradation revealed a second E3 ligase paradigm—adapter within a cullin–RING complex—distinct from its intrinsic U-box activity.

    Evidence Pulldown, Co-IP, ubiquitination assay, viral replication assay, mouse infection model

    PMID:38265236

    Open questions at the time
    • Whether CRL4B-adapter function extends to endogenous cellular substrates beyond VDR not systematically tested
    • Structural basis of CUL4B–DDB1–PRPF19 assembly unknown
  13. 2025 Medium

    Identification of VDR as a PRPF19 ubiquitination substrate linked PRPF19 to ferroptosis regulation in diabetic nephropathy via GPX4 downregulation, expanding its substrate repertoire to nuclear receptors.

    Evidence Proteomics, ubiquitination assay, VDR knockout, SPR and molecular docking for berberine as inhibitor

    PMID:40414879

    Open questions at the time
    • Whether VDR ubiquitination uses the intrinsic U-box or CRL4B adapter mode not determined
    • Berberine specificity for PRPF19 over other E3 ligases not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include how PRPF19 partitions between its splicing, DNA repair, and substrate-degradation functions in vivo; whether its E3 ligase activity within the NTC has distinct substrates from its CRL4B-adapter activity; and what structural transitions underlie the damage-induced NTC remodeling.
  • No systematic substrate screen for NTC-associated E3 activity performed
  • Structural basis of damage-induced NTC disassembly unresolved
  • Relative contribution of splicing-dependent vs. splicing-independent roles in DDR phenotypes not dissected

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016874 ligase activity 6 GO:0140096 catalytic activity, acting on a protein 6 GO:0003677 DNA binding 3 GO:0060090 molecular adaptor activity 2
Localization
GO:0005634 nucleus 4 GO:0005694 chromosome 3
Pathway
R-HSA-392499 Metabolism of proteins 6 R-HSA-73894 DNA Repair 6 R-HSA-8953854 Metabolism of RNA 4 R-HSA-5357801 Programmed Cell Death 3 R-HSA-168256 Immune System 2 R-HSA-9612973 Autophagy 1
Partners
CDC5LEXOC7PLRG1PSMB4RPA1SETMARSPF27WRN
Complex memberships
CRL4B complex (CUL4B–DDB1–RBX1–PRPF19)NTC/Prp19 complex (PRPF19–CDC5L–PLRG1–SPF27)

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 PSO4 is allelic to PRP19 in S. cerevisiae, encoding a spliceosome-associated protein essential for viability; loss-of-function causes sensitivity to DNA cross-linking agents, blocked sporulation, and reduced mutagenesis, placing PSO4/PRP19 at the intersection of pre-mRNA splicing and DNA repair pathways Genetic complementation, gene disruption, sequence analysis Nucleic acids research High 8918805
2003 Human Pso4 (hPso4/PRPF19) binds double-stranded DNA in a sequence-nonspecific manner (but not single-stranded DNA), is induced by gamma radiation and chemical mutagens, and its loss via siRNA causes accumulation of DNA double-strand breaks and apoptosis, establishing a direct role in mammalian DSB repair DNA binding assay (purified protein), siRNA knockdown, comet assay, cell survival assay Proceedings of the National Academy of Sciences of the United States of America High 12960389
2005 The Pso4/Prp19 complex (composed of Pso4/Prp19, Cdc5L, Plrg1, and Spf27) is required for processing of DNA interstrand cross-links in vitro, and interacts physically with WRN helicase through a direct association between WRN and Cdc5L; WRN helicase activity (but not exonuclease activity) is required for ICL processing Biochemical ICL processing assay (in vitro), co-immunoprecipitation, pulldown, mutagenesis of WRN The Journal of biological chemistry High 16223718
2005 SNEV/PRPF19 is the human ortholog of yeast Prp19; its homo-oligomerization (self-interaction domain mapped to amino acids 56–74) is essential for spliceosome assembly and stability, as demonstrated by immunodepletion from HeLa nuclear extracts abolishing in vitro splicing and synthetic peptides from the self-interaction domain inhibiting spliceosome formation Immunodepletion of nuclear extracts, in vitro splicing assay, yeast complementation, synthetic peptide inhibition, mapping of self-interaction domain Nucleic acids research High 16332694
2005 SNEV/PRPF19 associates with the proteasome by directly binding the beta7 subunit (PSMB4) of the 20S proteasome; SNEV exhibits E3 ligase activity in vivo and escorts ubiquitinated substrates to the proteasome, with co-localization increasing upon proteasome inhibition Co-immunoprecipitation, immunofluorescence co-localization, in vitro E3 ligase assay The Biochemical journal High 15660529
2007 hPrp19 forms a ubiquitylated oligomeric species (likely via thiolester between ubiquitin and a cysteine residue) that is enhanced by DNA damage; ubiquitylated hPrp19 fails to interact with Cdc5L or Plrg1, indicating DNA damage induces structural alterations to the Prp19 core complex; overexpression of hPrp19 reduces apoptosis after DNA damage SDS-PAGE under non-reducing conditions, chromatin fractionation, co-immunoprecipitation, overexpression/apoptosis assay Biochemical and biophysical research communications Medium 17276391
2008 hPso4/PRPF19 forms a stable complex with Metnase (SETMAR) on both TIR and non-TIR DNA; hPso4 is required to localize Metnase to DSB sites after ionizing radiation; hPso4 depletion abolishes Metnase-mediated stimulation of DNA end joining coupled to genomic integration Co-immunoprecipitation, siRNA knockdown, immunofluorescence colocalization, DNA end-joining assay The Journal of biological chemistry High 18263876
2010 In the Metnase-hPso4 complex, hPso4 is solely responsible for DNA binding; hPso4 negatively regulates Metnase's TIR-specific DNA binding activity, and Metnase's DNA binding is not required for formation of the Metnase-hPso4-DNA complex; the complex is competitively inhibited by both TIR and non-TIR DNA Electrophoretic mobility shift assay, stoichiometric analysis, competition assay Archives of biochemistry and biophysics Medium 20416268
2011 Exo70 (a subunit of the exocyst complex) directly interacts with SNEV/PRPF19 via its N-terminal 100 amino acids, shuttles to the nucleus, associates with the spliceosome, and addition of Exo70 N-terminal peptides inhibits pre-mRNA splicing in vitro; Exo70 influences splice site selection in vivo Co-immunoprecipitation, pulldown, in vitro splicing assay, minigene splicing assay, immunofluorescence The Biochemical journal Medium 21639856
2012 SNEV/PRPF19 is phosphorylated at S149 in an ATM-dependent manner in response to oxidative stress and DSB-inducing agents; S149 phosphorylation is necessary for resistance to apoptosis upon oxidative stress and is partially required for cellular lifespan extension Mass spectrometry (phosphorylation site identification), ATM inhibition, phosphorylation-deficient point-mutant overexpression, apoptosis assay, lifespan assay Aging Medium 22529335
2014 Both BCAS2 and PSO4 subunits of the PSO4 core complex directly interact and colocalize with RPA; depletion of BCAS2 or PSO4 impairs ATRIP recruitment to DNA damage sites and compromises CHK1 activation and RPA2 phosphorylation; the RPA1-binding ability of BCAS2 and E3 ligase activity of PSO4 are both required for efficient ATRIP accumulation and downstream ATR signaling Co-immunoprecipitation, immunofluorescence, siRNA knockdown, CHK1/RPA2 phosphorylation assay, domain mutagenesis The Journal of biological chemistry High 24443570
2014 The hPso4 complex is required for timely S-phase progression, G2/M checkpoint transition, and repair of DSBs by homologous recombination; hPso4 depletion delays replication restart after hydroxyurea-induced fork stalling, reduces BRCA1 levels, and decreases ssDNA generation at DSBs siRNA knockdown, flow cytometry (cell cycle), γ-H2AX assay, hydroxyurea treatment, PARP inhibitor sensitivity, HR reporter assay The Journal of biological chemistry Medium 24675077
2018 Prp19/PRPF19 is autoinhibited as a homotetramer; stepwise assembly of SPF27, CDC5L, and PLRG1 onto the Prp19 tetramer activates its E3 ubiquitin ligase activity; the elongated coiled coils of Prp19 serve as the assembly axis for SPF27 and CDC5L; communication between PLRG1 and Prp19 enables E3 activity Crystal structure, cryo-EM/SAXS, mutagenesis, in vitro ubiquitin ligation assay, protein crosslinking mass spectrometry Molecular cell High 29547724
2021 PRPF19 knockdown causes a switch in MDM4 splicing from the stable full-length MDM4-FL to the unstable MDM4-S isoform (lacking exon 6), activating p53-p21 pathway and inducing cellular senescence; PRPF19 promotes MDM4 full-length splicing by facilitating physical interaction between splicing factors PRPF3 and PRPF8 (components of U4/U6.U5 tri-snRNP) siRNA knockdown, RNA-sequencing, RT-PCR, co-immunoprecipitation, western blot, cell cycle analysis The Journal of biological chemistry High 34144037
2021 Prpf19 promotes poly-ubiquitination and proteasomal degradation of mutant ATXN3-polyQ protein; nuclear localization of Prpf19 is essential for this modulatory function; Exoc7/Exo70 interacts with Prpf19 and antagonizes its E3 ligase function toward ATXN3-polyQ Overexpression/knockdown in mammalian and Drosophila models, ubiquitination assay, immunofluorescence (nuclear localization), co-immunoprecipitation Cell death & disease Medium 33542212
2022 PRPF19 recruits E3 ubiquitin ligase MARCH8 to the PEDV N (capsid) protein for ubiquitination; the ubiquitinated N protein is recognized by cargo receptor NDP52 and transported to autolysosomes for selective autophagy-mediated degradation, thereby inhibiting PEDV replication Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, overexpression, autophagy flux assay Journal of virology Medium 36541804
2023 PRPF19 ubiquitinates MYL9 via K63-linked ubiquitination, enhancing MYL9 stability; the PRPF19/MYL9 axis activates the Src-YAP1 signaling cascade to promote colorectal cancer cell migration and invasion Co-immunoprecipitation, ubiquitination assay (K63-specific), gain/loss-of-function assays, migration/invasion assays Cell death & disease Medium 37031206
2024 PRPF19 functions as a substrate recognition receptor for a CRL4B E3 ligase complex (with CUL4B, DDB1, RBX1) that catalyzes ubiquitination and proteasomal degradation of SARS-CoV-2 ORF6; PRPF19 overexpression promotes ORF6 degradation, releases ORF6-mediated IFN inhibition, and inhibits SARS-CoV-2 replication Pulldown (identifying interacting partners), co-immunoprecipitation, ubiquitination assay, overexpression, viral replication assay, mouse infection model mBio Medium 38265236
2025 PRPF19 mediates ubiquitination and proteasomal degradation of VDR (vitamin D receptor); loss of VDR reduces GPX4 expression and promotes ferroptosis in renal tubular epithelial cells in diabetic nephropathy; berberine identified as a PRPF19 inhibitor by molecular docking, affinity bead technology, and surface plasmon resonance Proteomics, luciferase reporter assay, chromatin immunoprecipitation, ubiquitination assay, VDR knockout, SPR, molecular docking Cell communication and signaling : CCS Medium 40414879
2024 The 5' UTR of PRPF19 mRNA contains an upstream open reading frame (uORF) that is translated in human cells; inactivation of this uORF reduces cell viability, indicating the microprotein or uORF regulatory function is important for cell survival Ribosome profiling data analysis, uORF inactivation, cell viability assay Doklady. Biochemistry and biophysics Low 38472668

Source papers

Stage 0 corpus · 50 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 The Pso4 mRNA splicing and DNA repair complex interacts with WRN for processing of DNA interstrand cross-links. The Journal of biological chemistry 112 16223718
2003 Role of human Pso4 in mammalian DNA repair and association with terminal deoxynucleotidyl transferase. Proceedings of the National Academy of Sciences of the United States of America 94 12960389
2008 Human Pso4 is a metnase (SETMAR)-binding partner that regulates metnase function in DNA repair. The Journal of biological chemistry 68 18263876
2007 The Prp19/Pso4 core complex undergoes ubiquitylation and structural alterations in response to DNA damage. Biochemical and biophysical research communications 58 17276391
2006 SNEV overexpression extends the life span of human endothelial cells. Experimental cell research 56 16388800
1996 Allelism of PSO4 and PRP19 links pre-mRNA processing with recombination and error-prone DNA repair in Saccharomyces cerevisiae. Nucleic acids research 56 8918805
1989 PSO4: a novel gene involved in error-prone repair in Saccharomyces cerevisiae. Mutation research 55 2671705
2005 Interaction of U-box E3 ligase SNEV with PSMB4, the beta7 subunit of the 20 S proteasome. The Biochemical journal 52 15660529
2014 The PSO4 protein complex associates with replication protein A (RPA) and modulates the activation of ataxia telangiectasia-mutated and Rad3-related (ATR). The Journal of biological chemistry 51 24443570
2005 SNEV is an evolutionarily conserved splicing factor whose oligomerization is necessary for spliceosome assembly. Nucleic acids research 44 16332694
2007 Early embryonic lethality of mice lacking the essential protein SNEV. Molecular and cellular biology 40 17283042
2018 Prp19/Pso4 Is an Autoinhibited Ubiquitin Ligase Activated by Stepwise Assembly of Three Splicing Factors. Molecular cell 37 29547724
2023 Comprehensive analysis of PRPF19 immune infiltrates, DNA methylation, senescence-associated secretory phenotype and ceRNA network in bladder cancer. Frontiers in immunology 36 38022515
1989 The PSO4 gene is responsible for an error-prone recombinational DNA repair pathway in Saccharomyces cerevisiae. Molecular & general genetics : MGG 36 2671661
2021 PRPF19 regulates p53-dependent cellular senescence by modulating alternative splicing of MDM4 mRNA. The Journal of biological chemistry 35 34144037
2015 hPso4/hPrp19: a critical component of DNA repair and DNA damage checkpoint complexes. Oncogene 31 26364595
2014 The role of the human psoralen 4 (hPso4) protein complex in replication stress and homologous recombination. The Journal of biological chemistry 21 24675077
2012 ATM-dependent phosphorylation of SNEVhPrp19/hPso4 is involved in extending cellular life span and suppression of apoptosis. Aging 21 22529335
2022 PRPF19 Limits Porcine Epidemic Diarrhea Virus Replication through Targeting and Degrading Viral Capsid Protein. Journal of virology 20 36541804
2011 Exo70, a subunit of the exocyst complex, interacts with SNEV(hPrp19/hPso4) and is involved in pre-mRNA splicing. The Biochemical journal 19 21639856
2021 PRPF19 promotes tongue cancer growth and chemoradiotherapy resistance. Acta biochimica et biophysica Sinica 15 33954334
2009 Blom7alpha is a novel heterogeneous nuclear ribonucleoprotein K homology domain protein involved in pre-mRNA splicing that interacts with SNEVPrp19-Pso4. The Journal of biological chemistry 15 19641227
1996 Further characterization of the yeast pso4-1 mutant: interaction with rad51 and rad52 mutants after photoinduced psoralen lesions. Current genetics 15 8595666
2010 Regulation of Metnase's TIR binding activity by its binding partner, Pso4. Archives of biochemistry and biophysics 14 20416268
2002 Thermoconditional modulation of the pleiotropic sensitivity phenotype by the Saccharomyces cerevisiae PRP19 mutant allele pso4-1. Nucleic acids research 14 12434004
2024 CRL4B E3 ligase recruited by PRPF19 inhibits SARS-CoV-2 infection by targeting ORF6 for ubiquitin-dependent degradation. mBio 13 38265236
2023 PRPF19 facilitates colorectal cancer liver metastasis through activation of the Src-YAP1 pathway via K63-linked ubiquitination of MYL9. Cell death & disease 13 37031206
2022 An Integrated Analysis of the Identified PRPF19 as an Onco-immunological Biomarker Encompassing the Tumor Microenvironment, Disease Progression, and Prognoses in Hepatocellular Carcinoma. Frontiers in cell and developmental biology 12 35252202
1992 The pso4-1 mutation reduces spontaneous mitotic gene conversion and reciprocal recombination in Saccharomyces cerevisiae. Molecular & general genetics : MGG 12 1465105
1994 The E. coli recA gene can restore the defect in mutagenesis of the pso4-1 mutant of S. cerevisiae. Mutation research 11 7513054
2021 A fine balance between Prpf19 and Exoc7 in achieving degradation of aggregated protein and suppression of cell death in spinocerebellar ataxia type 3. Cell death & disease 10 33542212
1995 The PSO4 gene of S. cerevisiae is important for sporulation and the meiotic DNA repair of photoactivated psoralen lesions. Current genetics 10 7736603
2021 BTK, NUTM2A, and PRPF19 Are Novel KMT2A Partner Genes in Childhood Acute Leukemia. Biomedicines 9 34440129
2016 SNEVhPrp19/hPso4 Regulates Adipogenesis of Human Adipose Stromal Cells. Stem cell reports 9 28041875
1991 Analysis of bleomycin-induced mutagenic functions related to the PSO4 (= xs9) gene of Saccharomyces cerevisiae. Environmental and molecular mutagenesis 8 1715270
2005 Establishment of a strategy for the rapid generation of a monoclonal antibody against the human protein SNEV (hNMP200) by flow-cytometric cell sorting. Journal of immunological methods 7 16289093
2023 Report of PRPF19 as a novel partner of RARG and the recurrence of interposition-type fusion in variant acute promyelocytic leukemia. Hematological oncology 6 37132198
2016 SNEV(Prp19/PSO4) deficiency increases PUVA-induced senescence in mouse skin. Experimental dermatology 6 26663487
2025 Deucravacitinib in plaque psoriasis: Safety and efficacy through 3 years in Japanese patients in the phase 3 POETYK PSO-1, PSO-4, and LTE trials. The Journal of dermatology 4 40066907
2025 Deucravacitinib, an Oral, Selective, Allosteric Tyrosine Kinase 2 Inhibitor, in Japanese Patients With Plaque Psoriasis: In-Depth Analysis of Efficacy and Safety in the Phase 3 POETYK PSO-4 Trial. The Journal of dermatology 4 40304108
2024 Deucravacitinib in Japanese patients with plaque, generalized pustular, or erythrodermic psoriasis: Patient-reported outcomes in the POETYK PSO-4 study. The Journal of dermatology 4 39641509
2023 PRPF19 modulates morphology and growth behavior in a cell culture model of human skin. Frontiers in aging 2 37214773
2023 PRPF19 promotes the proliferation, migration, and inhibits autophagy in prostate cancer by suppressing SLC40A1. The Chinese journal of physiology 2 37929350
2023 PRPF19 functions in DNA damage repair and gemcitabine sensitivity via regulating DDB1 in bladder cancer cells. Cytotechnology 2 38304628
2025 Hypoxia-induced PRPF19 modulates TPT1 alternative splicing to facilitate cisplatin resistance in high-grade serous ovarian cancer. Biochimica et biophysica acta. Molecular basis of disease 1 39983558
1997 Searching for a functional analogy between yeast Pso4 and bacterial RecA proteins in induced mitotic recombination. Neoplasma 1 9605011
2025 PRPF19 mediates the proteasomal degradation of VDR to exacerbate ferroptosis in diabetic nephropathy. Cell communication and signaling : CCS 0 40414879
2025 Hub Genes PRPF19 and PPIB: Molecular Pathways and Potential Biomarkers in COPD. International journal of chronic obstructive pulmonary disease 0 40524719
2025 AI-aided identification of dual-purpose therapeutic targets PRPF19 and MAPK9 in hepatocellular carcinoma and cellular senescence. npj aging 0 41407697
2024 PRPF19 mRNA Encodes a Small Open Reading Frame That Is Important for Viability of Human Cells. Doklady. Biochemistry and biophysics 0 38472668