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Showing PRPF19 — PRP19 is a alias.

PRPF19

Pre-mRNA-processing factor 19 · UniProt Q9UMS4

Length
504 aa
Mass
55.2 kDa
Annotated
2026-06-10
50 papers in source corpus 22 papers cited in narrative 22 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PRPF19 (PSO4/SNEV/hPrp19) is an essential, evolutionarily conserved nuclear protein that couples pre-mRNA splicing to genome maintenance, and its loss is lethal in yeast and arrests early mouse development at the inner cell mass stage (PMID:8918805, PMID:17283042). Structurally, PRPF19 assembles into a homotetramer whose elongated coiled coils form an assembly axis for the NTC/Pso4 core complex; the tetramer is autoinhibited and catalytically silent as an E3 ubiquitin ligase until stepwise loading of SPF27, CDC5L, and PLRG1 activates ubiquitin ligation, with PLRG1–Prp19 communication relieving autoinhibition (PMID:29547724, PMID:15660529). As a splicing factor, its self-interaction (mapped to residues 56–74) is required for spliceosome assembly and stability, and it promotes the PRPF3–PRPF8 interaction within the U4/U6.U5 tri-snRNP to control alternative splicing such as the MDM4 isoform switch that gates p53-p21–dependent senescence (PMID:16332694, PMID:34144037). In the DNA damage response, the Pso4 complex binds RPA and, together with BCAS2's RPA1-binding and PRPF19's E3 activity, drives ATRIP recruitment, CHK1 activation, and RPA2 phosphorylation, while supporting interstrand crosslink repair through Cdc5L-mediated WRN recruitment, homologous recombination, replication fork restart, and recruitment of Metnase to double-strand breaks (PMID:24443570, PMID:16223718, PMID:24675077, PMID:18263876). PRPF19 also functions broadly as a substrate-selective ubiquitin ligase—escorting substrates to the 20S proteasome via direct PSMB4/β7 binding and ubiquitinating diverse targets including expanded ataxin-3, viral proteins, MYL9, and VDR (PMID:15660529, PMID:33542212, PMID:37031206, PMID:40414879).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 1996 High

    Established that a single essential gene underlies both splicing and DNA repair, defining PRPF19's dual functional identity from the outset.

    Evidence Genetic complementation and gene disruption in S. cerevisiae showing PSO4/PRP19 allelism and haploid lethality

    PMID:8918805

    Open questions at the time
    • Does not resolve whether splicing and repair roles are mechanistically coupled or separable
    • No molecular activity assigned to the protein
  2. 2003 Medium

    Showed the human protein directly engages DNA and protects against breaks, providing the first biochemical link to genome integrity.

    Evidence In vitro DNA-binding assays and Co-IP with TdT, plus siRNA knockdown with γ-H2AX/comet readout in lymphoid cells

    PMID:12960389

    Open questions at the time
    • dsDNA binding is sequence-nonspecific, leaving target selectivity unexplained
    • Mechanism linking DNA binding to break suppression undefined
  3. 2005 High

    Resolved that PRPF19 is an E3 ubiquitin ligase that escorts substrates to the proteasome and that its oligomerization is structurally required for spliceosome assembly, unifying its catalytic and splicing roles.

    Evidence In vitro ubiquitination assay, PSMB4 Co-IP, yeast two-hybrid self-interaction mapping (aa 56–74), immunodepletion/rescue and peptide-inhibition splicing assays, plus reconstituted in vitro ICL processing with WRN

    PMID:15660529 PMID:16223718 PMID:16332694

    Open questions at the time
    • Physiological ubiquitination substrates not yet identified in these studies
    • How proteasome escort relates to splicing function unclear
  4. 2007 High

    Defined PRPF19 as functionally non-redundant in vivo and showed DNA damage remodels its core complex, hinting at a damage-responsive conformational switch.

    Evidence Mouse knockout with blastocyst outgrowth/MEF proliferation assays; non-reducing SDS-PAGE and chromatin fractionation after DNA damage

    PMID:17276391 PMID:17283042

    Open questions at the time
    • The ubiquitylated damage-induced species is biochemically inferred, not structurally proven
    • Developmental phenotype not assigned to splicing vs repair function
  5. 2008 Medium

    Demonstrated PRPF19 acts as a DNA-binding recruitment platform that targets repair effectors to break sites, extending its role beyond catalysis.

    Evidence Co-IP, IR-induced co-localization, siRNA depletion, and end-joining assays with Metnase; EMSA and competitive binding showing PRPF19 controls Metnase DNA selectivity

    PMID:18263876 PMID:20416268

    Open questions at the time
    • Single lab characterization of the Metnase axis
    • Generality across repair pathways not established
  6. 2012 Medium

    Identified ATM-dependent S149 phosphorylation as a post-translational switch linking PRPF19 to stress-resistance and lifespan, placing it downstream of damage signaling.

    Evidence MS phosphosite mapping, ATM inhibitor treatment, and S149A mutant apoptosis assays under oxidative stress

    PMID:22529335

    Open questions at the time
    • Downstream effectors of S149 phosphorylation unknown
    • Single-lab finding without structural context
  7. 2014 High

    Positioned PRPF19 as an upstream activator of ATR signaling and a regulator of replication-coupled repair, defining its mechanistic role in the DNA damage response.

    Evidence Co-IP and co-localization with RPA, siRNA depletion with ATRIP recruitment/CHK1/RPA2 readouts and E3 mutant analysis; BrdU, HR reporter, PARP-inhibitor sensitivity and BRCA1 Western assays

    PMID:24443570 PMID:24675077

    Open questions at the time
    • Direct ubiquitination substrate driving ATR activation not identified
    • Mechanism of BRCA1 level regulation undefined
  8. 2018 High

    Provided the structural basis for activity by showing the Prp19 tetramer is autoinhibited and activated only by stepwise NTC assembly, explaining how E3 activity is gated.

    Evidence X-ray crystallography, mutagenesis, crosslinking MS, and stepwise in vitro reconstitution of E3 activity with SPF27/CDC5L/PLRG1

    PMID:29547724

    Open questions at the time
    • How DNA damage signals release autoinhibition in vivo not addressed
    • Substrate engagement geometry of the active complex unresolved
  9. 2021 Medium

    Connected PRPF19's splicing activity to a defined biological output by showing it controls the MDM4 isoform switch governing p53-p21 senescence, and broadened its substrate repertoire to neurodegeneration.

    Evidence siRNA/RNA-seq/RT-PCR splicing analysis with PRPF3/PRPF8 Co-IP; ubiquitination and proteasome assays for ATXN3-polyQ in Drosophila and mammalian cells with Exo70 antagonism

    PMID:33542212 PMID:34144037

    Open questions at the time
    • Whether MDM4 regulation requires E3 activity vs splicing alone unclear
    • Nuclear-localization requirement for ATXN3 clearance not mechanistically dissected
  10. 2024 Medium

    Established PRPF19 as a substrate-recognition receptor within a CRL4B complex and an antiviral/disease-relevant E3 ligase across multiple substrates.

    Evidence Co-IP/pulldown, ubiquitination, and viral replication assays for PEDV-N (via MARCH8/NDP52), SARS-CoV-2 ORF6 (via CUL4B/DDB1/RBX1), MYL9 (K63-linked), and VDR with knockout/SPR validation

    PMID:36541804 PMID:37031206 PMID:38265236 PMID:40414879

    Open questions at the time
    • Each substrate characterized by a single lab
    • How PRPF19 selects among diverse substrates and ligase partners is unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How PRPF19's splicing, DNA-repair, and substrate-degradation activities are coordinately regulated and selectively deployed within a single autoinhibited scaffold remains unresolved.
  • No unified model linking conformational state to substrate/pathway choice
  • Determinants of substrate selectivity for the E3 activity undefined
  • In vivo trigger releasing autoinhibition during DNA damage unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016874 ligase activity 7 GO:0140096 catalytic activity, acting on a protein 5 GO:0003677 DNA binding 2 GO:0060089 molecular transducer activity 1
Localization
GO:0005694 chromosome 3 GO:0005634 nucleus 2
Pathway
R-HSA-392499 Metabolism of proteins 5 R-HSA-73894 DNA Repair 4 R-HSA-8953854 Metabolism of RNA 3 R-HSA-8953897 Cellular responses to stimuli 2
Partners
BCAS2CDC5LCUL4BPLRG1PSMB4RPA1SETMARWRN
Complex memberships
CRL4B E3 ligase complexNTC/Pso4 complexspliceosome

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 PSO4 is allelic to PRP19, encoding a spliceosome-associated protein; gene disruption is lethal in haploid yeast, establishing it as an essential gene with dual roles in pre-mRNA splicing and DNA repair/recombination. Genetic complementation, gene disruption, sequence analysis in S. cerevisiae Nucleic acids research High 8918805
2003 Human hPso4 (PRPF19) binds double-stranded DNA in a sequence-nonspecific manner but does not bind single-stranded DNA; it associates physically with terminal deoxynucleotidyl transferase (TdT) in lymphoid cells; siRNA-mediated loss of hPso4 causes accumulation of DNA double-strand breaks and apoptosis after DNA damage. Co-immunoprecipitation, DNA binding assays (purified protein), siRNA knockdown with γ-H2AX/comet assay readout Proceedings of the National Academy of Sciences of the United States of America Medium 12960389
2005 The Pso4/Prp19 complex (composed of Pso4/Prp19, Cdc5L, Plrg1, and Spf27) is required for processing of DNA interstrand cross-links (ICLs) in vitro; WRN helicase activity (but not exonuclease activity) is also required; WRN physically interacts with the Pso4 complex via direct binding to Cdc5L. In vitro ICL processing biochemical assay with site-specific psoralen substrate, co-immunoprecipitation, pulldown The Journal of biological chemistry High 16223718
2005 SNEV (PRPF19) has in vitro E3 ubiquitin ligase activity and interacts directly with the β7 subunit (PSMB4) of the 20S proteasome; upon proteasome inhibition, SNEV co-localizes with ubiquitin without itself being ubiquitinated, suggesting it escorts substrates to the proteasome; this interaction is evolutionarily conserved (yeast Prp19 also binds yeast β7). In vitro ubiquitination assay, co-immunoprecipitation, immunofluorescence microscopy, yeast two-hybrid The Biochemical journal High 15660529
2005 SNEV (PRPF19) is the human ortholog of yeast Prp19; it functions in pre-mRNA splicing; its homo-oligomerization (self-interaction domain mapped to amino acids 56–74) is essential for spliceosome assembly and stability, as synthetic peptides from this region inhibit in vitro splicing by disrupting spliceosome formation. Yeast complementation, immunodepletion from HeLa nuclear extracts, in vitro splicing assay, peptide inhibition, yeast two-hybrid self-interaction mapping Nucleic acids research High 16332694
2007 hPrp19 forms an ubiquitylated oligomeric species (likely via thiolester between ubiquitin and a cysteine in Prp19) that is enhanced upon DNA damage and associates more with chromatin; this ubiquitylated form fails to interact with Cdc5L or Plrg1, indicating DNA damage induces structural alterations to the Prp19 core complex. SDS-PAGE under non-reducing conditions, co-immunoprecipitation, chromatin fractionation, DNA damage treatment Biochemical and biophysical research communications Medium 17276391
2007 SNEV (PRPF19) is essential for early mouse development; SNEV-null embryos initiate blastocyst formation but cells of the inner cell mass fail to proliferate and die; heterozygous MEFs show decreased proliferative potential, demonstrating the protein is functionally non-redundant in vivo. Homologous recombination knockout in mice, blastocyst outgrowth assays, MEF proliferation assays Molecular and cellular biology High 17283042
2008 hPso4 (PRPF19) forms a stable complex with Metnase (SETMAR) on both TIR and non-TIR DNA; hPso4 is required to recruit Metnase to DNA double-strand break sites in vivo; siRNA depletion of hPso4 abolishes Metnase localization at DSBs and Metnase-mediated stimulation of DNA end joining. Co-immunoprecipitation, immunofluorescence co-localization after ionizing radiation, siRNA knockdown, DNA end-joining functional assay The Journal of biological chemistry Medium 18263876
2010 When hPso4 forms a complex with Metnase, hPso4 is solely responsible for DNA binding within the complex and negatively regulates Metnase's TIR-specific DNA binding activity, redirecting Metnase to non-TIR sites such as DSBs. Electrophoretic mobility shift assay, competitive inhibition assay, stoichiometric analysis of protein-DNA complexes 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; Exo70 shuttles to the nucleus, associates with the spliceosome, and its N-terminal fragment inhibits pre-mRNA splicing in vitro; Exo70 influences splicing of a model substrate and its own pre-mRNA in vivo. Co-immunoprecipitation, yeast two-hybrid, in vitro splicing assay with peptide inhibition, minigene splicing assay in vivo The Biochemical journal Medium 21639856
2012 SNEVhPrp19/hPso4 is phosphorylated at serine 149 in an ATM-dependent manner in response to oxidative stress and DNA double-strand break-inducing agents; this S149 phosphorylation is necessary for mediating resistance to apoptosis upon oxidative stress and partially necessary for extending cellular life span. Mass spectrometry phosphorylation mapping, ATM inhibitor treatment, phosphorylation-deficient point-mutant (S149A) overexpression, apoptosis assays Aging Medium 22529335
2014 The PSO4 complex (PSO4/PRP19, CDC5L, PLRG1, BCAS2/SPF27) directly interacts and co-localizes with RPA; both BCAS2 and PSO4 interact with RPA1; depletion of BCAS2 or PSO4 impairs ATRIP recruitment to DNA damage sites and compromises CHK1 activation and RPA2 phosphorylation; both RPA1-binding ability of BCAS2 and E3 ligase activity of PSO4 are required for efficient ATR pathway activation. Co-immunoprecipitation, immunofluorescence, siRNA depletion, CHK1/RPA2 phosphorylation assays, E3 ligase activity mutant analysis The Journal of biological chemistry High 24443570
2014 The hPso4 complex is required for timely S-phase progression and G2/M checkpoint transition; hPso4 depletion results in delayed replication fork restart after hydroxyurea-induced stalling, reduced DSB repair, increased sensitivity to PARP inhibitors, and impaired homologous recombination; hPso4 regulates BRCA1 protein levels and single-strand DNA generation at DSBs. siRNA knockdown, BrdU incorporation (replication assay), γ-H2AX foci, PARP inhibitor sensitivity, HR reporter assay, Western blot for BRCA1 The Journal of biological chemistry Medium 24675077
2018 Prp19 forms a homotetramer whose elongated coiled coils serve as an assembly axis for the NTC (nineteen complex); Prp19 is autoinhibited and inactive as an E3 ligase on its own; stepwise assembly of SPF27, CDC5L, and PLRG1 onto the Prp19 tetramer activates ubiquitin ligation; structural basis for autoinhibition was determined by crystallography; communication between PLRG1 and Prp19 enables E3 activity. X-ray crystallography, mutational analysis, in vitro ubiquitination assay, protein-protein crosslinking mass spectrometry, stepwise complex reconstitution Molecular cell High 29547724
2021 PRPF19 knockdown causes a switch in MDM4 splicing from the stable full-length MDM4-FL isoform to the unstable MDM4-S isoform (lacking exon 6), thereby reducing MDM4-mediated p53 inactivation and inducing p53-p21-dependent cellular senescence; PRPF19 promotes the physical interaction between splicing factors PRPF3 and PRPF8 (components of U4/U6.U5 tri-snRNP). siRNA knockdown, RNA-seq, RT-PCR splicing isoform analysis, co-immunoprecipitation of PRPF3/PRPF8, p53-p21 pathway analysis The Journal of biological chemistry Medium 34144037
2021 Prpf19/prp19 promotes poly-ubiquitination and proteasomal degradation of mutant expanded ataxin-3 (ATXN3-polyQ); nuclear localization of Prpf19 is essential for its modulatory function; Exoc7/exo70 interacts with Prpf19 and opposes its E3 ligase function toward ATXN3-polyQ. Ubiquitination assay, proteasome inhibitor treatment, localization mutant analysis, co-immunoprecipitation, Drosophila and mammalian cell models Cell death & disease Medium 33542212
2022 PRPF19 recruits the E3 ubiquitin ligase MARCH8 to the PEDV nucleocapsid (N) protein to mediate its ubiquitination; the ubiquitinated N protein is recognized by cargo receptor NDP52 and transported to autolysosomes for degradation via selective autophagy, thereby inhibiting PEDV replication. Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, overexpression, selective autophagy assays Journal of virology Medium 36541804
2023 PRPF19 promotes K63-linked ubiquitination of myosin light chain 9 (MYL9), enhancing MYL9 stability, which activates the Src-YAP1 signaling cascade to promote migration and invasion in colorectal cancer cells. Co-immunoprecipitation, ubiquitination assay (K63-linkage specific), gain- and loss-of-function experiments, Src/YAP1 pathway analysis Cell death & disease Medium 37031206
2024 PRPF19 acts as a substrate recognition receptor that interacts with CUL4B, DDB1, and RBX1 to form a CRL4B-based E3 ubiquitin ligase complex; this complex catalyzes ubiquitination and proteasomal degradation of SARS-CoV-2 ORF6, relieving ORF6-mediated IFN suppression and inhibiting SARS-CoV-2 replication. Pulldown/Co-immunoprecipitation, ubiquitination assay, overexpression/knockdown with viral replication readout, mouse SARS-CoV-2 infection model mBio Medium 38265236
2025 PRPF19 mediates ubiquitin-dependent proteasomal degradation of the vitamin D receptor (VDR); loss of VDR reduces GPX4 transcription, promoting ferroptosis in renal tubular epithelial cells; berberine was identified as an inhibitor of PRPF19-VDR interaction via molecular docking and surface plasmon resonance. Proteomics, luciferase reporter assay, chromatin immunoprecipitation, co-immunoprecipitation, ubiquitination assay, SPR, VDR knockout mouse model Cell communication and signaling Medium 40414879
2009 Blom7α (a novel KH domain protein) directly interacts with SNEV(Prp19-Pso4), co-localizes and co-precipitates with splicing factors, and is present in affinity-purified spliceosomes; addition of Blom7α to HeLa nuclear extracts increases splicing activity; Blom7α overexpression alters both 5'- and 3'-splice site selection. Yeast two-hybrid, co-immunoprecipitation, affinity-purified spliceosome analysis, in vitro splicing assay, minigene splicing assay The Journal of biological chemistry Medium 19641227
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. Ribosome profiling, uORF mutagenesis, cell viability assays 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
2021 PRPF19 regulates p53-dependent cellular senescence by modulating alternative splicing of MDM4 mRNA. The Journal of biological chemistry 36 34144037
1989 The PSO4 gene is responsible for an error-prone recombinational DNA repair pathway in Saccharomyces cerevisiae. Molecular & general genetics : MGG 36 2671661
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
2024 CRL4B E3 ligase recruited by PRPF19 inhibits SARS-CoV-2 infection by targeting ORF6 for ubiquitin-dependent degradation. mBio 15 38265236
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
2023 PRPF19 facilitates colorectal cancer liver metastasis through activation of the Src-YAP1 pathway via K63-linked ubiquitination of MYL9. Cell death & disease 14 37031206
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
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 13 35252202
1992 The pso4-1 mutation reduces spontaneous mitotic gene conversion and reciprocal recombination in Saccharomyces cerevisiae. Molecular & general genetics : MGG 12 1465105
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 11 33542212
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 BTK, NUTM2A, and PRPF19 Are Novel KMT2A Partner Genes in Childhood Acute Leukemia. Biomedicines 10 34440129
1995 The PSO4 gene of S. cerevisiae is important for sporulation and the meiotic DNA repair of photoactivated psoralen lesions. Current genetics 10 7736603
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 5 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
2025 Hub Genes PRPF19 and PPIB: Molecular Pathways and Potential Biomarkers in COPD. International journal of chronic obstructive pulmonary disease 3 40524719
2025 PRPF19 mediates the proteasomal degradation of VDR to exacerbate ferroptosis in diabetic nephropathy. Cell communication and signaling : CCS 2 40414879
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 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

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