Affinage

OASL

2'-5'-oligoadenylate synthase-like protein · UniProt Q15646

Length
514 aa
Mass
59.2 kDa
Annotated
2026-06-10
55 papers in source corpus 24 papers cited in narrative 24 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

OASL is an interferon-inducible, catalytically inactive member of the OAS family that has lost 2'-5' oligoadenylate synthetase activity and instead carries two C-terminal ubiquitin-like (UBL) domains that repurpose it as a context-dependent regulator of innate immune signaling (PMID:9722630). Its induction is rapid and driven by IRF-3 independently of a functional type I IFN response, distinguishing it from IFN-dependent OAS1 (PMID:19203244). During RNA virus infection, OASL acts as a positive co-activator of RIG-I: its UBL domains mimic K63-linked polyubiquitin to potentiate RIG-I signaling, while its OAS-like domain adopts an activated OAS1-like fold with a dsRNA-binding groove whose integrity is required for this co-activator function (PMID:24931123, PMID:25925578). OASL also drives antiviral cell death by undergoing liquid-like phase condensation that scaffolds the RIPK3–ZBP1 necrosome, promoting RIPK3 fibril formation, autophosphorylation, and MLKL phosphorylation to execute virus-induced necroptosis (PMID:36604592). In opposition to this antiviral arm, OASL directly and non-competitively binds cGAS independently of DNA and inhibits cyclic GMP-AMP synthesis, dampening STING-dependent type I IFN responses during DNA virus infection and in tumor microenvironments (PMID:30635239, PMID:41330170). The mouse ortholog OASL1 functions predominantly as a negative regulator of type I IFN, repressing IRF7 translation and limiting IFN output, with loss of OASL1 sustaining IFN and accelerating viral clearance (PMID:23874199, PMID:27034232). Beyond infection, OASL contributes to disease-relevant processes including endothelial NOS3 mRNA destabilization via a PI3K/Akt–miR-584 axis in atherosclerosis (PMID:36333342), and immune evasion in cancer through NBR1/autophagy-lysosomal degradation of MHC-I (PMID:39990208). Rare OASL variants enhance type I IFN secretion by patient-derived dendritic cells, linking OASL function to systemic lupus erythematosus (PMID:37354689).

Mechanistic history

Synthesis pass · year-by-year structured walk · 23 steps
  1. 1998 Medium

    Established OASL as a distinct OAS family member that has lost canonical synthetase activity but gained ubiquitin-like domains, setting up the central question of what function the UBL-bearing protein serves.

    Evidence cDNA cloning, genomic sequencing, and domain analysis of human p59OASL

    PMID:9722630

    Open questions at the time
    • Lack of enzymatic activity inferred from sequence, not direct in vitro assay
    • No functional role assigned to the UBL domains
  2. 2004 Medium

    Identified the first OASL protein partner, showing the UBL domain mediates a specific interaction with the transcriptional repressor MBD1, indicating the UBL domains are protein-interaction modules.

    Evidence Yeast two-hybrid, in vitro pulldown, and reciprocal co-immunoprecipitation

    PMID:14728690

    Open questions at the time
    • Functional consequence of OASL-MBD1 interaction not established
    • No link to antiviral or IFN biology
  3. 2009 Medium

    Placed OASL induction in an IRF-3-dependent, IFN-independent pathway, distinguishing its regulation from IFN-dependent OAS1 and positioning it as an early-response gene.

    Evidence Gene expression analysis during Sendai and influenza A virus infection with IRF-3 pathway dissection

    PMID:19203244

    Open questions at the time
    • Does not define OASL molecular activity
    • Single lab
  4. 2012 Medium

    Functionally implicated the UBL domain in antiviral activity by showing splice variants retaining the UBL inhibit RNA viruses while those lacking it do not.

    Evidence RT-PCR cloning of natural splice variants, ectopic expression, and viral infection assays

    PMID:22531715

    Open questions at the time
    • Molecular mechanism of UBL-mediated antiviral effect not yet defined
    • Virus-specificity (HSV-2 vs RNA viruses) unexplained
  5. 2013 High

    Revealed an opposing negative-regulatory role for the mouse ortholog OASL1, which suppresses sustained type I IFN, establishing that OASL family members can both enhance and dampen innate immunity.

    Evidence Oasl1 knockout mice in chronic LCMV infection with cytokine, flow cytometry, and viral titer readouts

    PMID:23874199

    Open questions at the time
    • Molecular mechanism of IFN suppression not resolved in this study
    • Mouse-specific; human relevance unclear at this point
  6. 2014 High

    Defined the mechanism of OASL's RNA-virus antiviral activity: its UBL domain mimics K63-linked polyubiquitin to enhance RIG-I signaling, identifying RIG-I as the key effector.

    Evidence Reciprocal Co-IP, colocalization, RIG-I-dependent rescue, siRNA loss-of-function, and Oasl2 KO macrophages across multiple viruses

    PMID:24931123

    Open questions at the time
    • Structural basis of polyubiquitin mimicry not yet shown
    • Role of the OAS-like domain undefined
  7. 2015 High

    Provided the structural and functional basis for the OAS-like domain, showing it adopts an activated OAS1-like fold and binds dsRNA, and that dsRNA binding is essential for RIG-I co-activation.

    Evidence X-ray crystallography, dsRNA binding assays, site-directed mutagenesis, and RIG-I reporter assays

    PMID:25925578

    Open questions at the time
    • How dsRNA binding couples to UBL-mediated RIG-I enhancement not fully resolved
  8. 2018 Medium

    Resolved a temporal switch in OASL1 function: early stress-granule-mediated viral RNA trapping enhances RLR signaling, while late-stage interaction with IRF7 mRNA inhibits its translation to shut down IFN.

    Evidence Subcellular localization, stress granule assays, RNA-binding assays, and IRF7 translation assays

    PMID:29463066

    Open questions at the time
    • Direct IRF7 mRNA binding mechanism not structurally defined
    • Mouse ortholog; human OASL behavior not addressed
  9. 2018 Medium

    Showed that a tree shrew ortholog bridges MDA5 and MAVS at mitochondria to potentiate IFN, extending the RNA-sensing co-activator role beyond RIG-I.

    Evidence Co-IP, subcellular fractionation, and gain/loss-of-function IFN reporter assays for tupaia OASL1

    PMID:33188074

    Open questions at the time
    • Ortholog-specific; human OASL-MDA5/MAVS interaction not demonstrated
    • Single lab
  10. 2019 High

    Defined the DNA-virus arm of OASL biology: direct, non-competitive inhibition of cGAS that suppresses cGAMP and IFN, revealing OASL as a brake on the cGAS-STING pathway.

    Evidence Co-IP, in vitro cGAS enzymatic assays, OASL-deficient cells, Oasl2 KO mice, and cGAS epistasis across DNA viruses

    PMID:30635239

    Open questions at the time
    • Structural basis of non-competitive cGAS inhibition not defined
    • How OASL switches between RIG-I enhancement and cGAS inhibition unclear
  11. 2022 High

    Extended OASL function into vascular biology, showing it stabilizes eNOS mRNA via a PI3K/Akt-miR-584 axis, with loss accelerating atherosclerosis.

    Evidence Endothelial-specific Oasl1 KO mice, atherosclerosis model, miRNA inhibitor rescue, and mRNA stability assays

    PMID:36333342

    Open questions at the time
    • Direct molecular target of OASL in the PI3K/Akt-miR-584 axis not identified
    • Connection to its immune roles unclear
  12. 2022 Medium

    Placed OASL1 downstream of NRF2 in macrophages as a restraint on inflammatory and cell-death pathways during ischemia-reperfusion injury.

    Evidence Myeloid TXNIP KO mice, NRF2 disruption, and pathway analysis of TBK1/G3BP1 and apoptosis/necroptosis markers

    PMID:36035360

    Open questions at the time
    • Direct OASL1 molecular targets in these pathways not defined
    • Single lab
  13. 2023 High

    Established a third antiviral mechanism: OASL undergoes liquid-like phase condensation to scaffold the RIPK3-ZBP1 necrosome and execute virus-induced necroptosis.

    Evidence Phase condensation assays, Co-IP, RIPK3 fibril/MLKL phosphorylation assays, and Oasl1 KO mouse infection model

    PMID:36604592

    Open questions at the time
    • Which OASL domains drive condensation not fully mapped
    • Relationship between condensation and RIG-I co-activation unresolved
  14. 2023 Medium

    Connected the OASL1-IRF7 translational repression mechanism to antitumor immunity, showing loss boosts IFN-I and antitumor T/NK cell responses.

    Evidence Oasl1 KO mice in syngeneic tumor models with IRF7 protein, IFN-I, and immune cell readouts

    PMID:27034232

    Open questions at the time
    • Mouse ortholog; human OASL translational control of IRF7 not shown
    • Single lab
  15. 2023 Medium

    Identified OASL as an upstream activator of mTORC1 driving tumor cell proliferation and invasion in stomach adenocarcinoma.

    Evidence siRNA knockdown, overexpression, mTOR/RPS6KB1 phosphorylation, rapamycin rescue, and xenograft assays

    PMID:36809539

    Open questions at the time
    • Direct molecular link between OASL and mTORC1 activation unknown
    • Single lab
  16. 2023 Medium

    Linked OASL function to a human Mendelian/autoimmune phenotype, showing rare SLE-associated variants causally enhance type I IFN secretion.

    Evidence Patient-derived iPSC-differentiated DCs with bidirectional CRISPR genome editing and IFN secretion assays

    PMID:37354689

    Open questions at the time
    • Mechanism by which variants alter OASL function not defined
    • Single lab
  17. 2024 Medium

    Demonstrated a direct antiviral effector role distinct from signaling, targeting IBDV VP2 for p62/SQSTM1-mediated autophagic degradation.

    Evidence Co-IP, autophagy pathway assays, and VP2 K316R mutagenesis with viral replication readouts

    PMID:38639485

    Open questions at the time
    • Whether this autophagy-targeting role generalizes to other viral proteins unknown
    • Single lab
  18. 2024 Low

    Identified Pi16 as an OASL partner that promotes pancreatic cancer proliferation through OASL.

    Evidence Co-IP, Pi16 CRISPR knockout, and OASL functional rescue in proliferation assays

    PMID:38353288

    Open questions at the time
    • Single Co-IP without reciprocal validation; limited mechanistic detail on how OASL mediates proliferation
    • Direct binding interface undefined
  19. 2025 Medium

    Defined an immune-evasion mechanism in pancreatic cancer whereby OASL drives NBR1-mediated autophagy-lysosomal degradation of MHC-I to limit CD8+ T-cell infiltration.

    Evidence Co-IP, flow cytometry, immunofluorescence, and orthotopic PDAC mouse model with OASL knockdown

    PMID:39990208

    Open questions at the time
    • Direct OASL-NBR1 binding interface not defined
    • Single lab
  20. 2025 Low

    Placed OASL in a JAK1-STAT1 axis driving MAPK-dependent keratinocyte hyperproliferation in psoriasis.

    Evidence OASL knockdown/overexpression in HaCaT cells, JAK1 inhibitor treatment, and imiquimod psoriasis model

    PMID:40360089

    Open questions at the time
    • Limited mechanistic detail; direct OASL-p38 link not established
    • Single lab
  21. 2025 Medium

    Confirmed and extended the cGAS-inhibitory role to the tumor microenvironment, showing OASL suppresses cGAS-STING antitumor immunity and sustains matrix stiffness in HCC.

    Evidence Co-IP, immunofluorescence, cGAMP ELISA, STING inhibitor rescue, and subcutaneous HCC mouse model

    PMID:41330170

    Open questions at the time
    • Mechanistic basis of matrix stiffness regulation not defined
    • Single lab
  22. 2025 Medium

    Showed that intrinsic, pre-infection OASL expression is required for robust type III IFN induction during influenza, identifying OASL as a determinant of cellular IFN heterogeneity.

    Evidence Temporal single-cell RNA-seq and OASL loss-of-function validation in IAV infection

    PMID:41468430

    Open questions at the time
    • Molecular mechanism linking OASL to IFNL induction not defined
    • Single lab
  23. 2026 Low

    Linked OASL to PANoptosis, showing TRAF1 transcriptionally activates OASL, which associates with the ZBP1-PANoptosome during H. pylori infection.

    Evidence Co-IP of OASL-ZBP1-PANoptosome, TRAF1 knockdown/OASL overexpression rescue, and in vivo H. pylori model

    PMID:41942799

    Open questions at the time
    • Single Co-IP without reciprocal validation; newly published and unreplicated
    • Direct OASL contribution to PANoptosome assembly undefined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How OASL switches between its opposing roles — enhancing RIG-I/RLR signaling versus inhibiting cGAS, and promoting versus suppressing IFN — remains unresolved at the molecular level.
  • No structural model explaining context-dependent partner selection (RIG-I vs cGAS)
  • Determinants of human vs mouse functional divergence (enhancer vs IFN repressor) unclear
  • How phase condensation, dsRNA binding, and UBL polyubiquitin mimicry are coordinated within one protein not integrated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0003723 RNA binding 2 GO:0060089 molecular transducer activity 2 GO:0031386 protein tag activity 1 GO:0060090 molecular adaptor activity 1
Localization
GO:0005829 cytosol 2 GO:0005634 nucleus 1 GO:0005739 mitochondrion 1
Pathway
R-HSA-168256 Immune System 4 R-HSA-162582 Signal Transduction 3 R-HSA-9612973 Autophagy 2 R-HSA-5357801 Programmed Cell Death 1
Partners
CGASMAVSMBD1MDA5NBR1RIGIRIPK3ZBP1
Complex memberships
RIPK3-ZBP1 necrosomeZBP1-PANoptosome

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 OASL (p59OASL) was identified as a novel OAS family member with a conserved N-terminal OAS-like domain but lacking 2'-5' oligoadenylate synthetase activity; its C-terminus contains two ubiquitin-like domains, distinguishing it from other OAS family members. cDNA cloning, genomic sequencing, sequence/domain analysis Nucleic acids research Medium 9722630
2004 OASL (p59OASL) interacts with the transcriptional repressor MBD1 (methyl CpG-binding protein 1) via its C-terminal ubiquitin-like domain; the interaction was confirmed by yeast two-hybrid, in vitro pulldown, and in vivo co-immunoprecipitation, and was specific (OASL did not interact with other MBD family members, and MBD1 did not interact with OAS1). Yeast two-hybrid, in vitro pulldown, co-immunoprecipitation European journal of biochemistry Medium 14728690
2009 OASL gene induction by viral infection is rapid and mediated by IRF-3 (IFN regulatory factor 3), independently of a functional type I IFN response, in contrast to OAS1 which requires type I IFN signaling for its induction. Gene expression analysis during Sendai virus and Influenza A virus infection; IRF-3 pathway dissection Journal of interferon & cytokine research Medium 19203244
2012 A splice variant of human OASL (OASL d), derived by deletion of exons 4 and 5 and retaining the ubiquitin-like domain, exhibits antiviral activity against RNA viruses (EV71, VSV) but not HSV-2; OASL b, which lacks the ubiquitin-like domain but shares the N-terminus, has no antiviral activity, implicating the ubiquitin-like domain in antiviral function. RT-PCR cloning, ectopic expression, viral infection assays, immunoblotting The international journal of biochemistry & cell biology Medium 22531715
2013 Mouse OASL1 negatively regulates type I IFN production; OASL1 deficiency leads to sustained type I IFN levels (primarily from plasmacytoid dendritic cells) during chronic LCMV infection, accelerated viral clearance, and restored CD8+ T-cell function, demonstrating OASL1 as a negative regulator of the innate antiviral response. Oasl1 knockout mice, LCMV chronic infection model, serum cytokine measurements, flow cytometry, viral titer assays PLoS pathogens High 23874199
2014 Human OASL enhances RIG-I activation by mimicking K63-linked polyubiquitin through its C-terminal ubiquitin-like domain; OASL interacts and colocalizes with RIG-I, and its expression suppresses replication of multiple RNA viruses in a RIG-I-dependent manner; loss of OASL reduces RIG-I signaling and enhances virus replication. Mouse Oasl2 is the functionally equivalent ortholog. Co-immunoprecipitation, colocalization imaging, RIG-I-dependent rescue experiments, loss-of-function (siRNA knockdown), gain-of-function (overexpression), Oasl2 KO bone-marrow-derived macrophages, multi-virus replication assays Immunity High 24931123
2015 The OAS-like domain of human OASL adopts a crystal structure resembling activated OAS1 and contains a positively charged dsRNA binding groove; OASL binds dsRNA through this domain, and mutation of key residues in the dsRNA binding site abolishes the ability of OASL to enhance RIG-I signaling, demonstrating that dsRNA binding is essential for OASL's co-activator function. X-ray crystallography, dsRNA binding assays, site-directed mutagenesis, RIG-I signaling reporter assays Nucleic acids research High 25925578
2018 Mouse OASL1 forms stress granules that trap viral RNAs during early viral infection, promoting efficient RLR (RIG-I-like receptor) signaling; this stress granule formation depends on the RNA binding activity of OASL1. In late stages of infection, OASL1 interacts with IRF7 mRNA transcripts to inhibit IRF7 translation, thereby downregulating type I IFN production. Subcellular localization imaging, stress granule assays, viral RNA trapping experiments, RNA-binding assays, IRF7 translation assays Molecules and cells Medium 29463066
2019 Human OASL and mouse Oasl2 directly bind cGAS (independently of dsDNA) and inhibit cGAS enzymatic activity (cyclic GMP-AMP production) via non-competitive inhibition, thereby suppressing type I IFN induction during DNA virus infection; OASL-deficient cells and Oasl2-/- mice show increased IFN production and reduced DNA virus (vaccinia, HSV, adenovirus) replication, and cGAS is required for this phenotype. Co-immunoprecipitation, cGAS enzymatic activity assays, OASL-deficient human cells and Oasl2 KO mice, multi-virus replication assays, genetic epistasis (cGAS knockdown rescue) Immunity High 30635239
2018 Tupaia OASL1 (tree shrew ortholog) associates with mitochondria and directly interacts with both MDA5 and MAVS via its OAS and UBL domains; upon RNA virus infection, tOASL1 enhances MDA5-MAVS interaction to potentiate type I IFN signaling. Co-immunoprecipitation, subcellular fractionation/localization, overexpression and knockdown assays, IFN signaling reporter assays Journal of immunology Medium 33188074
2022 OASL1/OASL regulates eNOS (NOS3) mRNA stability in endothelial cells; endothelial Oasl1 deficiency leads to reduced eNOS expression through PI3K/Akt-dependent upregulation of miR-584 (a negative regulator of NOS3 mRNA), resulting in impaired NO bioavailability and accelerated atherosclerotic plaque progression. miR-584 inhibition rescues the effects of OASL knockdown. Endothelial-specific Oasl1 knockout mice, atherosclerosis model, miRNA inhibitor rescue experiments, PI3K/Akt pathway inhibition, mRNA stability assays, Western blot Nature communications High 36333342
2022 Mouse OASL1 acts downstream of NRF2 in macrophages; OASL1 deficiency enhances G3BP1- and TBK1-mediated inflammatory responses and induces apoptosis/necroptosis via APAF1/cytochrome c/caspase-9 and RIPK3 pathways during hepatic ischemia-reperfusion injury. Myeloid-specific TXNIP KO mice, NRF2 disruption experiments, OASL1 deficiency experiments, pathway analysis (STING/TBK1, apoptosis/necroptosis markers), histological and biochemical assays JHEP reports Medium 36035360
2023 OASL promotes virus-induced necroptosis by undergoing liquid-like phase condensation, which scaffolds the RIPK3-ZBP1 necrosome complex; OASL phase-separated droplets recruit RIPK3 and ZBP1 via protein-protein interactions, providing spatial segregation that facilitates RIPK3 amyloid-like fibril formation, autophosphorylation, and subsequent MLKL phosphorylation. Oasl1-deficient mice show severely impaired necroptosis and succumb to uncontrolled viral infection. Phase condensation assays, co-immunoprecipitation, RIPK3 fibril/amyloid assays, MLKL phosphorylation assays, Oasl1 KO mouse viral infection model, live cell imaging Nature cell biology High 36604592
2023 OASL1 negatively regulates IRF7 translation (not transcription), thereby reducing type I IFN production; mouse Oasl1 KO leads to increased IRF7 protein and enhanced type I IFN in response to tumors, promoting antitumor immunity with increased CD8+ T cells, NK cells, and CD8α+ DCs in tumors. Oasl1 KO mice, syngeneic tumor transplant models, IRF7 protein measurement, flow cytometry, IFN-I measurement Cancer immunology, immunotherapy Medium 27034232
2023 OASL knockdown in stomach adenocarcinoma cells suppresses mTORC1 signaling (reduced p-mTOR and p-RPS6KB1), inhibiting cell proliferation, migration, and invasion; OASL overexpression activates mTORC1 signaling, and rapamycin reverses OASL overexpression-induced tumor cell growth, establishing OASL as an upstream activator of mTORC1 in STAD. siRNA knockdown, overexpression, mTOR/RPS6KB1 phosphorylation Western blot, rapamycin rescue, xenograft tumor formation assay FASEB journal Medium 36809539
2023 Rare OASL variants (R60W, T261S, A447V, 202Q) found in SLE patients enhance type I IFN secretion by dendritic cells differentiated from patient-derived iPSCs; genome editing of the 202Q variant to wild-type 202R reduced IFN secretion, and introduction of 202Q into wild-type iPSCs enhanced it, confirming functional causality. Patient-derived iPSC differentiation to DCs, CRISPR/Cas9 genome editing, IFN secretion assays Journal of autoimmunity Medium 37354689
2024 OASL interacts with viral protein VP2 of IBDV (infectious bursal disease virus) and targets it for degradation via the autophagy receptor p62/SQSTM1 through the autophagy pathway; lysine 316 of VP2 is the critical site for this autophagy-mediated degradation, and K316R mutation abolishes VP2 degradation and enhances IBDV replication. Co-immunoprecipitation, overexpression/knockdown assays, autophagy pathway assays, site-directed mutagenesis (VP2 K316R), viral replication assays Journal of virology Medium 38639485
2024 Pi16 (peptidase inhibitor 16) binds to OASL by co-immunoprecipitation and promotes pancreatic ductal adenocarcinoma cell proliferation via OASL; functional rescue experiments confirmed that Pi16's proliferative effect depends on OASL. Co-immunoprecipitation, CRISPR/Cas9 knockout of Pi16, functional rescue with OASL, in vitro and in vivo proliferation assays Molecular carcinogenesis Low 38353288
2025 OASL promotes immune evasion in pancreatic ductal adenocarcinoma by enhancing NBR1-mediated autophagy-lysosomal degradation of MHC-I; OASL knockdown restores total and surface MHC-I levels, increases CD8+ T-cell infiltration, and slows tumor growth in vivo. Co-immunoprecipitation, flow cytometry, Western blot, immunofluorescence, orthotopic PDAC mouse model, OASL knockdown Theranostics Medium 39990208
2025 OASL promotes mTOR-independent and MAPK (p38)-dependent keratinocyte hyperproliferation and inflammatory/lipid metabolic dysregulation in psoriasis; OASL expression is regulated by the JAK1-STAT1 axis (Upadacitinib inhibits STAT1 and reduces OASL), and OASL knockdown suppresses p38 MAPK activation. OASL knockdown and overexpression in HaCaT cells, JAK1 inhibitor treatment, p38 MAPK pathway analysis, imiquimod-induced psoriasis mouse model Life sciences Low 40360089
2025 OASL directly binds cGAS (confirmed by Co-IP and immunofluorescence) and inhibits cGAMP generation, reducing STING-mediated antitumor immunity and sustaining matrix stiffness in hepatocellular carcinoma; OASL knockdown activates cGAS-STING signaling and promotes M1 macrophage polarization, and STING inhibitor C-176 reverses these effects. Co-immunoprecipitation, immunofluorescence, ELISA (cGAMP), Western blot, flow cytometry, subcutaneous HCC mouse model, STING inhibitor rescue International immunopharmacology Medium 41330170
2025 Intrinsic (pre-infection) expression of OASL is essential for robust type III IFN (IFNL) induction during influenza A virus infection; single-cell RNA-seq analysis of temporal infection data identified OASL as a correlate of IFN induction potential, and validation experiments confirmed OASL as necessary for this heterogeneous cellular IFN response. Temporal single-cell RNA sequencing, OASL knockdown/loss-of-function validation, IAV infection model, IFNL induction assays Proceedings of the National Academy of Sciences of the United States of America Medium 41468430
2026 OASL interacts with the ZBP1-PANoptosome complex via co-immunoprecipitation; TRAF1 transcriptionally activates OASL, and OASL promotes PANoptosis (combined apoptosis/necroptosis/pyroptosis) during H. pylori infection of gastric epithelial cells; OASL overexpression reverses the PANoptosis suppression caused by TRAF1 knockdown. Co-immunoprecipitation (OASL-ZBP1-PANoptosome interaction), TRAF1 knockdown/OASL overexpression rescue, functional assays (CCK-8, colony formation, TUNEL), in vivo H. pylori infection model Apoptosis Low 41942799
2022 OASL overexpression in SSc CD4+ T cells upregulates TET1 via IRF1 signaling, increasing hydroxymethylation of CD4+ T cell genomes and promoting aberrant expression of CD40L and CD70, driving CD4+ T cell hyperactivation; IRF1 binds the TET1 promoter as confirmed by dual luciferase reporter assay. RNA sequencing, overexpression experiments, dual luciferase reporter assay (IRF1 binding TET1 promoter), hydroxymethylation assays, flow cytometry Arthritis research & therapy Low 35183246

Source papers

Stage 0 corpus · 55 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 Antiviral activity of human OASL protein is mediated by enhancing signaling of the RIG-I RNA sensor. Immunity 224 24931123
2015 Oligoadenylate synthase-like (OASL) proteins: dual functions and associations with diseases. Experimental & molecular medicine 202 25744296
1998 p59OASL, a 2'-5' oligoadenylate synthetase like protein: a novel human gene related to the 2'-5' oligoadenylate synthetase family. Nucleic acids research 102 9722630
2009 Differential regulation of the OASL and OAS1 genes in response to viral infections. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 98 19203244
2019 Oligoadenylate-Synthetase-Family Protein OASL Inhibits Activity of the DNA Sensor cGAS during DNA Virus Infection to Limit Interferon Production. Immunity 97 30635239
2015 OASL-a new player in controlling antiviral innate immunity. Current opinion in virology 93 25676874
2011 Genetic variants in LPL, OASL and TOMM40/APOE-C1-C2-C4 genes are associated with multiple cardiovascular-related traits. BMC medical genetics 87 21943158
2015 Structural and functional analysis reveals that human OASL binds dsRNA to enhance RIG-I signaling. Nucleic acids research 71 25925578
2022 Novel role of macrophage TXNIP-mediated CYLD-NRF2-OASL1 axis in stress-induced liver inflammation and cell death. JHEP reports : innovation in hepatology 59 36035360
2017 The Association of OASL and Type I Interferons in the Pathogenesis and Survival of Intracellular Replicating Bacterial Species. Frontiers in cellular and infection microbiology 51 28580319
2013 Negative regulation of type I IFN expression by OASL1 permits chronic viral infection and CD8⁺ T-cell exhaustion. PLoS pathogens 43 23874199
2020 MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL. Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas 41 32321151
2023 OASL phase condensation induces amyloid-like fibrillation of RIPK3 to promote virus-induced necroptosis. Nature cell biology 38 36604592
2023 Novel CH25H+ and OASL+ microglia subclusters play distinct roles in cerebral ischemic stroke. Journal of neuroinflammation 32 37183260
2018 Molecular Mechanisms for the Adaptive Switching Between the OAS/RNase L and OASL/RIG-I Pathways in Birds and Mammals. Frontiers in immunology 32 29973937
2018 Regulatory roles of OASL in lung cancer cell sensitivity to Actinidia chinensis Planch root extract (acRoots). Cell biology and toxicology 30 29508110
2017 Goose Mx and OASL Play Vital Roles in the Antiviral Effects of Type I, II, and III Interferon against Newly Emerging Avian Flavivirus. Frontiers in immunology 29 28878774
2022 2'-5' oligoadenylate synthetase‑like 1 (OASL1) protects against atherosclerosis by maintaining endothelial nitric oxide synthase mRNA stability. Nature communications 25 36333342
2021 Pseudorabies virus UL24 antagonizes OASL-mediated antiviral effect. Virus research 25 33476694
2020 OASL Triggered by Novel Goose Astrovirus via ORF2 Restricts Its Replication. Journal of virology 24 32967952
2016 OASL1 deficiency promotes antiviral protection against genital herpes simplex virus type 2 infection by enhancing type I interferon production. Scientific reports 23 26750802
2004 Interaction between the 2'-5' oligoadenylate synthetase-like protein p59 OASL and the transcriptional repressor methyl CpG-binding protein 1. European journal of biochemistry 22 14728690
2023 OASL knockdown inhibits the progression of stomach adenocarcinoma by regulating the mTORC1 signaling pathway. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 20 36809539
2018 OASL1 Traps Viral RNAs in Stress Granules to Promote Antiviral Responses. Molecules and cells 17 29463066
2023 ATM Inhibition-Induced ISG15/IFI27/OASL Is Correlated with Immunotherapy Response and Inflamed Immunophenotype. Cells 15 37174688
2021 Positive Feedback Loop of Long Noncoding RNA OASL-IT1 and Innate Immune Response Restricts the Replication of Zika Virus in Epithelial A549 Cells. Journal of innate immunity 15 33626545
2016 2'-5' Oligoadenylate synthetase-like 1 (OASL1) deficiency in mice promotes an effective anti-tumor immune response by enhancing the production of type I interferons. Cancer immunology, immunotherapy : CII 14 27034232
2022 OASL1-Mediated Inhibition of Type I IFN Reduces Influenza A Infection-Induced Airway Inflammation by Regulating ILC2s. Allergy, asthma & immunology research 13 34983110
2012 Identification of OASL d, a splice variant of human OASL, with antiviral activity. The international journal of biochemistry & cell biology 13 22531715
2024 OASL suppresses infectious bursal disease virus replication by targeting VP2 for degrading through the autophagy pathway. Journal of virology 12 38639485
2023 Functional evaluation of rare OASL variants by analysis of SLE patient-derived iPSCs. Journal of autoimmunity 12 37354689
2013 Differential upregulation of human 2'5'OAS genes on systemic sclerosis: Detection of increased basal levels of OASL and OAS2 genes through a qPCR based assay. Autoimmunity 12 24328427
2023 Host DNA Demethylation Induced by DNMT1 Inhibition Up-Regulates Antiviral OASL Protein during Influenza a Virus Infection. Viruses 10 37631988
2022 Overexpression of OASL upregulates TET1 to induce aberrant activation of CD4+ T cells in systemic sclerosis via IRF1 signaling. Arthritis research & therapy 9 35183246
2017 Identification of a novel porcine OASL variant exhibiting antiviral activity. Virus research 9 29155034
2025 OASL promotes immune evasion in pancreatic ductal adenocarcinoma by enhancing autolysosome-mediated degradation of MHC-I. Theranostics 8 39990208
2025 Activation of HTR2B Suppresses Osteosarcoma Progression through the STAT1-NLRP3 Inflammasome Pathway and Promotes OASL1+ Macrophage Production to Enhance Antitumor Immunity. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 7 40387572
2020 Tupaia OASL1 Promotes Cellular Antiviral Immune Responses by Recruiting MDA5 to MAVS. Journal of immunology (Baltimore, Md. : 1950) 7 33188074
2021 Interferon Lambda 3/4 (IFNλ3/4) rs12979860 Polymorphisms Is Not Associated With Susceptibility to Systemic Lupus Erythematosus, Although It Regulates OASL Expression in Patients With SLE. Frontiers in genetics 6 34149799
2025 Intrinsic OASL expression licenses interferon induction during influenza A virus infection. bioRxiv : the preprint server for biology 4 40166309
2025 OASL activates MAPK to drive psoriatic pathogenesis: Astilbin targeting this axis improves metabolic-inflammation crosstalk. Life sciences 3 40360089
2019 Enhanced Antitumor Immune Response in 2'-5' Oligoadenylate Synthetase-Like 1- (OASL1-) Deficient Mice upon Cisplatin Chemotherapy and Radiotherapy. Journal of immunology research 3 31049360
2025 Intrinsic OASL expression governs heterogeneity in interferon induction during influenza A virus infection. Proceedings of the National Academy of Sciences of the United States of America 2 41468430
2024 Peptidase inhibitor 16 promotes proliferation of pancreatic ductal adenocarcinoma cells through OASL signaling. Molecular carcinogenesis 2 38353288
2025 Research on expression patterns of endogenous OASL and IFN-α in duck embryos infected with DHAV-3. Polish journal of veterinary sciences 1 40130293
2025 Effect of OASL on oxaliplatin-induced immunogenic cell death in gastric cancer via the cGAS-STING signaling pathway. Cell death discovery 1 41271618
2025 Matrix stiffening-driven hepatocellular carcinoma progression through OASL-mediated cGAS-STING repression and subsequent macrophage activation. International immunopharmacology 1 41330170
2024 The role of 2'-5'-oligoadenylate synthase-like protein (OASL1) in biliary and hepatotoxin-induced liver injury in mice. Scientific reports 1 39300174
2026 An OASL homologue involved in IFN-like antiviral signal by binding MDA5 in the Pacific oyster Crassostrea gigas. Fish & shellfish immunology 0 41580101
2026 In silico structural and functional characterization of high-risk missense variants in MMP8, GZMK, and OASL genes associated with epidemic viral infections. Scientific reports 0 41807577
2026 2'-5' Oligoadenylate Synthetase-Like 1- (OASL1-) deficient mice promote antiviral protection against pseudorabies virus infection associated with enhanced production of type I interferon. Scientific reports 0 41813805
2026 Helicobacter pylori activates the TRAF1/OASL/ZBP1-PANoptosome pathway to induce PANoptosis in the gastric mucosa. Apoptosis : an international journal on programmed cell death 0 41942799
2026 Expression dynamics and antiviral role of chicken OASL during infectious bronchitis virus infection. Poultry science 0 42102758
2025 Elucidating OASL-RNA Interactions: Structural and energetic insights into vault RNAs binding. Journal of molecular graphics & modelling 0 40378427
2025 HERC5, IFI6, IFIT3, and OASL as potential diagnostic biomarkers for systemic lupus erythematosus: an integrated bioinformatics, machine learning and clinical validation. Clinical rheumatology 0 41432807

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