Affinage

ZSWIM8

Zinc finger SWIM domain-containing protein 8 · UniProt A7E2V4

Length
1837 aa
Mass
197.3 kDa
Annotated
2026-06-11
41 papers in source corpus 18 papers cited in narrative 16 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

ZSWIM8 is the substrate-receptor subunit of a Cullin-RING E3 ubiquitin ligase that controls miRNA stability by executing target-directed miRNA degradation (TDMD), a pathway conserved across bilaterian animals (PMID:33184237, PMID:33184234, PMID:37532519, PMID:37553261). It recognizes Argonaute (AGO) complexes specifically when the loaded miRNA is extensively base-paired to a highly complementary 'trigger' RNA, polyubiquitinates AGO, and routes it for proteasomal degradation, thereby exposing the miRNA to nucleolytic decay in a manner independent of miRNA tailing and trimming (PMID:33184237, PMID:33184234, PMID:41851464, PMID:39433399). Cryo-EM and in vitro reconstitution show that trigger pairing extracts the miRNA from a binding pocket in AGO2 and that ZSWIM8 reads out both the exposed pocket and the distinct trajectory of the trigger RNA — a 'two-RNA-factor authentication' mechanism that specifies ubiquitylation without a conventional degron (PMID:41851464, PMID:41542392). Through this activity ZSWIM8 sets the half-lives of most short-lived miRNAs in mammals, and its loss causes perinatal lethality with lung sacculation and ventricular septal defects, while genetic removal of the miR-322/miR-503 cluster rescues the embryonic growth restriction of Zswim8-null mice, establishing TDMD of specific miRNAs as a developmental requirement (PMID:37532519, PMID:37553261, PMID:41213800). The complex assembles with CRL3 components (Cul3, EloB, EloC) in invertebrate cells, and in C. elegans EBAX-1 requires a Cullin-2 binding motif for one of its activities, indicating context-dependent cullin usage (PMID:40328417, PMID:41542532). Beyond miRNA control, ZSWIM8 performs protein quality control on intrinsically disordered substrates: it eliminates misfolded Disabled-1 (Dab1) via a 'disorder targets misorder' mechanism in the developing nervous system (PMID:35989311), and it can be hijacked by Zika virus NS5, which scaffolds STAT2 onto the ZSWIM8-CUL3 complex to drive STAT2 degradation and suppress type I interferon signaling (PMID:39145933). ZSWIM8/TDMD also shapes oligodendrocyte myelination, neural progenitor migration and synaptogenesis, and developmental cell-fate decisions including non-apoptotic linker-cell death in C. elegans (PMID:35989311, PMID:41787678, PMID:41542532).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2020 High

    Established the core function: how are mature miRNAs actively degraded when engaged by highly complementary targets, answered by identifying ZSWIM8 as a CRL substrate adaptor that destroys AGO to expose the miRNA.

    Evidence CRISPR loss-of-function, reciprocal Co-IP of ZSWIM8-CRL with AGO, and small-RNA sequencing across mammals, flies, and nematodes

    PMID:33184234 PMID:33184237

    Open questions at the time
    • Did not resolve how the complex structurally distinguishes trigger-paired AGO from canonical targets
    • Did not identify the full repertoire of affected miRNAs in vivo
  2. 2020 High

    Defined the rate-limiting step and substrate specificity: AGO polyubiquitination and proteasomal degradation is the key regulatory event, and the complex only recognizes extensively trigger-paired AGO.

    Evidence In vitro ubiquitylation reconstitution, cellular ubiquitination assays with mutagenesis, and cryo-EM of the AGO2-miRNA-trigger-ZSWIM8 complex

    PMID:41851464

    Open questions at the time
    • Atomic basis of conformational recognition not fully resolved here
    • E2 enzyme partners and ubiquitin chain topology not detailed
  3. 2026 High

    Resolved the recognition logic: how is ubiquitylation specified absent a linear degron, answered by a two-RNA-factor authentication mechanism in which trigger pairing extracts the miRNA and ZSWIM8 reads both the exposed AGO2 pocket and the trigger RNA path.

    Evidence Cryo-EM structural determination with in vitro reconstitution, active-site mutagenesis, and cellular assays (preprint and journal versions)

    PMID:41542392 PMID:41851464

    Open questions at the time
    • Whether all triggers engage identical contacts is untested
    • Kinetics of conformational capture versus dissociation not quantified
  4. 2023 High

    Demonstrated the physiological scope in mammals: ZSWIM8 specifies the half-lives of most short-lived miRNAs and is required for cardiac and pulmonary development.

    Evidence Constitutive Zswim8 knockout mouse with small-RNA sequencing across 12 tissues and mRNA target analysis

    PMID:37532519 PMID:37553261

    Open questions at the time
    • The triggers for most affected miRNAs were not identified
    • Tissue-specific trigger sources not mapped
  5. 2023 High

    Provided causal proof that a defined developmental phenotype results from failed degradation of specific miRNAs, by rescuing growth restriction through miR-322/miR-503 deletion.

    Evidence Mouse genetic epistasis with double knockout (Zswim8-null x miR-322/503-null) and embryonic growth measurement

    PMID:37553261 PMID:41213800

    Open questions at the time
    • Other ZSWIM8 phenotypes (cardiac, pulmonary) not attributed to specific miRNAs
    • Trigger RNA for miR-322/503 not defined in this work
  6. 2023 Medium

    Broadened ZSWIM8 function beyond miRNAs to protein quality control, showing it eliminates misfolded Dab1 via recognition of intrinsically disordered regions, with neurodevelopmental consequences.

    Evidence Conditional CRISPR knockout in mouse nervous system, Co-IP, ubiquitination assays, and neuronal spine/synapse imaging

    PMID:35989311

    Open questions at the time
    • Single lab; generality of the 'disorder targets misorder' rule across substrates untested
    • Relative contribution of TDMD versus Dab1 quality control to the neural phenotype unresolved
  7. 2026 Medium

    Extended ZSWIM8's role to glial development, linking AGO2 stabilization and disrupted miR-7 TDMD plus IDR-protein accumulation to myelination defects.

    Evidence Conditional ZSWIM8 brain knockout with proteomics, AGO2 ubiquitination assays, miRNA sequencing, and myelination histology

    PMID:41787678

    Open questions at the time
    • Single lab; which IDR-protein substrates drive the phenotype not pinned down
    • Causal separation of TDMD versus protein-quality-control contributions incomplete
  8. 2024 High

    Revealed ZSWIM8 as a hijackable substrate receptor: Zika virus NS5 scaffolds STAT2 onto ZSWIM8-CUL3 to drive its degradation and dampen interferon signaling.

    Evidence Genome-wide CRISPR screen, ZSWIM8/CUL3 depletion, bridging Co-IP, and ubiquitination assays in A549/Huh7 and neural progenitor cells

    PMID:39145933

    Open questions at the time
    • Whether other viral or endogenous adaptors redirect ZSWIM8 similarly is unknown
    • Structural basis of NS5-mediated bridging not determined
  9. 2021 Medium

    Addressed substrate determinants by showing AGO protein identity, not small-RNA modification, governs TDMD sensitivity in Drosophila.

    Evidence Dora loss-of-function with small-RNA sequencing comparing Ago1- versus Ago2-loaded siRNAs and 2'-O-methylation analysis

    PMID:33853897

    Open questions at the time
    • The AGO2 features conferring protection were not mapped
    • Single-organism observation
  10. 2023 High

    Identified endogenous triggers and an autoregulatory loop, showing the AGO1 3'UTR itself encodes a trigger that drives miR-999 degradation in flies.

    Evidence AGO1-CLASH in Dora-KO S2 cells with in vivo CRISPR deletion of the trigger site and miRNA/mRNA sequencing

    PMID:37055443

    Open questions at the time
    • Conservation of the AGO1-encoded trigger to mammals untested
    • Functional consequence of the autoregulatory loop on AGO homeostasis unclear
  11. 2024 Medium

    Confirmed conservation of the degradation mechanism in C. elegans, where EBAX-1 polyubiquitinates AGO to expose miRNAs to nucleases with developmental-stage specificity.

    Evidence ebax-1 mutant small-RNA sequencing across stages and miRNA 3'-region replacement experiments

    PMID:39433399

    Open questions at the time
    • The nucleases degrading exposed miRNAs not identified
    • Variable role of the miRNA 3' region not mechanistically explained
  12. 2025 Medium

    Clarified cullin and granule context in flies, associating Dora with CRL3 (Cul3/EloB/EloC) and localizing it to distinct protein granules, with loss impairing Notch signaling.

    Evidence Co-IP with CRL3 components, dora KO with miRNA sequencing, CRL3 RNAi, neddylation inhibition, and fluorescence localization

    PMID:40328417

    Open questions at the time
    • Composition and function of the Dora granules undefined
    • Direct miRNA connecting Dora loss to Notch defects not established
  13. 2026 Medium

    Linked ZSWIM8/EBAX-1 to a developmental cell-death program, showing it drives non-apoptotic linker-cell death cell-autonomously via TDMD of miR-35 family miRNAs.

    Evidence Genetic epistasis of ebax-1 with argonaute/mir-35/biogenesis mutants, cell-autonomous rescue, and viln-1 expression analysis (preprint)

    PMID:41542532

    Open questions at the time
    • Preprint, single lab
    • The trigger RNA inducing miR-35 degradation in dying cells not identified

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved which RNA features universally define a competent trigger across species and how the same complex partitions its activity between miRNA degradation and IDR-protein quality control in a given cell.
  • No general predictive rule for trigger RNA competence
  • No systematic catalog of non-AGO IDR substrates
  • Determinants selecting Cul3 versus Cul2 partners across contexts unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 5 GO:0016874 ligase activity 3 GO:0060090 molecular adaptor activity 3 GO:0003723 RNA binding 2
Localization
GO:0005829 cytosol 1 GO:0031410 cytoplasmic vesicle 1
Pathway
R-HSA-1266738 Developmental Biology 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-8953854 Metabolism of RNA 3 R-HSA-1643685 Disease 1 R-HSA-168256 Immune System 1
Partners
AGO2CDONCUL3DAB1ELOBELOCSTAT2
Complex memberships
Cdon/JLP/Bnip-2/CDC42 complexCullin3-RING E3 ubiquitin ligase (CRL3)

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2020 ZSWIM8 is a substrate adaptor of a Cullin-RING E3 ubiquitin ligase (CRL) that interacts with AGO proteins and mediates target-directed miRNA degradation (TDMD) by directing proteasomal decay of miRNA-containing AGO complexes engaged with highly complementary 'trigger' target RNAs, thereby exposing the miRNA for degradation. This mechanism is independent of miRNA tailing and trimming. CRISPR/Cas9 loss-of-function, co-immunoprecipitation of ZSWIM8 CRL with AGO proteins, small RNA sequencing in loss-of-function cells, genetic rescue experiments in mammals, flies, and nematodes Science (New York, N.Y.) High 33184234 33184237
2020 ZSWIM8 CRL-mediated AGO polyubiquitination and proteasomal degradation is the key regulatory step of TDMD; the ZSWIM8 CRL specifically recognizes AGO complexes only when the miRNA is extensively paired to a trigger RNA, not when engaged with typical target RNAs. Biochemical in vitro ubiquitylation assays, cryo-EM structural analysis of AGO2-miRNA-trigger complex bound to ZSWIM8, cellular ubiquitination assays with mutational analysis Nature High 41851464
2026 Cryo-EM analyses revealed that ZSWIM8 recognizes distinct AGO2 conformational states induced by miRNA-trigger pairing: the trigger RNA extracts the miRNA from a binding pocket within AGO2, allowing the pocket to be captured by ZSWIM8, and the trigger RNA itself follows a distinct trajectory also recognized by ZSWIM8. This establishes a 'two-RNA-factor authentication' mechanism for specifying AGO ubiquitylation that does not conform to a conventional degron. Cryo-EM structural determination, in vitro biochemical ubiquitylation reconstitution, active-site mutagenesis, cellular assays Nature High 41542392 41851464
2023 Conditional deletion of Zswim8 in the mouse embryonic nervous system causes global cellular stress, partial perinatal lethality, defective migration of neural progenitor cells, and impaired spine formation and synaptogenesis. Mechanistically, ZSWIM8 controls protein quality of Disabled 1 (Dab1) by recognizing intrinsically disordered regions (IDRs) of Dab1 through a 'disorder targets misorder' mechanism, eliminating misfolded Dab1 that cannot be properly phosphorylated. Conditional CRISPR knockout in mouse nervous system, Co-IP/pulldown for ZSWIM8-Dab1 interaction, ubiquitination assays, hippocampal neuron spine/synapse imaging Cerebral cortex (New York, N.Y. : 1991) Medium 35989311
2023 Constitutive Zswim8 knockout mice die perinatally with lung sacculation defects (failed alveolar epithelial maturation) and ventricular septal defects. Loss of ZSWIM8 results in aberrant accumulation of >50 miRNAs across 12 tissues, demonstrating that ZSWIM8 specifies the half-lives of most short-lived miRNAs in mice. ZSWIM8-sensitive miRNAs are preferentially produced from genomic miRNA clusters, and ZSWIM8 can cause strand/isoform switching from a miRNA hairpin. Constitutive Zswim8 knockout mouse generation, small RNA sequencing across 12 tissues, mRNA target repression analysis Genome research High 37532519 37553261
2023 Deletion of miR-322 and miR-503 rescued embryonic growth restriction in Zswim8-null mice, directly establishing that TDMD-mediated degradation of these specific miRNAs by ZSWIM8 is required for normal mammalian body size. Genetic epistasis in mice — double KO (Zswim8-null × miR-322/503-null) with embryonic growth measurements Genes & development High 37553261 41213800
2024 ZSWIM8, as the substrate receptor of the Cullin3-RING E3 ligase complex, is required for Zika virus NS5-mediated degradation of STAT2. NS5 acts as a scaffold that enhances the interaction between STAT2 and the ZSWIM8-CUL3 complex, facilitating STAT2 ubiquitination and proteasomal degradation, thereby suppressing type I interferon signaling. Genome-wide CRISPR/Cas9 screen, genetic depletion of ZSWIM8 and CUL3, biochemical Co-IP showing NS5 bridges STAT2 and ZSWIM8-CUL3, ubiquitination assays, ZSWIM8 KO in A549/Huh7 and human neural progenitor cells Proceedings of the National Academy of Sciences of the United States of America High 39145933
2022 The Drosophila ZSWIM8 ortholog Pelado/CG34401 promotes linear actin filament polymerization at the expense of branched filaments. Loss of Pelado causes actin hair elongation defects in epithelial cells and loss of filopodia in hemocytes. This function is conserved in human cells, where ZSWIM8 knockdown inhibits cell migration by affecting branched actin polymerization. Drosophila pelado mutant analysis, genetic epistasis with actin regulators (linear vs. branched polymerization), human cell ZSWIM8 knockdown with migration assay and actin cytoskeleton imaging Life science alliance Medium 35940847
2021 ZSWIM8 is induced during C2C12 myoblast differentiation and is incorporated into the Cdon/JLP/Bnip-2/CDC42 complex. ZSWIM8 knockdown accelerates C2C12 differentiation, indicating that ZSWIM8 partly prevents myogenic differentiation. However, ZSWIM8-dependent ubiquitination or degradation of Bnip2, Cdon, or JLP was not detected. Co-immunoprecipitation of ZSWIM8 with Cdon complex components, siRNA knockdown of Zswim8 in C2C12 cells with differentiation assay, ubiquitination assay (negative for Bnip2/Cdon/JLP as substrates) Scientific reports Medium 34686700
2021 In Drosophila, siRNAs loaded into Ago2 are insensitive to Dora (ZSWIM8 ortholog)-mediated target-directed degradation. This protection is conferred by features of the Ago2 protein itself, not by 2'-O-methylation of the small RNA 3' termini. In contrast, the same siRNAs are sensitive to Dora when loaded into Ago1. Genetic Dora loss-of-function in Drosophila, small RNA sequencing comparing Ago1- vs. Ago2-loaded siRNAs, 2'-O-methylation analysis RNA (New York, N.Y.) Medium 33853897
2023 In Drosophila S2 cells, the ZSWIM8 ortholog Dora is required for TDMD; AGO1-CLASH identified five TDMD trigger sequences, including a trigger in the 3' UTR of AGO1 mRNA itself that induces miR-999 degradation. Knockout of the AGO1 trigger in S2 cells and in Drosophila specifically elevated miR-999 with concurrent repression of miR-999 targets. AGO1-CLASH in Dora CRISPR KO Drosophila S2 cells, CRISPR-Cas9 knockout of the AGO1 3' UTR trigger site in S2 cells and in vivo, miRNA/mRNA sequencing Nature communications High 37055443
2024 In C. elegans, EBAX-1 (the ZSWIM8 ortholog) polyubiquitinates AGO, leading to its degradation and exposure of the miRNA to cellular nucleases; 22 miRNAs are sensitive to EBAX-1 loss, with the greatest effect in L1 larvae. The 3' region of a miRNA influences EBAX-1 sensitivity in a variable manner. ebax-1 mutant small RNA sequencing at multiple developmental stages, mRNA target repression analysis, miRNA 3' region replacement experiments RNA (New York, N.Y.) Medium 39433399
2025 In Drosophila ovarian somatic cells, Dora (ZSWIM8 ortholog) associates with CRL3 complex proteins (Cul3, EloB, EloC), and depletion of CRL3 components or inhibition of Cul3 neddylation (via UbcE2M) upregulates miR-7-5p. Dora localizes to protein granules distinct from P-bodies and GW-bodies. Loss of Dora impairs Notch signaling pathway activity. Co-immunoprecipitation of Dora with CRL3 components, dora CRISPR KO with miRNA sequencing, CRL3 component RNAi, neddylation inhibition, fluorescence localization of tagged Dora Biochimica et biophysica acta. Gene regulatory mechanisms Medium 40328417
2026 ZSWIM8 is indispensable for oligodendrocyte maturation and myelination. Loss of ZSWIM8 in brain causes accumulation of IDR-rich proteins including RNA-binding proteins; AGO2 stabilization in ZSWIM8-null tissues disrupts TDMD of miR-7, leading to altered gene expression and myelination defects in vivo. ZSWIM8-mediated ubiquitination of AGO2 also requires microRNA binding to AGO2. Conditional ZSWIM8 KO in mouse brain, proteomic analysis of IDR protein accumulation, AGO2 ubiquitination assays, miRNA sequencing, myelination phenotype histology Glia Medium 41787678
2026 In C. elegans, EBAX-1/ZSWIM8 promotes linker cell-type death (LCD) non-apoptotically and cell-autonomously through TDMD. EBAX-1 requires its Cullin-2 binding motif for LCD. Loss of mir-35 family miRNAs, argonautes, or miRNA biogenesis factors restores LCD to ebax-1 mutants. The predicted miR-35 target viln-1/villin mRNA is upregulated in dying cells and required for LCD. Genetic epistasis (ebax-1 mutant × argonaute/mir-35/biogenesis factor mutants), cell-autonomous rescue, mRNA expression analysis of viln-1, LCD quantitation bioRxiv : the preprint server for biologypreprint Medium 41542532
2024 In Pristionchus pacificus, EBAX-1/ZSWIM8 destabilizes the clustered miRNA family miR-2235a/miR-35, and this is required for transgenerational epigenetic memory of the predatory mouth form after dietary switching. Ppa-ebax-1 mutants show no transgenerational memory; deletion of a cluster of 44 miR-2235a copies results in precocious and extended transgenerational inheritance. ebax-1 mutant analysis, miRNA cluster deletion, dietary induction and food-reversal experiments across multiple generations, miRNA sequencing bioRxiv : the preprint server for biologypreprint Low bio_10.1101_2024.09.10.612280

Source papers

Stage 0 corpus · 41 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2020 The ZSWIM8 ubiquitin ligase mediates target-directed microRNA degradation. Science (New York, N.Y.) 187 33184237
2020 A ubiquitin ligase mediates target-directed microRNA decay independently of tailing and trimming. Science (New York, N.Y.) 182 33184234
2022 MicroRNA turnover: a tale of tailing, trimming, and targets. Trends in biochemical sciences 59 35811249
2024 To kill a microRNA: emerging concepts in target-directed microRNA degradation. Nucleic acids research 49 38224449
2021 Widespread microRNA degradation elements in target mRNAs can assist the encoded proteins. Genes & development 48 34819352
2022 The developmentally timed decay of an essential microRNA family is seed-sequence dependent. Cell reports 45 35947946
2024 Zika virus NS5 protein inhibits type I interferon signaling via CRL3 E3 ubiquitin ligase-mediated degradation of STAT2. Proceedings of the National Academy of Sciences of the United States of America 37 39145933
2023 Target-directed microRNA degradation regulates developmental microRNA expression and embryonic growth in mammals. Genes & development 34 37553261
2023 ZSWIM8 destabilizes many murine microRNAs and is required for proper embryonic growth and development. Genome research 31 37532519
2023 Screening of Drosophila microRNA-degradation sequences reveals Argonaute1 mRNA's role in regulating miR-999. Nature communications 30 37055443
2021 Ago2 protects Drosophila siRNAs and microRNAs from target-directed degradation, even in the absence of 2'-O-methylation. RNA (New York, N.Y.) 29 33853897
2024 Target-directed microRNA degradation: Mechanisms, significance, and functional implications. Wiley interdisciplinary reviews. RNA 26 38448799
2023 The ZSWIM8 ubiquitin ligase regulates neurodevelopment by guarding the protein quality of intrinsically disordered Dab1. Cerebral cortex (New York, N.Y. : 1991) 21 35989311
2024 Widespread destabilization of Caenorhabditis elegans microRNAs by the E3 ubiquitin ligase EBAX-1. RNA (New York, N.Y.) 17 39433399
2023 Genome-wide identification and spatiotemporal expression profiling of zinc finger SWIM domain-containing protein family genes. Zoological research 12 37161653
2022 The conserved Pelado/ZSWIM8 protein regulates actin dynamics by promoting linear actin filament polymerization. Life science alliance 12 35940847
2021 To Degrade a MicroRNA, Destroy Its Argonaute Protein. Molecular cell 10 33482091
2021 ZSWIM8 is a myogenic protein that partly prevents C2C12 differentiation. Scientific reports 10 34686700
2023 A statistical approach for identifying primary substrates of ZSWIM8-mediated microRNA degradation in small-RNA sequencing data. BMC bioinformatics 8 37170259
2023 Establishment and validation of the autophagy-related ceRNA network in irreversible pulpitis. BMC genomics 5 37208635
2026 Plagl1 and Lrrc58 control mammalian body size by triggering target-directed microRNA degradation of miR-322 and miR-503. Genes & development 4 41213800
2026 A lncRNA drives developmentally timed decay of all members of an essential microRNA family. Genes & development 4 41791866
2025 CLASHub: an integrated database and analytical platform for microRNA-target interactions. bioRxiv : the preprint server for biology 4 40799581
2024 Retargeting target-directed microRNA-decay sites to highly expressed viral or cellular miRNAs. Nucleic acids research 4 39588775
2025 Comparative structural insights and functional analysis for the distinct unbound states of Human AGO proteins. Scientific reports 3 40108192
2025 A lncRNA drives developmentally-timed decay of all members of an essential microRNA family. bioRxiv : the preprint server for biology 3 40766674
2026 The E3 ubiquitin ligase mechanism specifying targeted microRNA degradation. Nature 2 41851464
2025 Insights into the target-directed miRNA degradation mechanism in Drosophila ovarian cell culture. Biochimica et biophysica acta. Gene regulatory mechanisms 2 40328417
2025 Plagl1 and Lrrc58 control mammalian body size by triggering target-directed microRNA degradation of miR-322 and miR-503. bioRxiv : the preprint server for biology 2 40631113
2025 mRNA 3' UTRs direct microRNA degradation to participate in imprinted gene networks and regulate growth. bioRxiv : the preprint server for biology 2 41279844
2026 mRNA 3' UTRs direct microRNA degradation to participate in imprinted gene networks and regulate growth. Genes & development 1 41871909
2026 CLASHub is an integrated database and analytical platform for microRNA-target interactions. Nature communications 1 42098137
2025 Regulatory Mechanisms of miRNA Turnover: Insights into ZSWIM8-Mediated Target-Directed MicroRNA Degradation. Biomedicines 1 41007757
2023 Target-directed microRNA degradation regulates developmental microRNA expression and embryonic growth in mammals. bioRxiv : the preprint server for biology 1 37425885
2022 NeuroSCORE is a genome-wide omics-based model that identifies candidate disease genes of the central nervous system. Scientific reports 1 35361823
2026 The E3 ubiquitin ligase mechanism specifying target-directed microRNA degradation. bioRxiv : the preprint server for biology 0 41542392
2026 C. elegans E3 ubiquitin ligase EBAX-1 promotes non-apoptotic linker cell-type death through target-directed miRNA degradation. bioRxiv : the preprint server for biology 0 41542532
2026 MiRNA Stability and Degradation: Dynamic Regulators of Cellular Regulatory Networks. Wiley interdisciplinary reviews. RNA 0 41608885
2026 The Ubiquitin Ligase Zinc Finger SWIM Domain-Containing Protein 8 Regulates Oligodendrocyte Development Through the Argonaute2/MicroRNA-7 Axis. Glia 0 41787678
2026 Linking miRNAs to decay. Genes & development 0 41887800
2025 Dora, a key component of target-directed miRNA degradation, is essential for local genomic amplification in Drosophila ovarian follicle cells. Gene 0 40684817

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