Affinage

TASOR

Protein TASOR · UniProt Q9UK61

Length
1670 aa
Mass
189.0 kDa
Annotated
2026-06-10
26 papers in source corpus 20 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TASOR is the central scaffolding subunit of the HUSH (human silencing hub) complex, which it assembles with MPP8 and Periphilin to deposit H3K9me3 heterochromatin and transcriptionally silence retroviruses, repetitive transgenes, and evolutionarily young, full-length LINE-1 retrotransposons residing in euchromatin (PMID:26022416, PMID:29211708, PMID:33009411). TASOR organizes the complex through defined interaction interfaces—an N-terminal catalytically-inactive pseudo-PARP (DUF3715/RDTS) domain required for targeted H3K9me3 deposition and silencing, a SPOC and novel-fold module engaging the MPP8 C-terminal domain, and a minimal core that binds a Periphilin homodimer—and through these contacts recruits the methyltransferase SETDB1 to establish and maintain silencing (PMID:33009411, PMID:32976585, PMID:37433650, PMID:39638237, PMID:39489739). Targeting is RNA-directed and co-transcriptional: Periphilin's N-terminal domain binds nascent transcripts to initiate silencing (PMID:39658355), while TASOR couples the complex to elongating RNA Polymerase II and to RNA-degradation machinery including the CNOT1/CCR4-NOT deadenylase complex and the RNA exosome, and accumulates at sites of high RNAPII occupancy and transcription termination through the WDR82/CPSF termination machinery (PMID:35013187, PMID:37164018). During replication, HUSH interacts with leading-strand polymerase Pol ε to propagate asymmetric H3K9me3 onto leading strands at LINE-1 elements (PMID:37938774). Loss of TASOR de-represses LINE-1s, triggering replication stress and activating innate immune sensing via MAVS and cGAS/STING (PMID:39453814, PMID:42190982). The HIV-2/SIV accessory protein Vpx antagonizes this pathway by stabilizing a ternary complex between TASOR's N-terminal PARP-like domain, DCAF1, and the CUL4 E3 ligase to drive proteasomal degradation of TASOR, reactivating latent proviruses (PMID:29891865, PMID:30297740, PMID:34699574).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2015 High

    Established that TASOR is a core subunit of a previously unknown silencing complex that maintains H3K9me3 heterochromatin, answering how certain integrated retroviruses and genomic loci are kept transcriptionally silent.

    Evidence Forward genetic screen in haploid KBM7 cells with ChIP for H3K9me3

    PMID:26022416

    Open questions at the time
    • Did not define how HUSH is targeted to specific loci
    • Did not assign TASOR a distinct molecular function within the complex
  2. 2017 High

    Identified the principal endogenous targets of HUSH as young, full-length LINE-1 elements in permissive euchromatin, explaining the complex's role in genome surveillance and its impact on host gene expression.

    Evidence Genome-wide CRISPR screen and ChIP-seq in two human cell lines

    PMID:29211708

    Open questions at the time
    • Did not establish how young L1 elements are recognized
    • Mechanism of co-transcriptional targeting unresolved
  3. 2018 High

    Revealed that HIV-2/SIV Vpx counteracts HUSH by inducing proteasomal degradation of TASOR via DCAF1-CUL4, linking the complex to retroviral latency and host antiviral defense.

    Evidence Proteomic screen, co-IP, proteasome inhibitor rescue, and HIV latency reactivation assays (two concurrent papers)

    PMID:29891865 PMID:30297740

    Open questions at the time
    • Did not map the TASOR domains engaged by Vpx/DCAF1
    • Did not address whether degradation is selective for specific HUSH functions
  4. 2018 High

    Showed HUSH/TASOR is recruited by NP220 to silence unintegrated retroviral DNA together with SETDB1 and HDACs, broadening the range of foreign DNA the complex restricts.

    Evidence Genome-wide CRISPR screen, ChIP, and knockout validation

    PMID:30487602

    Open questions at the time
    • Did not define TASOR's direct contribution versus other recruited factors
    • Generality of NP220-dependent recruitment unclear
  5. 2020 High

    Defined TASOR as the central scaffold whose pseudo-PARP domain is required for H3K9me3 deposition independent of complex assembly, and resolved the Periphilin-TASOR core interface, providing the architectural basis of HUSH.

    Evidence Biochemical reconstitution, domain mutagenesis, ChIP-seq, reporter assays, and X-ray crystallography of the Periphilin-TASOR core

    PMID:32976585 PMID:33009411

    Open questions at the time
    • Did not establish the catalytic or binding function of the pseudo-PARP domain
    • Did not resolve the TASOR-MPP8 interface
  6. 2021 Medium

    Mapped TASOR's N-terminal PARP-like domain as the DCAF1-binding region and showed TASOR-DCAF1 association is constitutive but Vpx-stabilized into a degradative ternary complex, clarifying the molecular logic of Vpx antagonism.

    Evidence Co-IP with domain and Vpx point mutants plus HIV reporter assay

    PMID:34699574

    Open questions at the time
    • Single lab
    • Physiological role of basal TASOR-DCAF1 interaction unknown
  7. 2022 Medium

    Connected TASOR to post-transcriptional repression by demonstrating interactions with CNOT1, the RNA exosome, and elongating RNA Pol II, indicating HUSH couples chromatin silencing to RNA degradation at transcription centers.

    Evidence Yeast two-hybrid screen, co-IP, RNA Pol II co-IP, and HIV LTR reporter assays

    PMID:35013187

    Open questions at the time
    • Single lab
    • Direct versus indirect nature of RNA-degradation coupling not fully resolved
  8. 2022 Medium

    Identified CDK1-mediated phosphorylation of TASOR at T819 in mitosis, but showed it is dispensable for HIV-1 silencing, indicating this modification is not required for the repressive function tested.

    Evidence Phospho-specific antibody, cell cycle arrest, CDK1 inhibition, and T819 point mutant assays in an HIV-1 latency model

    PMID:36309692

    Open questions at the time
    • Positive functional role of T819 phosphorylation, if any, undefined
    • Single lab and limited mechanistic follow-up
  9. 2023 Medium

    Established the DUF3715/pseudo-PARP domain as a conserved RNA-directed silencing module by showing TEX15's homologous domain functionally substitutes in TASOR, deepening understanding of how this domain enables transposon silencing.

    Evidence Structural homology analysis and domain-swap transposon silencing assays

    PMID:37433650

    Open questions at the time
    • Single lab
    • Biochemical activity contributed by the domain remains undefined
  10. 2023 High

    Showed HUSH co-transcriptional targeting requires the termination factor WDR82 and CPSF, with the complex accumulating at high-RNAPII-occupancy regions, explaining how silencing is directed to actively transcribed repetitive loci.

    Evidence Reciprocal co-IP, ChIP-seq, epistatic WDR82/CPSF knockouts, and a Sox2 genomic rearrangement experiment

    PMID:37164018

    Open questions at the time
    • How the RNA signal is converted to chromatin recruitment unresolved
    • TASOR-specific role within this targeting not isolated
  11. 2023 High

    Demonstrated HUSH interacts with leading-strand polymerase Pol ε to propagate asymmetric H3K9me3 at replication forks, providing a mechanism for heritable maintenance of LINE-1 silencing through replication.

    Evidence Co-IP with Pol ε, strand-specific H3K9me3 ChIP, POLE3/POLE4 and MPP8/TASOR knockouts, and interaction-defective TASOR mutants

    PMID:37938774

    Open questions at the time
    • Structural basis of TASOR-Pol ε interaction not defined
    • Lagging-strand restoration mechanism unaddressed
  12. 2024 Medium

    Resolved the TASOR-MPP8 interface using crystallography and AlphaFold3 modeling validated by mutagenesis, completing the structural map of HUSH subunit contacts required for repression.

    Evidence X-ray crystallography of MPP8 CTD, AlphaFold3 modeling, point mutagenesis, and reporter assays

    PMID:39638237

    Open questions at the time
    • Model-derived interfaces partly predictive rather than experimentally resolved
    • Single lab
  13. 2024 Medium

    Revealed a paralogous HuSH2 complex centered on TASOR2 occupying distinct genomic loci, with TASOR-HUSH dedicated to LINE-1 repression and HUSH stoichiometry tuning L1 activity.

    Evidence ChIP-seq, in silico structural prediction, MPP8-TASOR interface mutagenesis, and LINE-1 reporter assays

    PMID:39489739

    Open questions at the time
    • Functional division of labor between HUSH and HuSH2 incompletely defined
    • Single lab
  14. 2024 Medium

    Connected TASOR loss to physiological consequences by showing de-repressed LINE-1 triggers replication stress and MAVS-dependent innate immune death during exit from naive pluripotency.

    Evidence CRISPR knockout, H3K9me3 ChIP, L1 expression analysis, caspase inhibition, and MAVS deletion in stem cells

    PMID:39453814

    Open questions at the time
    • Single lab
    • Whether replication stress is a direct or downstream consequence of L1 activation unresolved
  15. 2024 Medium

    Linked HUSH to PRC1.6 components L3MBTL2 and MGA at active promoters, with promoter-specific MPP8-dependent PRC1.6 recruitment, expanding the repressive cofactor network.

    Evidence Proximity labeling (dCas9-APEX2), forward genetic screen, and ChIP-seq co-localization (preprint)

    PMID:39026796

    Open questions at the time
    • Preprint, not peer-reviewed
    • Direct TASOR contribution to PRC1.6 recruitment not isolated
  16. 2025 Medium

    Demonstrated that Vpx-driven TASOR degradation activates both RNA (MAVS) and DNA (cGAS/STING) innate sensing pathways via increased LINE-1 activity, integrating HUSH antagonism with antiviral signaling.

    Evidence Vpx mutant dissection, transcriptomics, and MAVS and cGAS/STING pathway inhibition

    PMID:42190982

    Open questions at the time
    • Single lab
    • Relative contributions of RNA versus DNA sensing not quantified
  17. 2025 Medium

    Established Periphilin as the RNA-binding initiator of HUSH silencing, showing its N-terminal domain binds nascent transcripts and that tethering Periphilin suffices to silence a HUSH-insensitive transcript, defining the upstream targeting trigger.

    Evidence Unbiased RNA-binding assay, domain truncation, Periphilin NTD mutagenesis, and tethering reporter assay

    PMID:39658355

    Open questions at the time
    • Single lab
    • How Periphilin RNA recognition is converted to TASOR/MPP8-dependent chromatin modification unresolved
  18. 2025 Medium

    Showed combined MPP8/TASOR loss locks mouse ES cells in pluripotency by suppressing keratin 18/19 adhesion genes, with keratin re-expression rescuing differentiation, linking HUSH to a developmental gene-regulatory output.

    Evidence CRISPR double knockout, pluripotency exit assay, gene expression analysis, and ectopic keratin rescue

    PMID:41291012

    Open questions at the time
    • Single lab
    • Mechanistic link between HUSH silencing and keratin regulation undefined

Open questions

Synthesis pass · forward-looking unresolved questions
  • The biochemical activity contributed by TASOR's pseudo-PARP domain and how nascent-RNA recognition by Periphilin is mechanistically transduced into TASOR-directed SETDB1 recruitment and H3K9me3 deposition remain unresolved.
  • No catalytic activity assigned to the pseudo-PARP domain
  • Step-wise coupling from RNA binding to chromatin modification not reconstituted
  • Full-complex structure with SETDB1 not determined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0140110 transcription regulator activity 3
Localization
GO:0000228 nuclear chromosome 3 GO:0005634 nucleus 3
Pathway
R-HSA-1643685 Disease 3 R-HSA-4839726 Chromatin organization 3 R-HSA-168256 Immune System 2 R-HSA-74160 Gene expression (Transcription) 2 R-HSA-8953854 Metabolism of RNA 1
Partners
CNOT1DCAF1MPP8POLEPPHLN1RNA POL IISETDB1WDR82
Complex memberships
HUSH complex

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2015 TASOR is a core subunit of the HUSH (human silencing hub) complex, together with MPP8 and Periphilin. Loss of HUSH components, including TASOR, results in decreased H3K9me3 at endogenous genomic loci and at retroviruses integrated into heterochromatin. The HUSH complex is recruited to H3K9me3-rich genomic loci, where it recruits the methyltransferase SETDB1 for further H3K9me3 deposition to maintain transcriptional silencing. Forward genetic screen in near-haploid KBM7 cells, loss-of-function analysis, chromatin immunoprecipitation Science High 26022416
2017 TASOR (as part of the HUSH complex) selectively binds evolutionarily young, full-length L1 elements located in transcriptionally permissive euchromatic environments and promotes H3K9me3 deposition for transcriptional silencing. HUSH-mediated silencing events within introns of transcriptionally active genes lead to downregulation of host gene expression in a HUSH- and L1-dependent manner. CRISPR-Cas9 genome-wide screen, ChIP-seq, loss-of-function in two distinct human cell lines Nature High 29211708
2018 HIV-2/SIV Vpx protein associates with the HUSH complex and induces proteasomal degradation of TASOR (and other HUSH subunits) through recruitment of the DCAF1-CUL4A/B E3 ubiquitin ligase, independently of SAMHD1 antagonism. This degradation reactivates HIV latent proviruses and increases LINE-1 ORF1p levels. Proteomic screen, co-immunoprecipitation, proteasome inhibitor rescue, knockdown rescue experiments, HIV latency reactivation assay Nature microbiology High 29891865 30297740
2018 NP220 recruits the HUSH complex (including TASOR) along with SETDB1 and histone deacetylases HDAC1 and HDAC4 to silence unintegrated retroviral DNA; TASOR/HUSH is required for this silencing as shown by CRISPR knockout de-repression. Genome-wide CRISPR-Cas9 screen, chromatin immunoprecipitation, knockout validation Nature High 30487602
2020 TASOR is the central scaffolding subunit of the HUSH complex; it bears a catalytically-inactive (pseudo-)PARP domain that is necessary for targeted H3K9me3 deposition and transgene repression, independently of overall complex assembly. TASOR associates with RNA processing components. The modular architecture of HUSH resembles the yeast RNA-induced transcriptional silencing (RITS) complex. Biochemical reconstitution, structure-function mutagenesis of TASOR domains, H3K9me3 ChIP-seq, transgene repression reporter assay, co-immunoprecipitation Nature communications High 33009411
2020 A crystal structure of the Periphilin-TASOR minimal core complex shows that Periphilin forms an α-helical homodimer bound by a single TASOR molecule. Residues required for TASOR binding and Periphilin aggregation are required for HUSH-dependent silencing and genome-wide H3K9me3 deposition. X-ray crystallography, mutagenesis, H3K9me3 ChIP, silencing reporter assay Nucleic acids research High 32976585
2021 The N-terminal PARP-like domain of TASOR is involved in DCAF1 binding (but not in Vpx binding). TASOR can interact with DCAF1 in the absence of Vpx, and this interaction is stabilized by Vpx to form a ternary TASOR-Vpx-DCAF1 complex that leads to TASOR ubiquitination and degradation. Co-immunoprecipitation, Vpx point mutant analysis, domain mapping, functional HIV reporter assay PLoS pathogens Medium 34699574
2022 TASOR interacts with the CCR4-NOT complex scaffold CNOT1 (identified by yeast two-hybrid screen), and TASOR and CNOT1 synergistically repress HIV LTR-driven expression. TASOR also interacts with the RNA exosome and with RNA Polymerase II predominantly in its elongating state, and facilitates the association of RNA degradation proteins with RNA Pol II at transcriptional centers. Yeast two-hybrid screen, co-immunoprecipitation, HIV LTR reporter assay, RNA Pol II co-IP, immunofluorescence at transcriptional centers Nature communications Medium 35013187
2022 TASOR is phosphorylated at T819 by a Cyclin/CDK1 complex, especially in cells arrested in early mitosis. However, this phosphorylation does not correlate with TASOR-mediated HIV-1 silencing, as T819A and T819E TASOR mutants repress HIV-1 LTR-driven expression similarly to wild-type TASOR. Phospho-specific antibody, nocodazole/etoposide cell cycle arrest, CDK1 inhibitor, TASOR point mutant overexpression in HIV-1 latency model Retrovirology Medium 36309692
2023 TASOR's DUF3715 domain adopts a pseudo-PARP (RDTS) structure with extensive structural homology to TEX15's DUF3715 domain. The DUF3715 domain from divergent TEX15 sequences can functionally substitute the DUF3715 domain of TASOR and mediate transposon silencing, establishing a conserved functional role for this domain in RNA-directed transposon silencing. Structural homology analysis, functional domain-swap experiments, transposon silencing reporter assay RNA Medium 37433650
2023 The HUSH complex (including TASOR) interacts with the transcription termination factor WDR82 and accumulates at sites of high RNAPII occupancy including long exons and transcription termination sites in a WDR82- and CPSF-dependent manner, demonstrating co-transcriptional chromatin targeting for genome surveillance. Co-immunoprecipitation, ChIP-seq, genetic epistasis with WDR82/CPSF knockouts, genomic rearrangement at Sox2 locus Molecular cell High 37164018
2023 HUSH complex (MPP8 and TASOR subunits) interacts with the leading-strand DNA polymerase Pol ε and contributes to asymmetric H3K9me3 distribution at replication forks (preferentially onto leading strands at LINE-1 elements). TASOR mutants with reduced Pol ε interaction show compromised H3K9me3 asymmetry and increased LINE expression. Co-immunoprecipitation, H3K9me3 strand-specific ChIP, TASOR interaction mutants, POLE3/POLE4 and MPP8/TASOR knockouts Nature High 37938774
2024 AlphaFold3 modeling of the MPP8-TASOR complex predicts that a SPOC domain and a domain with a novel fold in TASOR form extended interaction interfaces with the MPP8 C-terminal domain (ankyrin repeats + PINIT-like domain). Point mutations at these predicted interfaces resulted in loss of HUSH-dependent transcriptional repression, validating the structural model. X-ray crystallography (MPP8 CTD), AlphaFold3 structural modeling, point mutagenesis, cell-based transcriptional repression reporter assay Journal of molecular biology Medium 39638237
2024 TASOR loss in naive pluripotent stem cells triggers replication stress, disrupts H3K9me3 heterochromatin, and impairs silencing of LINE-1 transposable elements. Unscheduled L1 expression upon TASOR loss activates an innate immune response (MAVS pathway) leading to cell death specifically in cells exiting naive pluripotency; this is rescued by caspase inhibition or MAVS deletion. CRISPR knockout, H3K9me3 ChIP, LINE-1 expression analysis, caspase inhibitor treatment, MAVS genetic deletion, pluripotency transition assay Cell reports Medium 39453814
2024 HuSH (HUSH) complex centered on TASOR and a second paralogous HuSH2 complex centered on TASOR2 localize to distinct, non-overlapping genomic loci; HUSH/TASOR represses LINE-1 retrotransposons. MPP8 interaction with TASOR is disrupted by specific amino acid substitutions guided by in silico structural predictions, and the relative quantities of HuSH complexes regulate LINE-1 activity. ChIP-seq, in silico protein structure prediction, mutagenesis of MPP8-TASOR interface, LINE-1 reporter assay, CRISPR knockout Nature communications Medium 39489739
2025 Vpx-mediated degradation of TASOR leads to increased LINE-1 activity, which in turn activates innate immune sensing; ISG induction by Vpx-mediated TASOR degradation relies on both RNA sensing (MAVS signaling) and DNA sensing (cGAS/STING signaling). Vpx mutant analysis, transcriptomic analysis, TASOR degradation experiments, MAVS and cGAS/STING pathway inhibition Journal of molecular biology Medium 42190982
2025 Periphilin is the major RNA-binding component of the HUSH complex; its N-terminal domain is essential for both RNA binding and HUSH function. Artificial tethering of Periphilin to a HUSH-insensitive nascent transcript enables HUSH-dependent silencing of that transcript, establishing that Periphilin's RNA binding initiates HUSH silencing. Periphilin's RNA binding is independent of its interaction with TASOR or MPP8. Unbiased RNA-binding assay, domain truncation analysis, tethering reporter assay, mutagenesis of Periphilin NTD Nucleic acids research Medium 39658355
2025 In mouse embryonic stem cells, deficiency of both MPP8 and TASOR (double mutant) locks cells in pluripotent state even upon differentiation stimuli, and decreases expression of adhesion-related genes (keratins 18 and 19); ectopic co-expression of keratins 18 and 19 rescues the exit-from-pluripotency defect. CRISPR-based knockout, pluripotency exit assay, gene expression analysis, ectopic expression rescue Communications biology Medium 41291012
2024 PRC1.6 components L3MBTL2 and MGA contribute to HUSH complex-mediated provirus silencing in a promoter-specific manner. PRC1.6 and HUSH complexes co-localize on chromatin primarily at active promoters, and PRC1.6 binding at a subset of HUSH-silenced genes is dependent on core HUSH component MPP8. Proximity labeling (C-BERST/dCas9-APEX2), forward genetic screen, ChIP-seq co-localization, MPP8-dependent PRC1.6 binding analysis bioRxivpreprint Medium 39026796

Source papers

Stage 0 corpus · 26 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 Selective silencing of euchromatic L1s revealed by genome-wide screens for L1 regulators. Nature 273 29211708
2015 GENE SILENCING. Epigenetic silencing by the HUSH complex mediates position-effect variegation in human cells. Science (New York, N.Y.) 266 26022416
2018 Primate immunodeficiency virus proteins Vpx and Vpr counteract transcriptional repression of proviruses by the HUSH complex. Nature microbiology 110 30297740
2018 HIV-2/SIV viral protein X counteracts HUSH repressor complex. Nature microbiology 106 29891865
2018 NP220 mediates silencing of unintegrated retroviral DNA. Nature 102 30487602
2020 TASOR is a pseudo-PARP that directs HUSH complex assembly and epigenetic transposon control. Nature communications 75 33009411
2022 TASOR epigenetic repressor cooperates with a CNOT1 RNA degradation pathway to repress HIV. Nature communications 38 35013187
2023 Asymmetric distribution of parental H3K9me3 in S phase silences L1 elements. Nature 37 37938774
2023 Co-transcriptional genome surveillance by HUSH is coupled to termination machinery. Molecular cell 26 37164018
2020 Periphilin self-association underpins epigenetic silencing by the HUSH complex. Nucleic acids research 23 32976585
2023 LINE-1 repression in Epstein-Barr virus-associated gastric cancer through viral-host genome interaction. Nucleic acids research 15 36942479
2024 Interplay between Two Paralogous Human Silencing Hub (HuSH) Complexes in Regulating LINE-1 Element Silencing. Nature communications 14 39489739
2024 DNA methylation governs the sensitivity of repeats to restriction by the HUSH-MORC2 corepressor. Nature communications 10 39214989
2020 Genomic Fabric Remodeling in Metastatic Clear Cell Renal Cell Carcinoma (ccRCC): A New Paradigm and Proposal for a Personalized Gene Therapy Approach. Cancers 10 33302383
2023 The DUF3715 domain has a conserved role in RNA-directed transposon silencing. RNA (New York, N.Y.) 9 37433650
2025 RNA binding by Periphilin plays an essential role in initiating silencing by the HUSH complex. Nucleic acids research 5 39658355
2021 Binding to DCAF1 distinguishes TASOR and SAMHD1 degradation by HIV-2 Vpx. PLoS pathogens 4 34699574
2016 Retinoblastoma-associated protein 140 as a candidate for a novel etiological gene to hypertension. Clinical and experimental hypertension (New York, N.Y. : 1993) 4 27391979
2022 HUSH-mediated HIV silencing is independent of TASOR phosphorylation on threonine 819. Retrovirology 3 36309692
2025 Efficacy of Larimichthys crocea TASOR protein-derived peptide FAM286 against Staphylococcus aureus. Current research in food science 2 39995466
2024 Interplay between Two Paralogous Human Silencing Hub (HuSH) Complexes in Regulating LINE-1 Element Silencing. bioRxiv : the preprint server for biology 2 38313255
2024 TASOR expression in naive embryonic stem cells safeguards their developmental potential. Cell reports 2 39453814
2024 Structure and Methyl-lysine Binding Selectivity of the HUSH Complex Subunit MPP8. Journal of molecular biology 2 39638237
2024 PRC1.6 localizes on chromatin with the human silencing hub (HUSH) complex for promoter-specific silencing. bioRxiv : the preprint server for biology 1 39026796
2026 Human Immunodeficiency Virus Type 2 Vpx-mediated Degradation of TASOR Activates Innate Immune Sensing of Nucleic Acids in Infected Cells. Journal of molecular biology 0 42190982
2025 The HUSH complex facilitates the exit of pluripotency. Communications biology 0 41291012

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