Affinage

MOV10

Helicase MOV-10 · UniProt Q9HCE1

Length
1003 aa
Mass
113.7 kDa
Annotated
2026-04-28
64 papers in source corpus 37 papers cited in narrative 37 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MOV10 is an ATP-dependent 5′-to-3′ RNA helicase that serves as a broad post-transcriptional regulator linking mRNA surveillance, translational control, retrotransposon defense, and innate antiviral immunity. It translocates along mRNA 3′ UTRs to resolve secondary structures, cooperates with UPF1 as an RNA clearance factor in nonsense-mediated mRNA decay, and forms an FMRP–AGO2 inhibitory complex at synapses whose activity-dependent disassembly derepresses translation of plasticity-related mRNAs (PMID:24726324, PMID:20064393, PMID:25464849, PMID:31291981). MOV10 restricts LINE-1 and other retrotransposons by associating with L1 RNPs, recruiting the decapping enzyme DCP2 within phase-separated cytoplasmic granules, and inhibiting cDNA synthesis, with dosage-dependent effects on retrotransposition confirmed in vivo (PMID:23093941, PMID:37437058, PMID:37126510, PMID:28662698). MOV10 also restricts diverse viruses—retroviruses, influenza A, HBV, and coronaviruses—through both helicase-dependent mechanisms (blocking reverse transcription, sequestering viral RNPs) and helicase-independent mechanisms (disrupting viral nucleoprotein–importin interactions, enhancing IKKε-dependent type I interferon induction) (PMID:20215113, PMID:26842467, PMID:31722967, PMID:34517762, PMID:27016603).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2008 Medium

    An initial functional link between MOV10 and viral RNA-directed transcription was established when MOV10 was identified as a hepatitis delta antigen interactor required for HDV replication but not HDAg translation.

    Evidence HDAg interaction screen with siRNA knockdown and replication/translation assays in human cells

    PMID:18552826

    Open questions at the time
    • Single screen-based identification without independent replication
    • Mechanism by which MOV10 promotes HDV RNA-directed transcription undefined
    • Relationship to MOV10 helicase activity not tested
  2. 2009 High

    MOV10 was established as an activity-dependent translational repressor at synapses: NMDA receptor stimulation triggers its rapid proteasomal degradation, releasing specific mRNAs (CaMKII, Limk1, Lypla1) into polysomes for translation during synaptic plasticity.

    Evidence Proteasome inhibitor experiments, polysome fractionation after MOV10 knockdown, and photoconvertible Kaede reporter in neurons

    PMID:20064393

    Open questions at the time
    • Direct RNA-binding targets not mapped genome-wide at this point
    • Mechanism of MOV10-mediated translational block (RISC-dependent vs independent) unresolved
  3. 2010 High

    Three independent studies demonstrated that MOV10 restricts HIV-1 at multiple steps—reducing Gag levels, being packaged into virions, and blocking reverse transcription—establishing MOV10 as a broad antiretroviral factor, while domain-mapping showed the N-terminal region suffices for some anti-HIV activities.

    Evidence Overexpression and siRNA knockdown in producer/target cells, virion packaging assays, reverse transcription assays, truncation mutagenesis across HIV-1 and MLV

    PMID:20140200 PMID:20215113 PMID:20668078

    Open questions at the time
    • Whether MOV10 acts as a bona fide restriction factor at endogenous expression levels debated
    • Precise biochemical mechanism of reverse transcription inhibition unclear
    • Whether helicase activity is required for anti-HIV function yielded conflicting data across studies
  4. 2010 High

    A nuclear role for MOV10 was uncovered: it associates with PRC1 components on chromatin in an RNA-dependent manner and is required for PRC1-mediated transcriptional silencing at the INK4a locus, broadening MOV10 function beyond cytoplasmic post-transcriptional regulation.

    Evidence Co-purification with PRC1, ChIP for H3K27me3 and PRC1 components, shRNA knockdown in human fibroblasts

    PMID:20543829

    Open questions at the time
    • Whether MOV10 directly unwinds RNA at chromatin or acts as a scaffold is unknown
    • Genome-wide scope of MOV10-PRC1 chromatin regulation not defined
    • Not independently replicated
  5. 2012 High

    MOV10 was shown to restrict LINE-1, Alu, and SVA retrotransposons through its helicase activity, associating with L1 RNPs and colocalizing with ORF1p in stress granules, while endogenous MOV10 knockdown confirmed selectivity for endogenous retroelements over exogenous retroviruses.

    Evidence Retrotransposition reporter assays across multiple element types, helicase domain mutagenesis, Co-IP with L1 RNP, RNAi knockdown with retroviral controls

    PMID:22727223 PMID:23093941

    Open questions at the time
    • Step in retrotransposition cycle targeted by MOV10 not pinpointed
    • Whether MOV10 degrades L1 RNA or blocks reverse transcription remained unclear
  6. 2014 High

    The biochemical basis of MOV10 was resolved: it possesses ATP-dependent 5′-to-3′ RNA unwinding activity, binds 3′ UTRs overlapping UPF1 sites, and cooperates with UPF1 in mRNA decay, while its interaction with FMRP creates a dual regulatory switch—facilitating or blocking AGO2-mediated silencing depending on FMRP binding proximity.

    Evidence In vitro helicase assays, PAR-CLIP of WT and helicase mutants, Co-IP with UPF1, mRNA half-life measurements; reciprocal Co-IP with FMRP, iCLIP, polysome assays

    PMID:24726324 PMID:25464849

    Open questions at the time
    • Structural basis of MOV10-UPF1 cooperation unknown
    • How FMRP switches MOV10 between silencing facilitation and blockade at individual mRNAs not defined
  7. 2016 High

    MOV10 was found to restrict influenza A virus by binding viral NP and preventing importin-α-mediated vRNP nuclear import, and independently to enhance IKKε-dependent type I IFN induction—both mechanisms operating without requiring helicase activity—while picornavirus proteases cleave MOV10 as a counter-defense.

    Evidence Co-IP, importin-α competition assay, confocal NP localization, helicase mutant analysis for IAV; genome-edited IRF3/IFNAR KO cells, IFN promoter reporter, viral protease cleavage assays

    PMID:26842467 PMID:27016603

    Open questions at the time
    • Whether the NP-sequestration and IFN-enhancing activities are coupled or independent in physiological infection unclear
    • Structural determinants of helicase-independent antiviral functions not mapped
  8. 2017 High

    In vivo mouse studies revealed that MOV10 suppresses LINE-1 retrotransposition in the brain, regulates cytoskeletal mRNAs for neurite outgrowth, and is essential for embryonic viability (Mov10 KO is lethal; heterozygotes show reduced dendritic arborization), while nuclear MOV10 associates with splicing factors in spermatogonia.

    Evidence Mov10 heterozygous and KO mice with L1 cDNA synthesis assays and dendritic imaging; knockdown/transplant in spermatogonia with PAR-CLIP and Co-IP with SRSF1

    PMID:28662698 PMID:31088452

    Open questions at the time
    • Whether splicing regulation by MOV10 is helicase-dependent not tested
    • Specific L1 loci targeted in vivo not identified
    • Cause of embryonic lethality in KO not mechanistically defined
  9. 2019 High

    The FMRP–MOV10–AGO2 complex was shown to be dynamically regulated: NMDAR stimulation dissociates MOV10 from AGO2, with FMRP phosphorylation serving as the regulatory switch, while MOV10 was independently demonstrated to block HBV reverse transcription through helicase-dependent binding of viral RNA.

    Evidence Co-IP in synaptoneurosomes with NMDAR stimulation, polysome analysis; HBV DNA quantification, RNA-IP, helicase mutagenesis, Southern blot

    PMID:31291981 PMID:31722967

    Open questions at the time
    • Kinase(s) responsible for FMRP phosphorylation switch in this context not identified
    • Whether MOV10 directly unwinds HBV pgRNA secondary structures not demonstrated
  10. 2020 High

    MOV10 was shown to disrupt bunyavirus RNP assembly by binding the N-arm domain of nucleoprotein N through its own N-terminus, blocking N polymerization and N-RNA binding in a helicase- and IFN-independent manner, extending MOV10's antiviral scope to negative-sense RNA viruses.

    Evidence Mass spectrometry, Co-IP, N polymerization and N-RNA binding assays, minigenome assay, domain mapping, in vivo knockdown

    PMID:33284835

    Open questions at the time
    • Whether MOV10 restriction of bunyaviruses occurs at endogenous expression levels in primary cells not shown
    • Structural basis of N-arm recognition undefined
  11. 2021 High

    CRL4-DCAF12 ubiquitin ligase was identified as the E3 ligase targeting MOV10's C-terminal degron for proteasomal degradation; Dcaf12 KO mice accumulate MOV10 and exhibit impaired spermatogenesis and altered T cell populations, demonstrating that MOV10 protein level must be tightly controlled.

    Evidence CRL4-DCAF12 complex purification, Co-IP, proteasome inhibitor rescue, Dcaf12 KO mouse phenotyping with flow cytometry

    PMID:34065512

    Open questions at the time
    • Whether elevated MOV10 is the sole cause of the spermatogenesis and T cell defects in Dcaf12 KO not formally demonstrated
    • Signals that modulate DCAF12-mediated MOV10 turnover unknown
  12. 2021 High

    MOV10 was established as a restriction factor for coronaviruses: it interacts with MERS-CoV and SARS-CoV-2 nucleocapsid proteins, sequesters viral RNA in cytoplasmic complexes, and requires helicase activity for antiviral function against coronaviruses.

    Evidence Co-IP of endogenous MOV10 with N protein, RNA-IP, CRISPR KO with WT/helicase-mutant rescue, virus titer assays

    PMID:34517762

    Open questions at the time
    • Whether MOV10 targets a specific step of CoV replication cycle not defined
    • Viral evasion mechanism against MOV10 during CoV infection not identified
  13. 2023 High

    Two key regulatory mechanisms were elucidated: MOV10 recruits DCP2 to LINE-1 RNA, forming phase-separated condensates that decap and degrade L1 transcripts; and phosphorylation of MOV10 at S970 inactivates its G-quadruplex unwinding activity, promoting AGO2-dependent target mRNA degradation.

    Evidence Co-IP of MOV10-DCP2-L1 RNP, decapping assay, LLPS characterization, retrotransposition assay; mass spectrometry phosphosite identification, S970D/A mutagenesis with in vitro unwinding and RNA-seq

    PMID:36871759 PMID:37437058

    Open questions at the time
    • Kinase responsible for S970 phosphorylation not identified
    • Whether DCP2-dependent decapping and S970 phosphorylation are coordinated mechanisms unknown
    • In vivo confirmation of LLPS-mediated L1 restriction pending
  14. 2023 High

    In vivo dosage-dependent LINE-1 restriction by MOV10 was confirmed: Mov10 heterozygous and KO mice show progressive L1 accumulation across somatic and reproductive tissues over generations, with MOV10-UPF1 complexes binding 3′ UTRs in testis.

    Evidence Mov10 KO/het mice, LINE-1 reporter transgene assay, CLIP-seq and RNA-seq in testis, Co-IP with UPF1

    PMID:37126510

    Open questions at the time
    • Whether transgenerational L1 accumulation causes measurable genomic instability not assessed
    • Relative contributions of MOV10 helicase activity vs. DCP2 recruitment in vivo not dissected
  15. 2025 Medium

    The functional architecture of MOV10 domains was further resolved: the N-terminal domain mediates UPF2 interaction and cytoplasmic RNA condensate (P-body/stress granule) localization; extended motif II (aa 563–675) is the primary determinant of L1 RNA/RNP binding and retrotransposition inhibition; and the C-terminal domain drives G3BP1-dependent granule formation providing an additional layer of L1 restriction. Brain-specific KO revealed MOV10 regulation of NUMA1 mRNA as a control point for dendritogenesis and fear memory.

    Evidence Domain deletion/mutagenesis with retrotransposition reporter, Co-IP with G3BP1, NMD reporter assays, in vitro binding; brain-specific KO mouse with behavioral testing, CLIP, NUMA1 rescue

    PMID:39915816 PMID:40408535 PMID:40570961

    Open questions at the time
    • Structural basis of N-terminal domain–UPF2 interaction not resolved
    • Whether the extended motif II contacts L1 RNA directly or via ORF1p unknown
    • Whether NUMA1 regulation is direct or indirect through other MOV10 targets not fully excluded

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the structural basis of MOV10's engagement with UPF1/UPF2 in NMD, the identity of the kinase(s) that phosphorylate S970 to toggle helicase activity, whether nuclear and cytoplasmic MOV10 pools are independently regulated, and the mechanism underlying embryonic lethality of Mov10 knockout.
  • No high-resolution structure of MOV10 or its complexes available
  • Kinase for S970 phosphorylation unknown
  • Cause of Mov10 KO embryonic lethality mechanistically undefined
  • Relative physiological importance of helicase-dependent vs. helicase-independent antiviral pathways not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 4 GO:0098772 molecular function regulator activity 3 GO:0140098 catalytic activity, acting on RNA 2 GO:0140110 transcription regulator activity 2 GO:0140657 ATP-dependent activity 2
Localization
GO:0005829 cytosol 4 GO:0031410 cytoplasmic vesicle 4 GO:0005634 nucleus 3
Pathway
R-HSA-1643685 Disease 6 R-HSA-392499 Metabolism of proteins 4 R-HSA-112316 Neuronal System 3 R-HSA-168256 Immune System 3 R-HSA-8953854 Metabolism of RNA 3 R-HSA-4839726 Chromatin organization 1
Partners
AGO2DCAF12DCP2FMRPG3BP1SRSF1UPF1UPF2
Complex memberships
FMRP-MOV10-AGO2 complexMOV10-UPF1 mRNA surveillance complexRISC/AGO2 complex

Evidence

Reading pass · 37 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2014 MOV10 has an ATP-dependent 5' to 3' RNA unwinding activity in vitro and translocates 5' to 3' along mRNA 3' UTRs to resolve local secondary structures. MOV10 interacts with UPF1, the key NMD component, and their RNA-binding sites are proximal; MOV10 knockdown increased mRNA half-lives of both MOV10-bound and UPF1-regulated transcripts, establishing MOV10 as an RNA clearance factor in UPF1-mediated mRNA degradation. In vitro helicase assay, PAR-CLIP of WT and helicase mutants, Co-IP with UPF1, mRNA half-life measurements after knockdown Molecular Cell High 24726324
2009 MOV10 is present at synapses and is rapidly degraded by the proteasome in an NMDA-receptor-mediated, activity-dependent manner. Upon MOV10 suppression, specific mRNAs (including alpha-CaMKII, Limk1, and Lypla1) selectively enter the polysome compartment, demonstrating that MOV10 acts as a translational repressor at the synapse whose proteasomal degradation relieves translational silencing during synaptic plasticity. Proteasome inhibitor experiments, polysome fractionation after MOV10 knockdown, photoconvertible reporter (Kaede) for activity-dependent translation Neuron High 20064393
2014 MOV10 directly associates with FMRP both directly and in an RNA-dependent manner. The FMRP-MOV10 complex exerts a dual translational regulatory function: MOV10 facilitates miRNA-mediated repression of some mRNAs, but FMRP, by binding in close proximity to MOV10 sites, prevents AGO2 access and thereby blocks miRNA-mediated suppression of a subset of mRNAs. RNA immunoprecipitation (RIP), iCLIP, Co-IP (direct and RNA-dependent), polysome and translation assays Cell Reports High 25464849
2010 MOV10 co-purifies and interacts with components of Polycomb-repressive complex 1 (PRC1). Endogenous MOV10 is predominantly nuclear and associates with chromatin in an RNA-dependent manner. shRNA-mediated MOV10 knockdown in human fibroblasts upregulates the INK4a tumor suppressor and causes dissociation of PRC1 from the INK4a locus along with a reduction in H3K27me3, indicating that MOV10 directly participates in PRC1-mediated transcriptional silencing. Co-purification, Co-IP, chromatin fractionation, shRNA knockdown, ChIP for H3K27me3 and PRC1 components Nature Structural & Molecular Biology High 20543829
2012 MOV10, a putative RNA helicase and RISC component, severely restricts LINE-1, Alu, and SVA retrotransposons. MOV10 associates with the L1 ribonucleoprotein particle and colocalizes with L1 ORF1 protein in stress granules; helicase domain integrity is required for retrotransposition inhibition. Retrotransposition reporter assays, Co-IP with L1 RNP components, helicase domain mutagenesis, immunofluorescence co-localization PLoS Genetics High 23093941
2013 MOV10 suppresses LINE-1 transposition through its helicase activity; helicase motif mutations impair this function. MOV10 post-transcriptionally reduces LINE-1 RNA levels and interacts with both LINE-1 RNA and ORF1 protein, suggesting it associates with the L1 RNP and causes RNA degradation. LINE-1 retrotransposition reporter assay, helicase motif mutagenesis, RT-PCR for L1 RNA levels, Co-IP with ORF1p, RNA-IP Journal of Biological Chemistry High 23754279
2010 MOV10 interacts with HIV-1 nucleocapsid (NC) protein in an RNA-dependent manner and is packaged into HIV-1 virions. Overexpression reduces HIV-1 Gag steady-state levels and virus infectivity; siRNA knockdown of MOV10 increased HIV-1 infectivity. MOV10 blocks HIV-1 replication at a post-entry step, and HIV-1 can suppress MOV10 protein expression as a counter-defense. Co-IP (RNA-dependent), Western blot for virion packaging, siRNA knockdown, infection/replication assays Journal of Biological Chemistry High 20215113
2010 MOV10 overexpression in HIV-1 producer cells inhibits production of infectious retroviruses and reduces virus infectivity by blocking reverse transcription. The N-terminal half of MOV10 is required for HIV-1 inhibition, while the C-terminal helicase domain is not essential; MOV10 also inhibits other lentiviruses and MLV. Overexpression and siRNA knockdown, reverse transcription assay, truncation/mutation analysis, infection assays across multiple retroviruses PLoS One High 20140200
2010 MOV10 inhibits HIV-1 at multiple stages: overexpression reduces Gag protein levels and virus production in producer cells, MOV10 is incorporated into virions, and virion-associated MOV10 reduces infectivity partly by inhibiting reverse transcription. APOBEC3G and MOV10 effects are additive, indicating they act through distinct mechanisms. Overexpression, siRNA knockdown, Western blot (Gag, virion-incorporated MOV10), reverse transcription assay, infectivity assay Journal of Virology High 20668078
2016 MOV10 inhibits influenza A virus (IAV) replication by interacting with the viral nucleoprotein (NP) via an RNA-mediated interaction, preventing NP from binding importin-α, thereby retaining NP in the cytoplasm and inhibiting vRNP nuclear import and polymerase activity. This antiviral mechanism is independent of MOV10's helicase activity. Co-IP, minigenome assay, importin-α binding competition assay, confocal localization of NP, MOV10 helicase mutant analysis Journal of Virology High 26842467
2008 MOV10 interacts with the hepatitis delta antigen (HDAg) as identified by an HDAg-interaction screen. MOV10 knockdown inhibited HDV replication but not HDAg mRNA translation, indicating a role for MOV10 specifically in RNA-directed transcription during HDV replication. HDAg interaction screen, siRNA knockdown with HDV replication and translation assays Nature Structural & Molecular Biology Medium 18552826
2011 MOV10 is packaged into HIV-1 virions via its N-terminal region (aa 261–305) binding to the NC basic linker of Gag. The Cys-His-rich domain (aa 93–305) containing residues C188, C195, H199, H201, H202 is critical for anti-HIV-1 activity. Nearly all MOV10 residues (aa 99–949) are required for antiviral activity, including C947, P948, F949 at the C-terminus, and packaging additionally requires most helicase motifs. Deletion and point mutagenesis, virion packaging assay, infection/infectivity assay, structural modeling Journal of Biological Chemistry High 22105071
2012 Endogenous MOV10 suppresses retrotransposition of LTR and non-LTR endogenous retroelements but does not affect production of infectious exogenous retrovirus particles, demonstrating selectivity. MOV10 is not required for miRNA or siRNA-mediated mRNA silencing. RNAi-mediated knockdown, retrotransposition reporter assays, retrovirus infectivity assay, miRNA/siRNA silencing reporter assays Retrovirology High 22727223
2012 APOBEC3G (A3G) inhibits miRNA-mediated translational repression by blocking the interaction between MOV10 and AGO2. A3G binds the C-terminus of MOV10, competing with AGO2 for the same domain, and this interaction depends on the 7SL RNA; the A3G mutant W127L (unable to bind 7SL RNA) cannot counteract miRNA repression. Co-IP of MOV10-AGO2 complex with/without A3G, MOV10 deletion mapping, miRNA reporter assay, A3G mutant analysis Journal of Biological Chemistry Medium 22791714
2018 MOV10 interacts with RNASEH2 (identified by proteomics). MOV10 and RNASEH2 co-localize in the nucleus, and RNASEH2 binds to LINE-1 RNAs in a MOV10-dependent manner. Knockdown of either RNASEH2A or MOV10 causes accumulation of LINE-1-specific RNA-DNA hybrids, indicating they cooperate to prevent formation of L1 heteroduplexes during retrotransposition. Mass spectrometry, Co-IP, immunofluorescence co-localization, shRNA knockdown, RNA-DNA hybrid detection (S9.6 antibody assay) Nucleic Acids Research Medium 29315404
2016 MOV10 exhibits antiviral activity against RNA viruses independent of its helicase function by enhancing IRF3-mediated type I IFN induction through a pathway requiring IKKε but not TBK1, and independent of the RIG-I/MAVS RNA-sensing pathway. Viral proteases from picornaviruses specifically cleave MOV10 as an immune evasion mechanism. Genome-edited knockout human cells (IRF3, IFN receptor), IFN promoter reporter assay, virus infection assays with helicase mutants, MOV10 cleavage by viral proteases Journal of Immunology High 27016603
2019 MOV10 suppresses IAV infection by binding viral NP and sequestering viral RNP in the cytoplasm within P-body-dependent structures, causing degradation of viral vRNA. The IAV NS1 protein antagonizes this by interfering with the MOV10-NP interaction and promoting MOV10 degradation via the lysosomal pathway. Co-IP of MOV10 with NP, immunofluorescence for P-body colocalization, vRNA quantification, NS1-MOV10 interaction assays, lysosomal pathway inhibitor experiments Biochemical Journal High 30617221
2017 MOV10 is a nucleocytoplasmic protein in spermatogonia; MOV10 deficiency reduces spermatogonial progenitor cell proliferation and in vivo repopulation capacity. Nuclear MOV10 associates with splicing factors, particularly SRSF1, and its intronic binding sites are proximal to splice sites, indicating a role in splicing regulation. MOV10 also impacts miRNA biogenesis partially through effects on primary miRNA transcript levels and splicing. Knockdown and transplantation assays, genome-wide RNA targetome analysis, nuclear fractionation, Co-IP with splicing factors, PAR-CLIP BMC Biology Medium 31088452
2021 CRL4-DCAF12 ubiquitin ligase targets the C-terminal degron of MOV10 to promote its proteasomal degradation. Dcaf12 knockout mice exhibit elevated MOV10 protein, reduced mature sperm production, and altered T cell populations (CD4+ T and NKT cells), demonstrating that DCAF12-mediated MOV10 degradation is required for normal spermatogenesis and T cell activation. CRL4-DCAF12 complex purification, Co-IP, proteasome inhibitor rescue, Dcaf12 knockout mouse phenotyping, flow cytometry, Western blot International Journal of Molecular Sciences High 34065512
2019 MOV10 interacts with HBV RNA via its helicase domain and blocks the early step of HBV reverse transcription, thereby impairing viral DNA synthesis, without affecting viral gene expression or pregenomic RNA encapsidation. Helicase domain mutations abolish both HBV RNA binding and anti-HBV activity. Overexpression and knockdown, HBV DNA quantification, RNA-IP, helicase domain mutagenesis, Southern blot for HBV DNA intermediates Journal of Biological Chemistry High 31722967
2020 MOV10 targets bunyavirus nucleoproteins (N) from SFTS virus and related high-pathogenic bunyaviruses in an RNA-independent manner. MOV10 binds the N-arm domain (34 aa) of N through its N-terminus and blocks N polymerization, N-RNA binding, and N-polymerase interaction, thereby disabling RNP assembly. This antiviral activity is independent of MOV10's helicase activity and the interferon pathway. Mass spectrometry, Co-IP, minigenome assay, N polymerization assay, N-RNA binding assay, domain mapping, animal knockdown experiments PLoS Pathogens High 33284835
2015 MOV10 functions as a co-factor of HIV-1 Rev by interacting with Rev in an RNA-independent manner to enhance Rev/RRE-dependent nuclear export of unspliced/partially spliced viral mRNAs, thereby increasing Gag expression. The DEAG-box of MOV10 is required for this activity; the DEAG-box mutant acts as a dominant-negative. Co-IP (RNA-independent), nuclear export reporter assay, Western blot for Gag, DEAG-box mutagenesis with dominant-negative analysis Virology Medium 26379090
2017 MOV10 suppresses LINE-1 retrotransposition in the mouse brain in vivo and inhibits complementary DNA synthesis directly in the nucleus, while cytosolic MOV10 regulates cytoskeletal mRNAs to influence neurite outgrowth. Mov10 heterozygote mice show reduced dendritic arborization in hippocampal neurons, and Mov10 knockout leads to embryonic lethality. Mov10 heterozygous and knockout mouse analysis, L1 cDNA synthesis assay, dendritic arborization imaging, RNA-seq, CLIP analysis in brain BMC Biology High 28662698
2018 Zygotic knockdown of Mov10 in Xenopus laevis causes defects in gastrulation, notochord and paraxial mesoderm development, and failure to neurulate. The Mov10 knockdown delays degradation of the miR-427 target mRNA cyclin A1, indicating MOV10 functions in miRNA-mediated regulation of the maternal-to-zygotic transition. Morpholino knockdown in Xenopus, RNA-seq of knockdown embryos, cyclin A1 mRNA stability assay Developmental Dynamics Medium 29266590
2019 MOV10 dissociates from AGO2 upon NMDAR stimulation in rat cortical synaptoneurosomes. The MOV10-FMRP-AGO2 inhibitory complex on NMDAR-responsive mRNAs is disrupted by NMDAR activation, promoting translation of target mRNAs. FMRP is required both to form the MOV10-AGO2 inhibitory complex and to promote translation of MOV10-associated mRNAs; FMRP phosphorylation is the regulatory switch. Co-IP in synaptoneurosomes, NMDAR stimulation experiments, polysome analysis, knockdown of FMRP Molecular Brain Medium 31291981
2020 The FMRP RGG box protects a subset of co-bound mRNAs from AGO association by working through the MOV10 N-terminus. The N-terminus of MOV10 is required to block AGO association and for neurite outgrowth. G-Quadruplex RNA structures modulate the FMRP-MOV10 regulatory switch, with the RGG box increasing binding to G-Quadruplex RNA in an N-terminus of MOV10-dependent manner. Domain mapping by Co-IP and RNA pulldown, G-Quadruplex binding assays, AGO association assays, neurite outgrowth assay Nucleic Acids Research Medium 31740951
2023 MOV10 recruits the decapping enzyme DCP2 to LINE-1 RNA and forms a MOV10-DCP2-LINE-1 RNP complex that undergoes liquid-liquid phase separation (LLPS). DCP2 cooperates with MOV10 to decap LINE-1 RNA, causing its degradation and reducing LINE-1 retrotransposition. Co-IP of MOV10-DCP2-L1 RNP, LINE-1 decapping assay, LLPS characterization (microscopy and biochemistry), retrotransposition reporter assay EMBO Reports High 37437058
2023 MOV10 is phosphorylated at serine 970 (S970) in the C-terminus. Phospho-mimic S970D blocks MOV10's ability to unfold RNA G-quadruplexes (similar to helicase-dead K531A), while S970A retains unwinding activity. In cells, S970D causes decreased expression of MOV10 CLIP target mRNAs in an AGO2-dependent manner, establishing that S970 phosphorylation restricts MOV10 helicase activity and thereby promotes AGO2-mediated mRNA degradation. Mass spectrometry identification of phosphosite, site-directed mutagenesis (S970D/S970A), in vitro G-quadruplex unwinding assay, RNA-seq, AGO2 Co-IP, AGO2 knockdown Journal of Biological Chemistry High 36871759
2021 MOV10 interacts with coronavirus nucleocapsid (N) protein during MERS-CoV infection, colocalizing in cytoplasmic structures. MOV10 silencing increases N protein and virus titer; MOV10 overexpression reduces viral titers ~10-fold. Viral RNAs are present in MOV10 cytoplasmic complexes (RNA immunoprecipitation). MOV10's helicase activity is required for its antiviral effect against MERS-CoV. MOV10-N interaction is conserved in SARS-CoV-2 and other human CoVs. Co-IP of endogenous MOV10 with N, RNA immunoprecipitation, CRISPR-Cas9 MOV10 KO cells with WT or helicase-mutant rescue, virus titer assay mBio High 34517762
2023 MOV10 forms a complex with UPF1 in mouse testis and primarily binds the 3' UTR of somatically expressed transcripts. Loss of MOV10 in mice causes a dosage-dependent increase in LINE-1 retrotransposition in somatic and reproductive tissues and reduces reproductive fitness over successive generations, establishing MOV10 as a dosage-dependent restriction factor for LINE-1 in vivo. Mov10 knockout and heterozygous mice, LINE-1 reporter transgene assay, CLIP-seq, RNA-seq in testis, Co-IP with UPF1 PLoS Genetics High 37126510
2025 MOV10's N-terminal domain (functionally distinct from UPF1's CH domain) mediates interaction with NMD factor UPF2 at a region distinct from UPF1's UPF2-binding site. The N-terminal domain of MOV10 dictates its localization to cytoplasmic RNA condensates (P-bodies and stress granules), unlike UPF1 whose localization is RNA-driven. MOV10 engages the NMD pathway as an RNA clearance factor downstream of UPF1, resolving RNA structures to facilitate mRNA degradation. In vitro biochemical binding assays, NMD reporter assays, domain deletion analysis, localization imaging Journal of Biological Chemistry Medium 40570961
2009 MOV10 was isolated as a telomerase-associated protein from porcine testis. Anti-MOV10 antibody precipitates telomerase activity from cancer cell extracts and inhibits telomerase in vitro. Recombinant MOV10 binds the G-rich strand of telomere-sequenced DNA (both single- and double-stranded) but not the C-rich strand, and ChIP shows MOV10 binds telomere chromatin in vivo. Co-purification with telomerase activity, antibody-mediated inhibition of telomerase in vitro, DNA binding assay, ChIP Biochemical and Biophysical Research Communications Low 19665004
2021 FMRP and MOV10 regulate DICER1 expression through its 3' UTR. In cells and tissues with reduced MOV10 or absent FMRP, DICER1 protein is significantly reduced. Introduction of a DICER1 transgene restores normal neurite outgrowth in Mov10 KO Neuro2A cells and branching in MOV10 heterozygote neurons. Loss of FMRP globally reduces AGO2-associated microRNAs in brain. Western blot for DICER1 in KD/KO cells and brain tissue, 3'UTR reporter assay, DICER1 transgene rescue of neurite phenotype, AGO2-IP followed by miRNA profiling PLoS One Medium 34847178
2025 The extended motif II (aa 563–675) of MOV10 mediates interaction with LINE-1 RNA/RNP and is the dominant contributor to anti-LINE-1 retrotransposition activity. The C-terminal domain (aa 907–1003) is required for MOV10 association with G3BP1 and formation of cytosolic granules; granule formation provides an additional layer of LINE-1 inhibition on top of LINE-1 RNA binding. Domain deletion and mutagenesis, retrotransposition reporter assay, Co-IP with G3BP1, granule formation imaging PLoS Genetics Medium 40408535
2022 In Dicer KO mouse embryonic stem cells, MOV10 is upregulated due to loss of direct miRNA regulation of Mov10 mRNA. Overexpression of L1 ORF1p together with MOV10 is sufficient to drive formation of cytosolic L1 RNP aggregates, and sequestration of L1 RNPs in these aggregates restricts retrotransposition. Dicer KO mESC analysis, MOV10 overexpression with L1 ORF1p co-expression, retrotransposition assay, aggregate imaging EMBO Reports Medium 35856394
2024 USP24 is an ISG15 cross-reactive deubiquitylase that deISGylates MOV10. ISGylated MOV10 enhances IFN-β production/secretion, whereas USP24-mediated deISGylation of MOV10 negatively regulates the innate immune response, establishing a USP24–MOV10–IFN-β regulatory axis. Activity-based protein profiling (ABPP), in vitro deISGylation assay with recombinant USP24, proteomic ISGylome analysis (total proteome, GG-peptidome, ISG15 interactome), cell-based IFN-β assay with USP24 depletion bioRxivpreprint Medium bio_10.1101_2024.09.06.611391
2025 Brain-specific Mov10 knockout mice exhibit enhanced fear memory and elongated distal dendrites in hippocampal neurons. NUMA1 mRNA is a MOV10 CLIP target and is decreased in Mov10 deletion hippocampus. Restoration of NUMA1 expression and knockdown of the antagonistic microtubule regulator HAUS rescues the dendritic phenotype, establishing translation regulation of NUMA1 by MOV10 as a control point in dendritogenesis. Brain-specific KO mouse (behavioral testing, dendritic morphology imaging), MOV10 CLIP, NUMA1 rescue and HAUS knockdown in cultured hippocampal neurons BMC Biology Medium 39915816

Source papers

Stage 0 corpus · 64 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 A coordinated local translational control point at the synapse involving relief from silencing and MOV10 degradation. Neuron 191 20064393
2012 MOV10 RNA helicase is a potent inhibitor of retrotransposition in cells. PLoS genetics 178 23093941
2014 MOV10 Is a 5' to 3' RNA helicase contributing to UPF1 mRNA target degradation by translocation along 3' UTRs. Molecular cell 158 24726324
2010 P body-associated protein Mov10 inhibits HIV-1 replication at multiple stages. Journal of virology 126 20668078
2012 Modulating human proteinase activated receptor 2 with a novel antagonist (GB88) and agonist (GB110). British journal of pharmacology 98 21806599
2010 Perturbation of the P-body component Mov10 inhibits HIV-1 infectivity. PloS one 98 20140200
2010 Moloney leukemia virus 10 (MOV10) protein inhibits retrovirus replication. The Journal of biological chemistry 98 20215113
2019 MOV10 binding circ-DICER1 regulates the angiogenesis of glioma via miR-103a-3p/miR-382-5p mediated ZIC4 expression change. Journal of experimental & clinical cancer research : CR 96 30621721
2014 MOV10 and FMRP regulate AGO2 association with microRNA recognition elements. Cell reports 94 25464849
2013 The MOV10 helicase inhibits LINE-1 mobility. The Journal of biological chemistry 89 23754279
2012 Endogenous MOV10 inhibits the retrotransposition of endogenous retroelements but not the replication of exogenous retroviruses. Retrovirology 85 22727223
2016 Host Protein Moloney Leukemia Virus 10 (MOV10) Acts as a Restriction Factor of Influenza A Virus by Inhibiting the Nuclear Import of the Viral Nucleoprotein. Journal of virology 75 26842467
2012 Mixture models and wavelet transforms reveal high confidence RNA-protein interaction sites in MOV10 PAR-CLIP data. Nucleic acids research 70 22844102
2008 Capped small RNAs and MOV10 in human hepatitis delta virus replication. Nature structural & molecular biology 65 18552826
2017 IRAV (FLJ11286), an Interferon-Stimulated Gene with Antiviral Activity against Dengue Virus, Interacts with MOV10. Journal of virology 62 27974568
2016 MOV10 Provides Antiviral Activity against RNA Viruses by Enhancing RIG-I-MAVS-Independent IFN Induction. Journal of immunology (Baltimore, Md. : 1950) 54 27016603
2010 Role for the MOV10 RNA helicase in polycomb-mediated repression of the INK4a tumor suppressor. Nature structural & molecular biology 54 20543829
2020 Caenorhabditis elegans ADAR editing and the ERI-6/7/MOV10 RNAi pathway silence endogenous viral elements and LTR retrotransposons. Proceedings of the National Academy of Sciences of the United States of America 47 32123111
2018 Interplay between RNASEH2 and MOV10 controls LINE-1 retrotransposition. Nucleic acids research 46 29315404
2012 APOBEC3G inhibits microRNA-mediated repression of translation by interfering with the interaction between Argonaute-2 and MOV10. The Journal of biological chemistry 46 22791714
2017 Mov10 suppresses retroelements and regulates neuronal development and function in the developing brain. BMC biology 42 28662698
2011 Identification of molecular determinants from Moloney leukemia virus 10 homolog (MOV10) protein for virion packaging and anti-HIV-1 activity. The Journal of biological chemistry 41 22105071
2013 Mov10 and APOBEC3G localization to processing bodies is not required for virion incorporation and antiviral activity. Journal of virology 35 23926332
2020 Host restriction of emerging high-pathogenic bunyaviruses via MOV10 by targeting viral nucleoprotein and blocking ribonucleoprotein assembly. PLoS pathogens 33 33284835
2019 Biological and RNA regulatory function of MOV10 in mammalian germ cells. BMC biology 29 31088452
2021 Unwinding the roles of RNA helicase MOV10. Wiley interdisciplinary reviews. RNA 26 34327836
2020 The FMRP-MOV10 complex: a translational regulatory switch modulated by G-Quadruplexes. Nucleic acids research 25 31740951
2019 MOV10L1 Binds RNA G-Quadruplex in a Structure-Specific Manner and Resolves It More Efficiently Than MOV10. iScience 22 31252377
2021 CRL4-DCAF12 Ubiquitin Ligase Controls MOV10 RNA Helicase during Spermatogenesis and T Cell Activation. International journal of molecular sciences 21 34065512
2019 The MOV10 helicase restricts hepatitis B virus replication by inhibiting viral reverse transcription. The Journal of biological chemistry 21 31722967
2018 MOV10 inhibits replication of porcine reproductive and respiratory syndrome virus by retaining viral nucleocapsid protein in the cytoplasm of Marc-145 cells. Biochemical and biophysical research communications 20 30172377
2015 RNA helicase MOV10 functions as a co-factor of HIV-1 Rev to facilitate Rev/RRE-dependent nuclear export of viral mRNAs. Virology 20 26379090
2019 NMDAR mediated translation at the synapse is regulated by MOV10 and FMRP. Molecular brain 18 31291981
1994 Interaction of several related GC-box- and GT-box-binding proteins with the intronic enhancer is required for differential expression of the gb110 gene in embryonal carcinoma cells. Molecular and cellular biology 18 8065313
2019 MOV10 sequesters the RNP of influenza A virus in the cytoplasm and is antagonized by viral NS1 protein. The Biochemical journal 17 30617221
2009 MOV10 as a novel telomerase-associated protein. Biochemical and biophysical research communications 17 19665004
2020 Effect of P-body component Mov10 on HCV virus production and infectivity. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 15 32496609
2017 Moloney leukemia virus 10 (MOV10) inhibits the degradation of APOBEC3G through interference with the Vif-mediated ubiquitin-proteasome pathway. Retrovirology 15 29258557
2016 MOV10 interacts with Enterovirus 71 genomic 5'UTR and modulates viral replication. Biochemical and biophysical research communications 14 27666477
2015 Regulation of lipid synthesis by the RNA helicase Mov10 controls Wnt5a production. Oncogenesis 14 26029828
2022 Host MOV10 is induced to restrict herpes simplex virus 1 lytic infection by promoting type I interferon response. PLoS pathogens 12 35157734
2021 Drosophila MOV10 regulates the termination of midgut regeneration. Genetics 12 33693718
2023 MOV10 recruits DCP2 to decap human LINE-1 RNA by forming large cytoplasmic granules with phase separation properties. EMBO reports 11 37437058
2014 Altered mRNA levels of MOV10, A3G, and IFN-α in patients with chronic hepatitis B. Journal of microbiology (Seoul, Korea) 11 24871977
2022 Sequestration of LINE-1 in cytosolic aggregates by MOV10 restricts retrotransposition. EMBO reports 10 35856394
2022 Evolutionary and Expression Analysis of MOV10 and MOV10L1 Reveals Their Origin, Duplication and Divergence. International journal of molecular sciences 10 35886872
1993 Consecutive inactivation of both alleles of the gb110 gene has no effect on the proliferation and differentiation of mouse embryonic stem cells. Gene 10 8482544
2021 FMRP and MOV10 regulate Dicer1 expression and dendrite development. PloS one 9 34847178
2020 Roles of MOV10 in Animal RNA Virus Infection. Frontiers in veterinary science 9 33195554
2021 MOV10 Helicase Interacts with Coronavirus Nucleocapsid Protein and Has Antiviral Activity. mBio 8 34517762
2018 RNA helicase Mov10 is essential for gastrulation and central nervous system development. Developmental dynamics : an official publication of the American Association of Anatomists 8 29266590
2023 The MOV10 RNA helicase is a dosage-dependent host restriction factor for LINE1 retrotransposition in mice. PLoS genetics 6 37126510
2017 s8ORF2 protein of infectious salmon anaemia virus is a RNA-silencing suppressor and interacts with Salmon salar Mov10 (SsMov10) of the host RNAi machinery. Virus genes 5 29218433
2023 Serine 970 of RNA helicase MOV10 is phosphorylated and controls unfolding activity and fate of mRNAs targeted for AGO2-mediated silencing. The Journal of biological chemistry 4 36871759
2024 S100A16 stabilizes the ITGA3‑mediated ECM‑receptor interaction pathway to drive the malignant properties of lung adenocarcinoma cells via binding MOV10. Molecular medicine reports 3 39450567
2023 Melatonin Regulates lncRNA NEAT1/miR-138-5p/HIF-1α Axis through MOV10 to Affect Acid-Related Esophageal Epithelial Cell Pyroptosis. Pharmacology 3 37231999
2019 Unraveling the role of the MOV10 RNA helicase during influenza A virus infection. The Biochemical journal 3 30918067
2014 [Host factor Moloney leukemia virus 10 (MOV10) protein inhibits replication of the xenotropic murine leukemia virus-related virus (XMRV)]. Bing du xue bao = Chinese journal of virology 2 25562960
2025 RNA helicase MOV10 suppresses fear memory and dendritic arborization and regulates microtubule dynamics in hippocampal neurons. BMC biology 1 39915816
2026 MOV10-mediated alternative splicing regulates mesangial cell proliferation in diabetic kidney disease. Biochimica et biophysica acta. Gene regulatory mechanisms 0 41638360
2026 MOV10 Promotes the Proliferation of Goat Mammary Epithelial Cells by Regulating the miR-21-5p-Mediated TGFβ/Smad7 Signaling Pathway. ACS omega 0 41867542
2025 Maximal inhibitory effect of MOV10 on LINE-1 retrotransposition requires both the MOV10/LINE-1 association and granule formation. PLoS genetics 0 40408535
2025 Functional investigation of the RNA helicase MOV10 with respect to its interplay with factors involved in nonsense-mediated mRNA decay. The Journal of biological chemistry 0 40570961
2021 Association study of hypertension susceptibility genes ITGA9, MOV10, and CACNB2 with preeclampsia in Chinese Han population. The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians 0 33491517