Affinage

RNF220

E3 ubiquitin-protein ligase RNF220 · UniProt Q5VTB9

Length
566 aa
Mass
62.8 kDa
Annotated
2026-06-10
28 papers in source corpus 22 papers cited in narrative 22 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RNF220 is a RING-domain E3 ubiquitin ligase that controls neural development, signal transduction, and cell proliferation by ubiquitinating a diverse set of substrates and switching between degradative (K48-linked) and non-degradative (K63-linked) outcomes depending on substrate and context (PMID:20170641, PMID:30177510, PMID:32814877). A central feature of its biology is partnership with the cofactor ZC4H2, which is required for RNF220 protein stability; the two proteins phenocopy one another in spinal cord patterning, and their abundance is set by an upstream RLIM–ZC4H2–RNF220 stabilization cascade (PMID:31336385, PMID:35040952). Through this complex RNF220 tunes Sonic hedgehog output during neural tube and cerebellar development — promoting K63-linked ubiquitination and nuclear export of Gli transcription factors, degrading the PRC2 component EED to alter H3K27me3 at Shh targets, and degrading the homeodomain factors Dbx1/2 and Nkx2.2 to specify ventral progenitor domains (PMID:30177510, PMID:32376680, PMID:33895473). RNF220 also monoubiquitinates Phox2a/Phox2b to enable noradrenergic neuron development and K63-stabilizes Olig1/2 to drive oligodendroglial myelination (PMID:32094113, PMID:38324685). Beyond development, it acts as a positive regulator of canonical Wnt signaling by recruiting USP7 to stabilize β-catenin, enhances IFN signaling via K63-linked ubiquitination of STAT1 at K110 to promote STAT1–JAK1 coupling, and drives cardiomyocyte hypertrophy through K63-linked stabilization of STAT3 (PMID:25266658, PMID:32814877, PMID:41219491). It additionally regulates synaptic transmission by ubiquitinating AMPA receptors and clears the ALS-associated protein TDP43 by K48-linked proteasomal degradation (PMID:33386850, PMID:36179027). Biallelic missense mutations in RNF220 cause leukodystrophy with ataxia and deafness, linked to disrupted binding to lamin B1 and deregulated Olig1/2 control (PMID:33964137, PMID:38324685). RNF220 protein levels are themselves controlled by GSK3β phosphorylation and by Smurf1/Smurf2-mediated degradation (PMID:25266658, PMID:37537194).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 2010 Medium

    Established RNF220 as a functional RING E3 ligase by identifying its first substrate, defining a role in corepressor complex turnover.

    Evidence Yeast two-hybrid, in vitro binding, Co-IP and ubiquitination assay showing Sin3B degradation

    PMID:20170641

    Open questions at the time
    • Substrate scope beyond Sin3B unknown
    • No in vivo phenotype
    • Chain linkage type not defined
  2. 2014 High

    Showed RNF220 can act non-canonically as a deubiquitination-promoting scaffold, recruiting USP7 to stabilize β-catenin and amplify Wnt signaling.

    Evidence Reciprocal Co-IP, ubiquitination assay, Wnt reporter and knockdown in colon cancer cells; GSK3β destabilizes RNF220

    PMID:25266658

    Open questions at the time
    • Mechanism by which RNF220 directs USP7 to β-catenin unclear
    • GSK3β phosphosites on RNF220 not mapped
  3. 2018 High

    Defined the RNF220/ZC4H2 complex as a fine-tuner of Shh/Gli morphogen gradients and ventral progenitor specification in vivo.

    Evidence Co-IP, ubiquitination assay, RNF220-null mouse and chick knockdown with progenitor domain phenotypes

    PMID:30177510

    Open questions at the time
    • How K63 ubiquitination drives Gli nuclear export mechanistically unclear
    • Determinants of degradative vs non-degradative output unresolved
  4. 2019 High

    Resolved the dependency within the complex by showing ZC4H2 is required for RNF220 stability, explaining their phenocopying KO phenotypes.

    Evidence ZC4H2 and RNF220 KO mice and zebrafish, protein stability and Gli ubiquitination assays

    PMID:31336385

    Open questions at the time
    • Structural basis of ZC4H2-mediated stabilization unknown
  5. 2020 High

    Expanded RNF220 substrate repertoire and ubiquitin-code usage across noradrenergic neuron development, cerebellar Shh/epigenetics, autophagic Gli clearance, STAT1-driven immunity, and cell-cycle control.

    Evidence Multiple KO mouse, Co-IP, ubiquitination, ChIP, aggresome fractionation, infection, RNA-seq and AML studies showing Phox2a/b monoubiquitination, EED degradation, Gli aggresome/p62 routing, STAT1 K110 K63-ubiquitination, and CyclinD1 stabilization via USP22

    PMID:32094113 PMID:32376680 PMID:32630355 PMID:32814877 PMID:32896826 PMID:33895473

    Open questions at the time
    • Rules governing K48 vs K63 vs monoubiquitination not unified
    • USP22 vs USP7 cofactor selection unexplained
    • Direct vs indirect cell-cycle effects partly inferential
  6. 2021 Medium

    Linked RNF220 to human disease and neurodegeneration, defining biallelic mutations causing leukodystrophy and a TDP43-clearance role relevant to ALS.

    Evidence WES, mass spectrometry, Co-IP with mutant comparison, Drosophila RNAi, patient fibroblasts (lamin B1); Co-IP, ubiquitination and RNF220+/− ALS-like mouse model (TDP43)

    PMID:33386850 PMID:33964137

    Open questions at the time
    • Whether lamin B1 is a ubiquitination substrate vs binding partner unclear
    • TDP43 degradation finding from single lab
    • Genotype-phenotype mechanism for missense mutants incomplete
  7. 2022 High

    Extended RNF220 function to synaptic regulation, hindbrain patterning, and the upstream RLIM–ZC4H2–RNF220 stabilization cascade controlling Shh-dependent development and medulloblastoma.

    Evidence Co-IP, ubiquitination, KO mice, electrophysiology and surface biotinylation (AMPAR); conditional KO IHC (hindbrain); Co-IP and KO models (RLIM-ZC4H2-RNF220)

    PMID:35040952 PMID:35399523 PMID:36179027

    Open questions at the time
    • AMPAR subunit selectivity and chain type not fully defined
    • Hindbrain study relies on single IHC method
  8. 2023 Medium

    Identified upstream control of RNF220 stability by Smurf1/2 and a USP22-dependent Wnt axis in gastric cancer, situating RNF220 in oncogenic signaling.

    Evidence Co-IP, ubiquitination, KD/OE in MB and gastric cancer cells, xenografts, USP22 rescue

    PMID:37295272 PMID:37537194

    Open questions at the time
    • Relationship between Smurf and ZC4H2 regulation of RNF220 unresolved
    • Direct USP22-RNF220 mechanism in Wnt axis indirect
  9. 2024 High

    Defined K63-linked stabilization of Olig1/2 in myelination (with a disease knock-in) and WDR5 degradation controlling late Hox expression, deepening the developmental gene-regulatory roles.

    Evidence Co-IP, ubiquitination, conditional KO and R365Q knock-in mice (Olig1/2); KO mice, snRNA-seq, ubiquitination, Wdr5 genetic and inhibitor rescue (WDR5/Hox)

    PMID:38324685 PMID:39526890

    Open questions at the time
    • How RNF220 chooses stabilizing vs degradative ubiquitination on different substrates unresolved
  10. 2025 High

    Broadened RNF220 into cancer immune evasion, cardiac hypertrophy, and isoform-specific myogenic function, including its own m6A-mediated mRNA regulation.

    Evidence Co-IP, MS, site-directed ubiquitination mapping, KO/OE mice and m6A analysis (PDE10A/PD-L1; STAT3 cardiac hypertrophy); isoform fractionation, Co-IP and KD differentiation assays (ΔN-RNF220/WDR5 in myoblasts)

    PMID:40158470 PMID:40609864 PMID:41219491

    Open questions at the time
    • Isoform-specific substrate selectivity not fully mapped
    • Tissue context driving K48 vs K63 STAT outcomes unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • The molecular determinant that switches RNF220 between K48-linked degradative and K63-linked/monoubiquitin non-degradative outputs, and how cofactor choice (ZC4H2, USP7, USP22) is dictated per substrate, remains unresolved.
  • No structural model of substrate or cofactor selection
  • Linkage-type determinants not defined
  • No unified model integrating its many substrates

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 6 GO:0016740 transferase activity 3 GO:0098772 molecular function regulator activity 3
Localization
GO:0005634 nucleus 3 GO:0005635 nuclear envelope 1 GO:0005856 cytoskeleton 1
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-1266738 Developmental Biology 4 R-HSA-392499 Metabolism of proteins 4 R-HSA-1640170 Cell Cycle 2 R-HSA-1643685 Disease 2 R-HSA-4839726 Chromatin organization 2 R-HSA-112316 Neuronal System 1 R-HSA-168256 Immune System 1
Partners
LMNB1STAT1STAT3TARDBPUSP22USP7WDR5ZC4H2
Complex memberships
RNF220–ZC4H2 complex

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2010 RNF220 is a RING domain E3 ubiquitin ligase that binds E2 ubiquitin-conjugating enzymes and mediates auto-ubiquitination; it interacts with Sin3B (identified by yeast two-hybrid and confirmed in vitro and in vivo) and promotes Sin3B ubiquitination and proteasomal degradation, thereby regulating the Sin3/HDAC corepressor complex. Yeast two-hybrid, in vitro binding assay, co-immunoprecipitation, ubiquitination assay, proteasome inhibitor rescue Biochemical and biophysical research communications Medium 20170641
2014 RNF220 physically interacts with β-catenin and with USP7; the RNF220/USP7 complex deubiquitinates β-catenin and stabilizes it, thereby enhancing canonical Wnt signaling. RNF220 itself is phosphorylated/destabilized by GSK3β, placing RNF220/USP7 as a positive feedback regulator of Wnt signaling. Co-immunoprecipitation, ubiquitination assay, knockdown in colon cancer cells, Wnt reporter assay, Western blot stability assay Molecular and cellular biology High 25266658
2018 RNF220 promotes K63-linked polyubiquitination and nuclear export of Gli transcription factors, thereby fine-tuning Shh/Gli gradients during ventral spinal cord patterning. RNF220 interacts with ZC4H2, and together they target Dbx1/2 and Nkx2.2 for degradation to specify ventral progenitor domains. RNF220-null mice show loss of the p2 progenitor domain. Co-immunoprecipitation, ubiquitination assay, RNF220-null mouse phenotypic analysis, chick spinal cord knockdown, immunofluorescence Development (Cambridge, England) High 30177510
2020 ZC4H2 is required for the stability of RNF220 protein and for proper Gli ubiquitination and Shh signaling in vivo; ZC4H2 and RNF220 knockouts phenocopy each other in spinal cord patterning in mouse and zebrafish. ZC4H2 and RNF220 knockout mice and zebrafish, Western blot protein stability assay, Gli ubiquitination assay, immunofluorescence Journal of molecular cell biology High 31336385
2020 The RNF220/ZC4H2 complex monoubiquitylates Phox2a and Phox2b transcription factors, and this monoubiquitylation is required for full transcriptional activity of Phox2a/Phox2b during locus coeruleus noradrenergic neuron development. Co-immunoprecipitation, ubiquitination assay, Rnf220 and Zc4h2 KO mice, transcriptional reporter assay, immunofluorescence Development (Cambridge, England) High 32094113
2020 RNF220 interacts with STAT1 and mediates K63-linked polyubiquitination of STAT1 at residue K110, which promotes the interaction between STAT1 and JAK1 kinase, enhancing STAT1 phosphorylation and activation of IFN-stimulated gene expression. Rnf220 deficiency reduces IFN signaling and increases susceptibility to bacterial and viral infection in mice. Co-immunoprecipitation, in vitro ubiquitination assay with K110 site-directed mutant, Rnf220 KO mice, ISG expression analysis, infection models Cell death and differentiation High 32814877
2020 RNF220 is required for proliferation of cerebellar granule neuron progenitors and promotes Shh signaling by targeting EED (a PRC2 component) for ubiquitination/degradation, thereby altering epigenetic marks (H3K27me3) on Shh target gene promoters. RNF220 haploinsufficiency in a Ptch1+/− background reduces spontaneous medulloblastoma occurrence. RNF220 conditional KO mice, ubiquitination assay, ChIP for histone marks, Daoy cell knockdown, xenograft, Western blot Development (Cambridge, England) High 32376680
2020 RNF220-polyubiquitinated Gli proteins accumulate in cytoskeletal aggresomes in an HDAC6-dependent manner and interact with p62 for autophagy-mediated degradation. RNF220 also inhibits Gli2 and Gli3 processing both in vitro and in vivo. Co-immunoprecipitation, ubiquitination assay, aggresome fractionation, HDAC6 knockdown, autophagy inhibitor assay, in vitro/in vivo Gli processing assay Biochemical and biophysical research communications Medium 33895473
2020 Loss of RNF220 or ZC4H2 in neural stem cells inhibits proliferation and promotes neuronal differentiation, coinciding with upregulation of Cend1 (a cell-cycle exit regulator) and downstream changes in CyclinD1, Notch1, Hes1, p53, and p21; RNF220-KO NSCs show G0/G1 arrest. RNF220 and ZC4H2 KO mouse-derived NSCs, cell proliferation assay, RNA-seq, Western blot, cell cycle analysis Cells Medium 32630355
2020 RNF220 promotes stabilization of Cyclin D1 protein via USP22; overexpression of RNF220 increases Cyclin D1 protein levels and decreases its ubiquitylation in the nucleus, accelerating G1-to-S phase transition in AML cells. RNF220 cannot stabilize Cyclin D1 without increased USP22 expression. RNF220 overexpression/knockdown in AML cells, co-immunoprecipitation, ubiquitination assay, Western blot, cell cycle analysis Blood cells, molecules & diseases Medium 32896826
2021 RNF220 interacts with TDP43 in vitro and in vivo and promotes its K48-linked polyubiquitination and proteasomal degradation. RNF220+/− mice progressively develop ALS-like motor neuron pathology including TDP43 cytoplasmic accumulation, astrocytosis, muscle denervation, and atrophy. Co-immunoprecipitation, ubiquitination assay, RNF220+/− mouse model, immunofluorescence, motor behavior assays Journal of molecular cell biology Medium 33386850
2021 Biallelic missense mutations in RNF220 (p.R363Q and p.R365Q) cause leukodystrophy with ataxia and deafness in humans. Mass spectrometry identified lamin B1 as an RNF220 binding partner; co-immunoprecipitation confirmed reduced binding of both mutants to lamin B1. RNF220 silencing in Drosophila disrupts localization of lamin Dm0, causes lamin aggregation, and produces a neurodegenerative phenotype. Patient fibroblasts with RNF220 mutations show nuclear morphology abnormalities (blebs, herniations, invaginations). Whole-exome sequencing, mass spectrometry, co-immunoprecipitation, Drosophila RNAi, immunofluorescence in patient fibroblasts Brain : a journal of neurology Medium 33964137
2022 RNF220 directly interacts with AMPA receptor subunits and mediates their polyubiquitination; RNF220 knockout specifically increases AMPAR protein levels and enhances basal synaptic transmission while impairing synaptic plasticity. Two neuropathology-related RNF220 variants fail to regulate AMPAR ubiquitination due to attenuated interaction, and forebrain RNF220-deficient mice show altered learning and memory. Co-immunoprecipitation, ubiquitination assay, RNF220 KO mice, electrophysiology (miniature EPSCs, LTP), surface biotinylation, behavioral testing Science advances High 36179027
2022 RLIM (an E3 ubiquitin ligase) stabilizes ZC4H2 via direct ubiquitination, which in turn stabilizes RNF220, establishing an RLIM–ZC4H2–RNF220 cascade required for full Shh signaling during cerebellar development and medulloblastoma progression. Disease-causative RLIM and ZC4H2 mutations disrupt their interaction and regulation within this cascade. Co-immunoprecipitation, ubiquitination assay, Western blot stability assay, ZC4H2/RLIM KO mouse models, clinical MB sample analysis Journal of molecular cell biology Medium 35040952
2022 RNF220 is required for dorsoventral patterning of the hindbrain neural tube; conditional knockout disrupts ventral progenitor domains (p1, p2, pMN) and alters development of oligodendrocyte precursor cells and serotonergic neurons in the hindbrain. Nestin-Cre conditional KO mice, immunofluorescence for domain markers at E10.5 and E12.5 Frontiers in cell and developmental biology Medium 35399523
2023 Smurf1 and Smurf2 interact with RNF220 and target it for polyubiquitination and proteasomal degradation; in medulloblastoma cells, knockdown or overexpression of Smurf1/Smurf2 controls RNF220 protein levels and consequently modulates Shh signaling and cell proliferation. Co-immunoprecipitation, ubiquitination assay, Smurf1/2 knockdown/overexpression in MB cells, xenograft, clinical sample protein level correlation Cell death & disease Medium 37537194
2023 RNF220 binds USP22 in gastric cancer cells; knockdown of RNF220 downregulates the Wnt/β-catenin axis via USP22, suppressing cell growth and stemness. This pathway dependence on USP22 was confirmed by USP22 overexpression rescue. Co-immunoprecipitation, RNF220 knockdown/overexpression, USP22 overexpression rescue, Western blot, xenograft Tissue & cell Medium 37295272
2024 RNF220 targets Olig1 and Olig2 transcription factors for K63-linked polyubiquitination, which stabilizes these proteins during oligodendroglial development. RNF220 depletion in oligodendrocyte lineage cells impairs OPC proliferation, differentiation, and myelination. A leukodystrophy-linked knock-in RNF220R365Q mutation deregulates Olig1/2 ubiquitination and stabilization, leading to oligodendroglial developmental defects and impaired myelination. Co-immunoprecipitation, ubiquitination assay, RNF220 conditional KO mice, RNF220R365Q knock-in mice, Western blot, immunofluorescence, behavioral testing Science advances High 38324685
2024 RNF220 promotes polyubiquitination and degradation of WDR5 (a TrxG complex component), and loss of RNF220 leads to de-repression of Hox gene expression in the hindbrain pons at late developmental stages (post-E15.5). Genetic ablation of Wdr5 or WDR5 inhibitor treatment in Rnf220-KO mice largely recovers normal Hox expression patterns. RNF220 KO mice, single-nucleus RNA-seq, co-immunoprecipitation, ubiquitination assay, WDR5 inhibitor treatment, Wdr5 conditional KO rescue, P19 cell retinoic acid induction eLife High 39526890
2025 RNF220 directly interacts with PDE10A and mediates its K48-linked ubiquitination and proteasomal degradation in cisplatin-resistant bladder cancer cells; this destabilization of PDE10A promotes PD-L1 expression. RNF220 mRNA is stabilized by m6A modification via METTL3 and IGF2BP2. Co-immunoprecipitation, ubiquitination assay, RNF220 overexpression/knockdown in vitro and in vivo, m6A methylation analysis, Western blot Biochemical pharmacology Medium 40158470
2025 RNF220 mediates K63-linked polyubiquitination of STAT3 at lysine residues K615, K626, K631, and K642 via direct binding through its N-terminal domain to the SH2 and TAD domains of STAT3, stabilizing STAT3 protein and driving pro-hypertrophic responses in cardiomyocytes. RNF220 KO suppresses Ang II-induced cardiac hypertrophy and fibrosis, while RNF220 overexpression aggravates it. Co-immunoprecipitation, proteomic mass spectrometry, ubiquitination assay with site-directed mutants, RNF220 KO and overexpression mice, Ang II cardiac hypertrophy model, STAT3 inhibitor rescue Cell death and differentiation High 41219491
2025 The short N-terminally deleted isoform of RNF220 (ΔN-RNF220/isoform 4) is the predominant and ubiquitously expressed isoform in non-brain tissues in mice. Isoform 4b shows distinct subcellular localization and interaction with nuclear protein WDR5. In murine myoblasts, isoform 4 is the sole expressed form and is required for MyoD and myogenin expression and muscle differentiation. Western blot isoform analysis, subcellular fractionation, co-immunoprecipitation (isoform 4b-WDR5), RNF220 isoform-specific KD in myoblasts, differentiation assay, ChIP-seq (ENCODE data) Molecules and cells Medium 40609864

Source papers

Stage 0 corpus · 28 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 The ubiquitin ligase RNF220 enhances canonical Wnt signaling through USP7-mediated deubiquitination of β-catenin. Molecular and cellular biology 81 25266658
2021 CircRNF220, not its linear cognate gene RNF220, regulates cell growth and is associated with relapse in pediatric acute myeloid leukemia. Molecular cancer 44 34702297
2010 RNF220, an E3 ubiquitin ligase that targets Sin3B for ubiquitination. Biochemical and biophysical research communications 39 20170641
2018 Rnf220 cooperates with Zc4h2 to specify spinal progenitor domains. Development (Cambridge, England) 37 30177510
2020 RNF220 mediates K63-linked polyubiquitination of STAT1 and promotes host defense. Cell death and differentiation 32 32814877
2020 ZC4H2 stabilizes RNF220 to pattern ventral spinal cord through modulating Shh/Gli signaling. Journal of molecular cell biology 28 31336385
2020 Rnf220/Zc4h2-mediated monoubiquitylation of Phox2 is required for noradrenergic neuron development. Development (Cambridge, England) 26 32094113
2022 RNF220 is an E3 ubiquitin ligase for AMPA receptors to regulate synaptic transmission. Science advances 24 36179027
2020 RNF220 is required for cerebellum development and regulates medulloblastoma progression through epigenetic modulation of Shh signaling. Development (Cambridge, England) 21 32376680
2021 Haploinsufficiency of the TDP43 ubiquitin E3 ligase RNF220 leads to ALS-like motor neuron defects in the mouse. Journal of molecular cell biology 20 33386850
2021 Biallelic mutations in RNF220 cause laminopathies featuring leukodystrophy, ataxia and deafness. Brain : a journal of neurology 19 33964137
2021 The many faces of the E3 ubiquitin ligase, RNF220, in neural development and beyond. Development, growth & differentiation 17 34716995
2020 Loss of ZC4H2 and RNF220 Inhibits Neural Stem Cell Proliferation and Promotes Neuronal Differentiation. Cells 17 32630355
2020 RNF220 promotes the proliferation of leukaemic cells and reduces the degradation of the Cyclin D1 protein through USP22. Blood cells, molecules & diseases 17 32896826
2023 RNF220 promotes gastric cancer growth and stemness via modulating the USP22/wnt/β-catenin pathway. Tissue & cell 14 37295272
2018 A homozygous RNF220 mutation leads to male infertility with small-headed sperm. Gene 13 30500349
2022 Sequential stabilization of RNF220 by RLIM and ZC4H2 during cerebellum development and Shh-group medulloblastoma progression. Journal of molecular cell biology 10 35040952
2025 N6-methyladenosine-modified RNF220 induces cisplatin resistance and immune escape via regulating PDE10A K48-linked ubiquitination in bladder cancer. Biochemical pharmacology 7 40158470
2024 RNF220-mediated K63-linked polyubiquitination stabilizes Olig proteins during oligodendroglial development and myelination. Science advances 7 38324685
2023 Smurf1 and Smurf2 mediated polyubiquitination and degradation of RNF220 suppresses Shh-group medulloblastoma. Cell death & disease 6 37537194
2022 Rnf220 is Implicated in the Dorsoventral Patterning of the Hindbrain Neural Tube in Mice. Frontiers in cell and developmental biology 5 35399523
2021 RNF220-mediated ubiquitination promotes aggresomal accumulation and autophagic degradation of cytoplasmic Gli via HDAC6. Biochemical and biophysical research communications 3 33895473
2024 The E3 ubiquitin ligase RNF220 maintains hindbrain Hox expression patterns through regulation of WDR5 stability. eLife 2 39526890
2025 N-Terminal deleted isoforms of E3 ligase RNF220 are ubiquitously expressed and required for mouse muscle differentiation. Molecules and cells 1 40609864
2025 Dual oncogenic role of RNF220 in AML: linking metabolic rewiring to cell proliferation and immune evasion. Frontiers in oncology 1 41244923
2023 The RNF220 domain nuclear factor Teyrha-Meyrha (Tey) regulates the migration and differentiation of specific visceral and somatic muscles in Drosophila. Development (Cambridge, England) 1 37642089
2025 RNF220 enhances USP22 to promote cell growth, metastasis and stemness in hepatocellular carcinoma by activating the Akt pathway. Cell cycle (Georgetown, Tex.) 0 40938201
2025 RNF220 mediates K63-linked polyubiquitination of STAT3 and aggravates pathological cardiac hypertrophy. Cell death and differentiation 0 41219491

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