Affinage

ARIH2

E3 ubiquitin-protein ligase ARIH2 · UniProt O95376

Length
493 aa
Mass
57.8 kDa
Annotated
2026-06-09
33 papers in source corpus 21 papers cited in narrative 21 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

ARIH2 (TRIAD1) is an RBR-family E3 ubiquitin ligase that operates as the catalytic partner of neddylated Cullin-RING ligase (CRL) complexes to control protein turnover across hematopoietic, immune, and neural contexts (PMID:24076655, PMID:23179078). In isolation ARIH2 is autoinhibited; binding to neddylated CUL5-RBX2 strongly stimulates its ligase activity, and structural analysis shows this activation is allosteric—CUL5-linked NEDD8 does not directly recruit ARIH2 but rearranges CUL5 to expose cryptic ARIH2-binding sites (PMID:24076655, PMID:34518685). The enzyme uses two RING domains that engage distinct E2s: RING1 binds UbcH7 to build K48-linked chains for proteasomal degradation, while RING2 binds Ubc13 to build K63-linked chains for non-proteolytic functions, and both are required to restrain myeloid progenitor proliferation (PMID:16118314, PMID:19340006). Through these activities ARIH2 ubiquitinates a range of substrates including NLRP3 to suppress inflammasome activation (PMID:29021376), p21 to promote its degradation (PMID:35732617), the Smoothened receptor via ER-associated degradation to limit basal Hedgehog signaling (PMID:35899529), and Gcn1 to suppress the integrated stress response in leukemic cells (PMID:40680841). ARIH2 also acts non-catalytically, competing with MDM2 to stabilize Gfi1 and p53 (PMID:17646546, PMID:22819825), and is essential for embryogenesis and for restraining NF-κB activation in dendritic cells via degradation of nuclear IκBβ (PMID:23179078). Additional substrate and trafficking roles—including dynein intermediate chain 1 in organelle positioning (PMID:41312386), vimentin and NUPR1 degradation (PMID:41572548, PMID:41998836), and multivesicular body sorting (PMID:23213454)—extend its reach into cytoskeletal and endosomal regulation.

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2005 High

    Established ARIH2/Triad1 as a functional E3 ligase by showing it binds the E2 UbcH7 through its RING fingers and that this activity restrains myeloid progenitor growth, defining its first biological role.

    Evidence E2 binding, ubiquitin chain assays, RING point mutants, and CFU-GM colony assays with proteasome inhibition

    PMID:16118314

    Open questions at the time
    • Specific physiological substrates not yet identified
    • Mechanism of ligase activation in cells not addressed
  2. 2007 High

    Revealed a catalysis-independent mode of action: ARIH2 stabilizes Gfi1 by competing with other E3 ligases rather than ubiquitinating it.

    Evidence Reciprocal Co-IP, siRNA knockdown, pulse-chase half-life, and domain-deletion mutants in U937 cells

    PMID:17646546

    Open questions at the time
    • Competing E3 ligase not identified
    • Whether this competition operates in primary cells unresolved
  3. 2009 High

    Dissected the dual-RING architecture, showing the two RING domains recruit different E2s (UbcH7 vs Ubc13) to assemble K48- versus K63-linked chains, explaining how one ligase serves both proteolytic and non-proteolytic outputs.

    Evidence E2 binding assays, ubiquitin linkage analysis, deletion/point mutants, and myeloid clonogenic assays

    PMID:19340006

    Open questions at the time
    • Substrate-specific deployment of each linkage type not mapped
    • Regulation of E2 choice unknown
  4. 2012 High

    Connected ARIH2 to immune homeostasis and embryogenesis, showing it degrades nuclear IκBβ to restrain NF-κB-driven dendritic cell activation, with loss causing lethal systemic immune activation.

    Evidence Gene-targeted knockout mice, hematopoietic reconstitution, and IκBβ-p65 interaction studies

    PMID:23179078

    Open questions at the time
    • Direct ubiquitination of IκBβ by ARIH2 not biochemically isolated here
    • CRL dependence of this activity not addressed
  5. 2012 Medium

    Defined a reciprocal regulatory relationship with MDM2: ARIH2 stabilizes p53 by displacing it from MDM2, while MDM2 in turn ubiquitinates and degrades ARIH2 to relieve its growth-inhibitory effect.

    Evidence Co-IP, p53-MDM2 dissociation and ubiquitination assays, siRNA, and stability assays (two studies)

    PMID:22819825 PMID:22940738

    Open questions at the time
    • Single-lab findings without reciprocal independent validation
    • Physiological context of the ARIH2-MDM2 feedback loop unclear
  6. 2012 Medium

    Extended ARIH2 function to membrane trafficking, showing it is required for endosomal sorting and multivesicular body function via dual K48/K63 chain formation.

    Evidence siRNA depletion, immunofluorescence, immune EM, and cargo transport assays

    PMID:23213454

    Open questions at the time
    • Trafficking substrate(s) of ARIH2 not identified
    • Link between ligase activity and MVB defect not biochemically resolved
  7. 2017 High

    Identified NLRP3 as a direct substrate, establishing ARIH2 as a brake on inflammasome activation through K48/K63 ubiquitination of the NACHT domain.

    Evidence Reciprocal Co-IP, RING2 and ubiquitin-linkage mutants, CRISPR KO, overexpression, and IL-1β readouts

    PMID:29021376

    Open questions at the time
    • Whether CRL5-NEDD8 activation is required for NLRP3 ubiquitination not tested
    • Functional roles of K48 vs K63 chains on NLRP3 not separated
  8. 2021 High

    Solved the structural basis of activation, showing NEDD8 on CUL5 acts allosterically—rearranging CUL5 to expose cryptic ARIH2 sites—rather than directly recruiting ARIH2 as occurs with CUL1-ARIH1.

    Evidence Cryo-EM/X-ray structural analysis with biochemical reconstitution and mutagenesis

    PMID:34518685

    Open questions at the time
    • Substrate engagement geometry in the activated E3-E3 complex not fully resolved
    • Whether other cullins activate ARIH2 by the same mechanism unknown
  9. 2022 High

    Identified p21 as a direct degradation substrate with defined linkage (K48) and acceptor lysine (K161), linking ARIH2 to cell cycle and chemosensitivity.

    Evidence Co-IP, in vitro ubiquitination, ubiquitin and substrate site mutants, knockdown, and xenografts

    PMID:35732617

    Open questions at the time
    • CRL dependence of p21 ubiquitination not addressed
    • Single-lab finding
  10. 2022 High

    Resolved isoform-specific function, showing the ER-localized Arih2β isoform mediates ERAD of Smoothened to suppress basal Hedgehog signaling and prevent ER stress.

    Evidence Mouse genetic KO with isoform-specific rescue, subcellular localization, cilia imaging, and UPR assays

    PMID:35899529

    Open questions at the time
    • Direct ubiquitination of Smo and chain type not specified
    • Determinants of α vs β isoform localization not defined
  11. 2022 Medium

    Added a second MDM2-competition substrate, showing Triad1 stabilizes PTN by reversing MDM2-mediated ubiquitination to promote neurite outgrowth after spinal cord injury.

    Evidence Ubiquitination assay, Co-IP, overexpression/knockdown, co-culture, and in vivo SCI model

    PMID:36055408

    Open questions at the time
    • Single-lab finding
    • Mechanism of MDM2 displacement vs deubiquitination not distinguished
  12. 2025 Medium

    Expanded the substrate landscape and revealed regulation of ARIH2's own neddylation state—ubiquitinating DIC1 for dynein-dependent organelle positioning, Gcn1 to suppress the integrated stress response in leukemia, and vimentin via K29 chains.

    Evidence Interaction proteomics, Co-IP, ubiquitination/linkage-site mutants, translatome profiling, organelle positioning, and AML/PDX models (three studies)

    PMID:40680841 PMID:41312386 PMID:41572548

    Open questions at the time
    • Each substrate from a single lab without independent confirmation
    • How Lis1/CSN-driven ARIH2 deneddylation integrates with CRL activation unclear
  13. 2026 Medium

    Linked ARIH2 to neurodegeneration and ferroptosis, identifying TPPP3 as a substrate required for ARIH2 effects on α-synuclein toxicity and NUPR1 as a substrate whose degradation modulates ferroptosis sensitivity.

    Evidence C. elegans genetic screen, iPSC-neuron proteomics, epistasis, IP-MS, Co-IP, ubiquitination, and ferroptosis marker analysis (two studies)

    PMID:41651665 PMID:41998836

    Open questions at the time
    • Direct ubiquitination assay for TPPP3 not detailed
    • Single-lab findings without orthogonal validation

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved which substrates depend on CRL5-NEDD8 allosteric activation versus CRL-independent activity, and how the dual K48/K63 (and K29) chain outputs are selected per substrate.
  • No unified rule linking activation state to substrate choice
  • Physiological substrate hierarchy across tissues unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 4 GO:0016874 ligase activity 3 GO:0098772 molecular function regulator activity 2
Localization
GO:0005634 nucleus 2 GO:0005768 endosome 1 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-392499 Metabolism of proteins 3 R-HSA-168256 Immune System 2 R-HSA-162582 Signal Transduction 1 R-HSA-1640170 Cell Cycle 1 R-HSA-8953897 Cellular responses to stimuli 1
Partners
CUL5GFI1MDM2NEDD8NLRP3RBX2UBC13UBCH7
Complex memberships
NLRP3 inflammasomeneddylated CUL5-RBX2 Cullin-RING ligase

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2013 TRIAD1 (ARIH2) associates with neddylated CUL5-RBX2-based Cullin-RING ligase (CRL) complexes, and binding of the cognate neddylated CRL greatly stimulates TRIAD1 RBR ligase activity in vitro (auto-ubiquitylation, UbcH7~ubiquitin thioester dissociation, and ubiquitin-vinyl methyl ester reactivity). TRIAD1 is auto-inhibited as an isolated protein but activated by neddylated CRL binding. In vitro ubiquitylation assays, auto-ubiquitylation, thioester dissociation assay, activity-based probe reactivity, genetic epistasis in vivo The EMBO journal High 24076655
2021 Crystal/cryo-EM structural analysis of the CUL5-ARIH2 E3-E3 assembly revealed that ARIH2 is autoinhibited in isolation, and activation on neddylated CUL5-RBX2 occurs through an allosteric mechanism: CUL5-linked NEDD8 does not directly recruit ARIH2 (unlike CUL1-NEDD8 recruiting ARIH1), but instead contacts CUL5 covalently and induces conformational rearrangements that expose cryptic ARIH2-binding sites on CUL5. Cryo-EM/X-ray structural analysis, biochemical reconstitution, mutational validation Nature chemical biology High 34518685
2005 Triad1 (ARIH2) binds the E2 ubiquitin-conjugating enzyme UbcH7 via its RING finger domains, supports formation of ubiquitin chains recognized by the proteasome, and inhibits clonogenic growth of primary myeloid progenitor cells. RING finger point mutants failing to bind UbcH7 lost the inhibitory effect; proteasome inhibition counteracted the growth inhibition. Binding assays, ubiquitin chain formation assays, retroviral transduction with RING finger mutants, CFU-GM colony assays, proteasome inhibition Blood High 16118314
2009 Triad1 contains two RING domains that differentially bind distinct E2 ubiquitin-conjugating enzymes: the first RING binds UbcH7 (supporting K48-linked chains for proteasomal degradation) and the second RING binds Ubc13 (supporting K63-linked chains for non-proteolytic functions). Both RING domains are required for inhibition of myeloid cell proliferation. E2 binding assays, ubiquitin chain linkage analysis, deletion/point mutants, myeloid clonogenic assays Leukemia High 19340006
2007 Triad1 interacts with the DNA-binding domain of Gfi1 and unexpectedly inhibits Gfi1 ubiquitination, resulting in prolonged Gfi1 half-life. This inhibition is independent of Triad1's own ubiquitin ligase activity, suggesting Triad1 competes with other E3 ligases for Gfi1 binding. Triad1 mutants lacking the Gfi1-binding domain lost this stabilizing effect. Co-immunoprecipitation, siRNA knockdown, ubiquitination assays, pulse-chase half-life analysis, deletion mutant analysis, U937 cell overexpression Blood High 17646546
2012 ARIH2 (Triad1) causes degradation of nuclear IκBβ in dendritic cells, abrogating IκBβ's ability to sequester, protect, and transcriptionally co-activate p65 in the nucleus. Loss of ARIH2 in hematopoietic cells leads to dysregulated NF-κB activation in dendritic cells and lethal systemic immune activation. Targeted gene deletion in mice showed ARIH2 is essential for embryogenesis. Gene-targeted knockout mice, hematopoietic stem cell reconstitution, NF-κB pathway analysis, IκBβ/p65 interaction studies Nature immunology High 23179078
2017 ARIH2 interacts with NLRP3 via NLRP3's NACHT domain (aa 220–575) in the inflammasome complex, and the RING2 domain of ARIH2 catalyzes K48- and K63-linked ubiquitination of NLRP3. CRISPR/Cas9 deletion of ARIH2 inhibited NLRP3 ubiquitination and promoted inflammasome activation (ASC oligomerization, pro-IL-1β processing, IL-1β secretion); overexpression of ARIH2 had the opposite effect. Co-immunoprecipitation, RING2 domain mutants, ubiquitin chain linkage mutants, CRISPR/Cas9 knockout, ARIH2 overexpression, ASC oligomerization assay, IL-1β ELISA Journal of immunology High 29021376
2012 TRIAD1 binds to the C-terminus of p53 and promotes its dissociation from MDM2, thereby inhibiting MDM2-mediated ubiquitination and degradation of p53. Ablation of TRIAD1 reduces p53 levels upon DNA damage, while ectopic TRIAD1 expression stabilizes p53. Co-immunoprecipitation, p53-MDM2 dissociation assay, ubiquitination assay, siRNA knockdown, overexpression FEBS letters Medium 22819825
2012 TRIAD1 is a ubiquitination substrate of MDM2: MDM2 interacts with and ubiquitinates TRIAD1, targeting it for proteasomal degradation. RNAi against MDM2 increased endogenous TRIAD1 protein stability, and MDM2-mediated TRIAD1 degradation suppressed TRIAD1-mediated cell growth inhibition. Co-immunoprecipitation, ubiquitination assay, siRNA knockdown of MDM2, protein stability assay Oncology reports Medium 22940738
2012 Triad1 depletion in cells disrupts endosomal sorting of growth hormone and EGF, causing accumulation of ligands in enlarged endosomes with irregular intraluminal vesicles and prominent clathrin coats, while reducing fluid-phase transport to lysosomes. Triad1 catalyzes both K48- and K63-linked polyubiquitin chain formation and is required for proper multivesicular body function. siRNA depletion, immunofluorescence, immune electron microscopy, fluid-phase transport assays, receptor recycling assay Biology open Medium 23213454
2011 TRIAD1 binds UBCH8 and PML-RARα, but this interaction does not affect PML-RARα turnover (negative finding), distinguishing TRIAD1 from SIAH1/SIAH2 in regulation of this leukemia oncoprotein. UBCH8 cooperates with SIAH1/SIAH2 but not TRIAD1 for PML-RARα degradation. Co-immunoprecipitation, protein stability/turnover assay, combined drug treatment (valproic acid + ATRA) The international journal of biochemistry & cell biology Medium 22037423
2022 ARIH2 interacts with p21 and induces K48-linked ubiquitination of p21 at lysine K161, targeting p21 for proteasomal degradation. ARIH2 was confirmed as a direct E3 ligase of p21 by in vitro ubiquitination assay. ARIH2 knockdown induced DNA damage and apoptosis and altered chemosensitivity. Co-immunoprecipitation, in vitro ubiquitination assay, site-directed mutagenesis (K48 ubiquitin and K161 p21 mutants), knockdown, in vivo tumor xenograft Cell death & disease High 35732617
2022 Arih2β (ER-localized isoform, cytoplasmic face of ER) regulates ER-associated degradation (ERAD) of Smoothened (Smo). Loss of Arih2 elevates cellular and ciliary Smo levels, activates basal Hedgehog signaling, and triggers ER protein aggregation and unfolded protein response. Re-expression of ER-localized Arih2β but not nuclear Arih2α rescues these phenotypes. Genetic loss-of-function (mouse model), isoform-specific re-expression, subcellular fractionation/localization, cilia imaging, UPR assays, protein accumulation assays Journal of cell science High 35899529
2025 ARIH2 ubiquitinates dynein intermediate chain 1 (DIC1), facilitating dynein function in organelle positioning. The Lis1 protein promotes ARIH2 deneddylation via the COP9 signalosome (CSN), thereby modulating ARIH2 ubiquitin ligase activity. Active (neddylated) ARIH2 is required for proper dynein-dependent intracellular transport. Proteomics-based interaction mapping, co-immunoprecipitation, ubiquitination assays, organelle positioning assays iScience Medium 41312386
2025 ARIH2 ubiquitinates Gcn1 (a regulator of the integrated stress response, ISR) among a set of ISR-regulatory proteins identified by proteomic screen. Triad1 knockdown causes a translatome shift consistent with ISR activation that is reversed by co-knockdown of Gcn1, linking Triad1-dependent ubiquitination to ISR suppression and leukemia suppression. Proteomic screen (ubiquitination proteomics), translatome profiling, Gcn1 co-knockdown epistasis, murine AML bone marrow transplant model The Journal of biological chemistry Medium 40680841
2026 In C. elegans and human iPSC-derived dopaminergic neurons, loss of ARIH2 (ari-2 in worm) suppresses α-synuclein-mediated dopaminergic neurodegeneration. Unbiased proteomics identified TPPP3 (a microtubule dynamics regulator) as a novel ARIH2 substrate; TPPP3 was required for ARIH2's effects on α-synuclein-induced neurodegeneration. C. elegans genetic screen, unbiased proteomics in human iPSC-derived neurons, loss-of-function studies, epistasis (TPPP3 requirement) The Journal of neuroscience Medium 41651665
2025 ARIH2 promotes K29-linked polyubiquitination of vimentin (VIM) at lysine K373 residue, leading to proteasomal degradation of VIM. LINC00476 lncRNA recruits ARIH2 to VIM to facilitate this ubiquitination. RNA pull-down, RIP, Co-IP, ubiquitination assays with linkage and site mutants, in vivo PDX model International journal of surgery Medium 41572548
2026 ARIH2 interacts with NUPR1 in bladder cancer cells and promotes its ubiquitin-mediated proteasomal degradation. ARIH2 depletion prolongs NUPR1 stability and reduces its ubiquitination, while ARIH2 overexpression decreases NUPR1 levels. NUPR1 suppresses ferroptosis (elevated GPX4, SLC7A11, reduced ACSL4), so ARIH2-mediated NUPR1 degradation indirectly modulates ferroptosis sensitivity. IP-MS, Co-IP, immunofluorescence, ubiquitination assay, protein stability assay, ferroptosis marker analysis Journal of cellular and molecular medicine Medium 41998836
2018 Triad1 interacts with DISC1 via specific protein fragments, and co-localization in neural stem cells was demonstrated. Overexpressing both TRIAD1 and DISC1 in primary neural stem cells significantly affected proliferation and differentiation after traumatic brain injury. Co-immunoprecipitation, truncation mutant mapping, immunofluorescence co-localization, lentiviral overexpression in primary neural stem cells Stem cell research & therapy Low 30409224
2018 Triad1 interacts with EHD1 (EH domain-containing protein 1) both in vitro and in vivo, mediated through the EH domain of EHD1. Triad1 regulates the expression and subcellular distribution of EHD1, influencing neurite outgrowth of PC12 cells after spinal cord injury. Co-immunoprecipitation, EH domain truncation interaction mapping, in vitro and in vivo binding assays, neurite outgrowth assay Journal of cellular biochemistry Low 30320922
2022 Triad1 overexpression promoted PTN (pleiotrophin) protein levels and inhibited MDM2-mediated PTN ubiquitination. MDM2 ubiquitinates PTN, and Triad1 reversed this ubiquitination, thereby stabilizing PTN and promoting astrocyte-dependent neurite outgrowth after spinal cord injury. Ubiquitination assay, co-immunoprecipitation, overexpression and shRNA knockdown, astrocyte-neuron co-culture, in vivo rat SCI model The Journal of biological chemistry Medium 36055408

Source papers

Stage 0 corpus · 33 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 ARIH2 Ubiquitinates NLRP3 and Negatively Regulates NLRP3 Inflammasome Activation in Macrophages. Journal of immunology (Baltimore, Md. : 1950) 118 29021376
2013 TRIAD1 and HHARI bind to and are activated by distinct neddylated Cullin-RING ligase complexes. The EMBO journal 97 24076655
2021 CUL5-ARIH2 E3-E3 ubiquitin ligase structure reveals cullin-specific NEDD8 activation. Nature chemical biology 58 34518685
2005 The E3 ubiquitin-protein ligase Triad1 inhibits clonogenic growth of primary myeloid progenitor cells. Blood 51 16118314
2022 Pyruvate dehydrogenase B regulates myogenic differentiation via the FoxP1-Arih2 axis. Journal of cachexia, sarcopenia and muscle 37 36564038
2012 ARIH2 is essential for embryogenesis, and its hematopoietic deficiency causes lethal activation of the immune system. Nature immunology 34 23179078
2009 The ubiquitin ligase Triad1 inhibits myelopoiesis through UbcH7 and Ubc13 interacting domains. Leukemia 29 19340006
2007 Gfi1 ubiquitination and proteasomal degradation is inhibited by the ubiquitin ligase Triad1. Blood 28 17646546
2014 A novel feed-forward loop between ARIH2 E3-ligase and PABPN1 regulates aging-associated muscle degeneration. The American journal of pathology 27 24486325
2011 HoxA10 influences protein ubiquitination by activating transcription of ARIH2, the gene encoding Triad1. The Journal of biological chemistry 27 21454682
2011 Differential regulation of PML-RARα stability by the ubiquitin ligases SIAH1/SIAH2 and TRIAD1. The international journal of biochemistry & cell biology 24 22037423
2015 HoxA10 Terminates Emergency Granulopoiesis by Increasing Expression of Triad1. Journal of immunology (Baltimore, Md. : 1950) 20 25895533
2012 Identification of the ubiquitin ligase Triad1 as a regulator of endosomal transport. Biology open 20 23213454
2024 A de novo ARIH2 gene mutation was detected in a patient with autism spectrum disorders and intellectual disability. Scientific reports 19 38982159
2018 The E3 ubiquitin ligase Triad1 influences development of Mll-Ell-induced acute myeloid leukemia. Oncogene 19 29459712
2022 ARIH2 regulates the proliferation, DNA damage and chemosensitivity of gastric cancer cells by reducing the stability of p21 via ubiquitination. Cell death & disease 17 35732617
2012 TRIAD1 inhibits MDM2-mediated p53 ubiquitination and degradation. FEBS letters 15 22819825
2022 Arih2 regulates Hedgehog signaling through smoothened ubiquitylation and ER-associated degradation. Journal of cell science 7 35899529
2021 E3 ubiquitin ligase Triad1 promotes neuronal apoptosis by regulating the p53-caspase3 pathway after spinal cord injury. Somatosensory & motor research 7 34641746
2017 TRIAD1 Is a Novel Transcriptional Target of p53 and Regulates Nutlin-3a-Induced Cell Death. Journal of cellular biochemistry 6 27935098
2012 TRIAD1 is negatively regulated by the MDM2 E3 ligase. Oncology reports 6 22940738
2022 Triad1 Promotes the Inflammatory Response and Neuronal Apoptosis to Aggravate Acute Spinal Cord Injury in Rats. Computational and mathematical methods in medicine 5 35912142
2020 Increased expression of Triad1 is associated with neuronal apoptosis after intracerebral hemorrhage in adult rats. The International journal of neuroscience 4 31842638
2018 Triad1 regulates the expression and distribution of EHD1 contributing to the neurite outgrowth of neurons after spinal cord injury. Journal of cellular biochemistry 4 30320922
2018 The expression of TRIAD1 and DISC1 after traumatic brain injury and its influence on NSCs. Stem cell research & therapy 4 30409224
2022 Ubiquitin ligase Triad1 promotes neurite outgrowth by inhibiting MDM2-mediated ubiquitination of the neuroprotective factor pleiotrophin. The Journal of biological chemistry 3 36055408
2019 Arih2 gene influences immune response and tissue development in chicken. Bioscience reports 3 31551339
2025 The ubiquitin ligase Triad1 influences myeloid leukemogenesis by regulating the integrated stress response. The Journal of biological chemistry 2 40680841
2025 A LisH-domain protein interaction map reveals a Lis1-ARIH2-dynein regulatory axis. iScience 2 41312386
2025 LINC00476 cooperates with ARIH2 and suppresses pancreatic cancer progression by inducing VIM ubiquitination. International journal of surgery (London, England) 1 41572548
2026 In Vivo Screen of Parkinson's Disease GWAS Risk Genes Identifies ARIH2 as a Novel Regulator of α-Synuclein Toxicity in Dopaminergic Neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience 0 41651665
2026 ARIH2 Ubiquitination Regulates NUPR1 to Inhibit Ferroptosis in Bladder Cancer. Journal of cellular and molecular medicine 0 41998836
2026 Cepharanthine inhibits NLRP3 inflammasome-induced pyroptosis through ARIH2-mediated degradation of NLRP3. International immunopharmacology 0 42217341

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