Affinage

USP48

Ubiquitin carboxyl-terminal hydrolase 48 · UniProt Q86UV5

Length
1035 aa
Mass
119.0 kDa
Annotated
2026-06-11
32 papers in source corpus 24 papers cited in narrative 26 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

USP48 is a nuclear-enriched ubiquitin-specific protease that removes K48-linked polyubiquitin from a diverse set of substrates to prevent their proteasomal degradation, positioning it at the intersection of DNA damage repair, NF-κB signaling, cell cycle control, and pyroptosis (PMID:29335415, PMID:25486460, PMID:34059922). Its catalytic ubiquitin-hydrolase activity is essential for function: disease-associated missense variants fail to cleave tetra-ubiquitin in vitro, and an auxiliary, non-cleaved ubiquitin allosterically modulates its activity (PMID:29335415, PMID:34059922). In the DNA damage response USP48 acts as a histone H2A deubiquitinase that antagonizes BRCA1-mediated ubiquitination at the C-terminal site, thereby restraining end resection and homology-directed repair pathway choice; loss of USP48 is synthetic viable in Fanconi anemia-deficient cells by enhancing BRCA1-dependent damage clearance (PMID:29335415, PMID:29891926). A second major axis is NF-κB: USP48 associates with the COP9 signalosome and trims K48 chains on nuclear RelA/p65 to stabilize it and tune induction and shutoff of NF-κB target genes, with activity gated by CK2-mediated phosphorylation (PMID:25486460, PMID:30628021, PMID:35913642). USP48 stabilizes additional substrates including Gli1 in Hedgehog signaling, TRAF2 in the TNFα/JNK pathway, Aurora B during mitosis, GSDME and NEK7 in pyroptosis, and SIRT6, HMGA2, DBF4, and YBX1 in cancer contexts (PMID:28623188, PMID:28874458, PMID:33903120, PMID:36607699, PMID:34445214, PMID:38572092, PMID:40580743, PMID:42163235, PMID:42142703). Its substrate selectivity is further regulated by GSK3β phosphorylation, SUMOylation at K258, and nuclear targeting via a defined nuclear localization signal (PMID:28874458, PMID:37781625, PMID:38572092). USP48 is recurrently mutated (M415I/M415V) in USP8 wild-type corticotroph adenomas, where mutants enhance POMC promoter activity, and recessive variants disrupt inner ear neuronal development with hearing and vestibular dysfunction (PMID:34059922, PMID:30093687).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2014 High

    Established USP48's first defined cellular substrate and an unusual catalytic mode—chain trimming rather than full disassembly—linking it to NF-κB signaling.

    Evidence siRNA screen, Co-IP with CSN and RelA, in vitro K48 chain-trimming assays, NF-κB reporters

    PMID:25486460

    Open questions at the time
    • Did not resolve structural basis of chain trimming
    • CK2 phosphosite not mapped
  2. 2017 High

    Extended USP48 beyond NF-κB by showing it directly deubiquitinates and stabilizes Gli1 (Hedgehog) and TRAF2 (TNFα/JNK), revealing substrate breadth and pathway-specific targeting.

    Evidence Co-IP, DUB/ubiquitination assays, Gli reporter, pathway-specific rescue, GSK3β phosphorylation assay

    PMID:28623188 PMID:28874458

    Open questions at the time
    • Mechanism of pathway-specific TRAF2 pool selection unresolved
    • Generality of feedback loops across tissues untested
  3. 2018 High

    Defined USP48 as the histone H2A deubiquitinase antagonizing BRCA1 and a synthetic viable target in Fanconi anemia, placing it in DNA repair pathway choice.

    Evidence In vitro DUB assays with auxiliary ubiquitin, cell-based BRCA1 ubiquitination, resection measurements, genome-wide screens across five FA backgrounds

    PMID:29335415 PMID:29891926

    Open questions at the time
    • Recruitment mechanism to damage sites not defined
    • Auxiliary ubiquitin binding site structurally uncharacterized
  4. 2018 Medium

    Identified recurrent USP48 mutations in corticotroph adenomas driving POMC transcription, the first disease-associated coding variants.

    Evidence Tumor DNA sequencing, POMC promoter reporter with mutant constructs

    PMID:30093687

    Open questions at the time
    • Mechanism connecting M415 mutation to POMC activation not dissected
    • DUB activity change of mutants not measured
  5. 2019 Medium

    Mapped the USP48–RelA interaction interface, localizing binding to the catalytic USP domain and the RHD N-terminus.

    Evidence Truncation Co-IP and nuclear co-localization

    PMID:30628021

    Open questions at the time
    • Domain mapping by overexpression only
    • No structural model of the interface
  6. 2021 Medium

    Broadened the substrate set to SIRT6 and Aurora B with site-mapped K48 deubiquitination, connecting USP48 to metabolism and mitotic progression.

    Evidence Co-IP, deubiquitination site mutagenesis, glycolysis assays, KO cell cycle and cytokinesis readouts

    PMID:33903120 PMID:34445214

    Open questions at the time
    • Single-lab findings without reciprocal independent validation
    • Regulation of substrate choice between contexts unknown
  7. 2021 High

    Confirmed catalytic ubiquitin-hydrolase requirement using disease mutants and tied USP48 to a Mendelian hearing/vestibular phenotype via an in vivo model.

    Evidence In vitro tetra-ubiquitin hydrolysis with mutants, structural modeling, human inner ear immunohistology, zebrafish knockdown

    PMID:34059922

    Open questions at the time
    • Relevant inner ear substrate not identified
    • Human genetics causality limited to candidate variants
  8. 2022 Medium

    Revealed context-dependent NF-κB regulation and a non-canonical ciliary/basal body role, complicating the uniform stabilizer model.

    Evidence siRNA + fractionation + reporter in RPE cells; Co-IP and basal body localization with ARL3/UNC119a; CSN1–RelA–A20 axis in H. pylori infection

    PMID:35913642 PMID:36077078 PMID:36293380

    Open questions at the time
    • RPE negative regulation lacks direct DUB assay (Low confidence)
    • Mechanism distinguishing stabilizing vs destabilizing RelA effects unknown
  9. 2023 High

    Linked USP48 to pyroptosis by stabilizing GSDME at mapped K48 sites, with tumor microenvironment and immunotherapy relevance.

    Evidence CRISPR screen, Co-IP, site-specific deubiquitination, pyroptosis assays, in vivo PD-1 blockade models

    PMID:36607699

    Open questions at the time
    • Direct regulation of USP48 activity in tumor immune context unclear
  10. 2024 Medium

    Defined SUMOylation at K258 as a regulator of substrate affinity (HMGA2) and demonstrated pharmacological tractability.

    Evidence MS, Co-IP, SUMOylation site mapping, DUB-IN-2 inhibition, invasion/metastasis assays

    PMID:38572092

    Open questions at the time
    • SUMO E3 ligase for K258 not identified
    • Selectivity of DUB-IN-2 not established
  11. 2025 Medium

    Expanded USP48 into chromatin–methylation crosstalk and DNMT1-inhibitor sensitization, plus multiple new disease-context substrates (NEK7, CNN1, MrgC, SLC1A5).

    Evidence CRISPR drug-modifier screens across >600 models, genomic localization to hypomethylated CpG islands, non-canonical histone DUB assays (preprints); Co-IP/DUB and in vivo models for NEK7, CNN1, MrgC, SLC1A5

    PMID:36864656 PMID:38427128 PMID:40513941 PMID:40580743

    Open questions at the time
    • Chromatin/methylation link from preprints not peer-reviewed
    • Recruitment to hypomethylated CpG islands mechanistically undefined
  12. 2026 Medium

    Implicated USP48 in cancer survival circuits by stabilizing DBF4, YBX1, and TAK1, including transcriptional feedback loops sustaining drug resistance.

    Evidence Functional USP screens, organoid CRISPR dropout, Co-IP, ubiquitination assays, promoter/ChIP feedback loop, xenograft and PDX models

    PMID:39971179 PMID:42142703 PMID:42163235

    Open questions at the time
    • Opposing NF-κB outcomes (TAK1 suppression vs RelA stabilization) not reconciled
    • Single-lab findings each

Open questions

Synthesis pass · forward-looking unresolved questions
  • How USP48 achieves substrate selectivity across such a broad target set, and what determines its context-dependent positive versus negative regulation of NF-κB, remain unresolved.
  • No structural model of substrate engagement across targets
  • PTM code (CK2/GSK3β/SUMO) governing context-specific activity incompletely defined
  • Mechanism of recruitment to damage sites and hypomethylated chromatin unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 7 GO:0016787 hydrolase activity 2
Localization
GO:0005634 nucleus 3 GO:0000228 nuclear chromosome 2 GO:0005815 microtubule organizing center 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-168256 Immune System 3 R-HSA-5357801 Programmed Cell Death 2 R-HSA-73894 DNA Repair 2 R-HSA-1640170 Cell Cycle 1
Partners
AURKBGLI1GSDMEHMGA2NEK7RELASIRT6TRAF2
Complex memberships
COP9 signalosome (CSN)

Evidence

Reading pass · 26 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2018 USP48 is a histone H2A deubiquitinase specific for the C-terminal BRCA1 ubiquitination site. Biochemical analysis showed that an auxiliary ubiquitin (itself not cleaved) modulates USP48 activity. In cells, USP48 antagonizes BRCA1 E3 ligase function; loss of USP48 results in 53BP1 positioned further from the break site and extended resection lengths, and confers survival benefit to camptothecin-treated cells. USP48 activity restrains gene conversion and mutagenic single-strand annealing. Detailed biochemical analysis, in vitro DUB assays, cell-based BRCA1 ubiquitination assays, epistasis with BRCA1 loss-of-function, resection length measurements, colony survival assays Nature communications High 29335415
2018 USP48 is identified as a synthetic viable interactor for FA-gene deficiencies (FANCA, FANCC, FANCG, FANCI, FANCD2). Loss of USP48 in FA-deficient cells reduces sensitivity to ICL agents, enhances BRCA1-dependent DNA damage clearance, and reduces chromosomal instability, placing USP48 in the DNA repair pathway downstream or parallel to the FA pathway. Genome-wide loss-of-function screens in haploid isogenic FA-defective human cells, ICL agent sensitivity assays, BRCA1-dependence epistasis, chromosomal instability measurements Nature communications High 29891926
2014 USP48 associates with the COP9 signalosome (CSN) and nuclear RelA (NF-κB p65). USP48 trims (rather than fully disassembles) K48-linked free and substrate-anchored ubiquitin chains on RelA, a catalytic property shared only with ataxin-3 and OTU1. USP48 chain-trimming activity is regulated by CK2-mediated phosphorylation in response to cytokine stimulation. CSN and USP48 cooperatively stabilize the nuclear pool of RelA to facilitate timely induction and shutoff of NF-κB target genes. siRNA screen identification, Co-IP (USP48–CSN, USP48–RelA), in vitro ubiquitin chain trimming assays, phosphorylation assays with CK2, NF-κB reporter assays Biochimica et biophysica acta High 25486460
2017 USP48 deubiquitinates and stabilizes Gli1 protein by directly cleaving its ubiquitin, activating Gli-dependent transcription. USP48 knockdown inhibits Gli1 target gene expression and glioblastoma cell proliferation and tumorigenesis. The Hedgehog pathway induces USP48 expression via Gli1-mediated transcription, forming a positive feedback loop. Co-IP (USP48–Gli1 interaction), DUB activity assay (ubiquitin cleavage from Gli1), Gli reporter assays, siRNA knockdown with proliferation and tumor growth readouts, Gli1 rescue experiments EMBO reports High 28623188
2017 USP48 deubiquitinates and stabilizes TRAF2 in epithelial cells, specifically targeting the TRAF2 pool linked to the JNK pathway but not the NF-κB or p38 pathways. USP48 is serine-phosphorylated in response to TNF-α by GSK3β, increasing its DUB activity. Knockdown of USP48 reduces TRAF2 stability, attenuates TNF-α/JNK signaling, and increases E-cadherin expression and epithelial barrier integrity. Co-IP (USP48–TRAF2), K48-polyubiquitination assays, pathway-specific rescue experiments, GSK3β phosphorylation assay, USP48 knockdown with E-cadherin and barrier function readouts FASEB journal High 28874458
2021 USP48 physically binds SIRT6 and stabilizes it by removing K48-linked ubiquitin chains specifically at K33 and K128 of SIRT6, preventing its proteasomal degradation and thereby impeding metabolic reprogramming (glycolysis) in hepatocellular carcinoma cells. Co-IP (USP48–SIRT6), K48-linked deubiquitination site-mapping (K33, K128 of SIRT6), glycolysis assays, cell-based ubiquitination assays Cancer research Medium 33903120
2023 USP48 promotes pyroptosis in cancer cells by binding GSDME (gasdermin E) and removing K48-linked ubiquitination at K120 and K189 of GSDME, thereby stabilizing it. CRISPR-Cas9 screen identified USP48 loss as inhibiting pyroptosis; USP48 knockout suppressed T cell and tumor-associated macrophage function in the tumor microenvironment. CRISPR-Cas9 loss-of-function screen, Co-IP (USP48–GSDME), site-specific K48-deubiquitination assays (K120, K189), pyroptosis assays, in vivo mouse tumor models with PD-1 blockade Cancer research High 36607699
2021 USP48 interacts with and stabilizes Aurora B protein by deubiquitinating it, maintaining its steady-state levels during the cell cycle. USP48 knockout causes delayed cell cycle progression, mitotic defects, and cytokinesis failure. Deubiquitinase knockout strategy, Co-IP (USP48–Aurora B), protein half-life assays, cell cycle progression analysis, cytokinesis failure quantification International journal of molecular sciences Medium 34445214
2019 The catalytic USP domain of USP48 mediates its physical interaction with the N-terminal region of the Rel homology domain (RHD) of nuclear RelA. This was mapped using overexpressed truncated proteins. Co-IP with truncated USP48 and RelA domain constructs, nuclear co-localization experiments Molecular biology reports Medium 30628021
2022 In H. pylori infection, USP48 interacts with CSN subunit CSN1 and stabilizes nuclear RelA by deubiquitination, prolonging de novo synthesis of DUB A20. A20 then suppresses caspase-8 activity and apoptotic cell death, defining a synergistic USP48–A20 mechanism that promotes cell survival. Co-IP (USP48–CSN1, USP48–RelA), deubiquitination assays, A20 expression measurement, caspase-8 activity assay, apoptosis readout in H. pylori-infected cells Cellular and molecular life sciences Medium 35913642
2022 USP48 downregulation stabilizes p65 (NF-κB) in the nuclear compartment of retinal pigment epithelium (RPE) cells, increasing NF-κB transcriptional activity — contrary to the stabilizing role described in other cell types. This delineates a negative regulatory role for USP48 on NF-κB in RPE cells. siRNA knockdown of USP48 in RPE cells, subcellular fractionation, NF-κB reporter assay, TNFα stimulation International journal of molecular sciences Low 36077078
2022 USP48 localizes to the basal body in retinal cells and interacts with the IRD-associated proteins ARL3 and UNC119a, stabilizing their protein levels. This suggests a role for USP48 in photoreceptor ciliary protein regulation and intracellular transport. Co-IP (USP48–ARL3, USP48–UNC119a), immunohistochemistry/subcellular localization in retinal cells, protein stability assays International journal of molecular sciences Medium 36293380
2021 USP48 has catalytic deubiquitinase (ubiquitin hydrolase) activity; disease-associated missense variants in USP48 are unable to hydrolyze tetra-ubiquitin in vitro, confirming the catalytic requirement for ubiquitin hydrolysis. USP48 is expressed in spiral ganglion neurons and other inner ear structures; zebrafish knocked down for usp48 show impaired statoacoustic neuron development and vestibular/hearing dysfunction. In vitro tetra-ubiquitin hydrolysis assay with mutant proteins, 3D structural modeling, immunohistology in human inner ear, zebrafish knockdown with acoustic startle response assay Human molecular genetics High 34059922
2018 Recurrent somatic mutations in USP48 (predominantly M415I or M415V) occur in USP8 wild-type corticotroph adenomas. Similar to USP8 mutants, USP48 mutants enhance promoter activity and transcription of the POMC gene (the ACTH precursor), providing a mechanism for ACTH overproduction in these tumors. Sanger/targeted sequencing of tumor DNA, POMC promoter reporter assay in cells transfected with mutant USP48 constructs Nature communications Medium 30093687
2023 USP48 (formerly USP31) is a nuclear deubiquitinase whose nuclear localization is mediated by a conserved 13-amino acid nuclear localization signal. USP48 interacts with NF-κB transcription factor and deubiquitinates p65, promoting its stability and activation, which upregulates NF-κB target genes that inhibit synaptogenesis. USP48 expression induces filopodia elaboration, spine loss, reduced synaptic protein clustering in vitro, and erases ~70% of functional synapses in vivo; depleting NF-κB prevents USP48-dependent spine pruning. NLS mutagenesis (nuclear localization signal), Co-IP (USP48–p65), deubiquitination assay (p65), NF-κB reporter assay, live imaging of spine dynamics, electrophysiological synapse counting in vivo, NF-κB depletion epistasis bioRxivpreprint Medium 37781625
2024 USP48 deubiquitinates HMGA2, stabilizing it and promoting tumor invasion and metastasis. USP48 undergoes SUMOylation at lysine K258, which enhances its binding affinity for HMGA2. A small-molecule inhibitor DUB-IN-2 blocks USP48 activity and induces HMGA2 destabilization. Mass spectrometry identification, Co-IP (USP48–HMGA2), overexpression/knockdown protein stability assays, SUMOylation site mapping (K258), DUB-IN-2 pharmacological inhibition, tumor invasion/metastasis assays Acta pharmaceutica sinica. B Medium 38572092
2023 USP48 interacts with MrgC (Mas-related G protein-coupled receptor C) in spinal cord neurons and reduces its K48-linked ubiquitination, stabilizing MrgC receptor levels. In a murine bone cancer pain model, spinal cord USP48 expression is reduced; AAV-mediated USP48 overexpression increased MrgC levels and alleviated pain behaviors. Co-IP (USP48–MrgC), overexpression/knockdown in N2a cells with receptor number quantification, ubiquitination assay, intrathecal AAV injection with pain behavior readout European journal of pain Medium 36864656
2025 USP48 stabilizes calponin 1 (CNN1) via deubiquitination in cardiomyocytes. The USP48/CNN1 axis inhibits release of CXCL1 and CXCL2 through inactivation of the ERK1/2 pathway, conferring cardioprotection in diabetes-aggravated myocardial ischemia-reperfusion injury. Proteomics identification of CNN1, cardiac-specific KO and OE in mice, Co-IP (USP48–CNN1), ubiquitination assay, RNA-seq, ERK1/2 pathway readout, CXCL1/2 antibody blockade rescue Metabolism: clinical and experimental Medium 40513941
2025 USP48 promotes NLRP3-dependent pyroptosis of alveolar macrophages in sepsis-induced acute lung injury by directly interacting with and deubiquitinating NEK7, stabilizing it and thereby activating the NEK7/NLRP3/caspase-1/GSDMD signaling axis. Co-IP (USP48–NEK7), NEK7 ubiquitination assay, USP48 knockdown in vivo and in vitro, NEK7 overexpression rescue experiment, NLRP3 inflammasome activation readout, murine sepsis model International immunopharmacology Medium 40580743
2025 USP48 is recruited to sites of DNA damage and deubiquitinates H2A variants and proteins important for DNA damage repair. Loss of USP48 increases chromatin accessibility upon HMA treatment, sensitizing AML cells to DNMT1 inhibition-induced cell death. CRISPR loss-of-function screens, chromatin accessibility assays (ATAC-seq implied), USP48 localization at DNA damage sites, H2A deubiquitination assay bioRxivpreprint Medium
2025 USP48 is recruited to newly hypomethylated CpG islands upon DNA demethylation and deubiquitinates non-canonical histones, establishing a molecular link between DNA methylation state and chromatin modification. Loss of USP48 (naturally occurring via biallelic deletions) sensitizes hematologic and solid tumors to DNMT1 inhibition in vitro and in vivo. CRISPR drug modifier screens across >600 cancer models, ChIP or genomic localization to hypomethylated CpG islands, non-canonical histone deubiquitination assay, in vitro and in vivo tumor sensitization experiments bioRxivpreprint Medium
2025 USP48 interacts with and stabilizes TAK1 through deubiquitination; this inhibits TAK1-triggered NF-κB activation and suppresses colorectal cancer tumorigenesis. USP48 expression also positively correlates with M1-type tumor-associated macrophage polarization. Co-IP (USP48–TAK1), deubiquitination assay, qRT-PCR for NF-κB targets, flow cytometry for macrophage polarization, cell proliferation/invasion/apoptosis assays Experimental cell research Medium 39971179
2026 USP48 interacts with and stabilizes DBF4 by modulating its ubiquitination. USP48 knockdown reduces DBF4 protein levels and inhibits ccRCC cell proliferation, migration, invasion, and causes cell cycle arrest and apoptosis. DBF4 overexpression rescues USP48-deficiency phenotypes in ccRCC cells. Luciferase-tagged DBF4 USP screen (40 USPs), Co-IP (USP48–DBF4), ubiquitination assay, KD + rescue experiments, xenograft in vivo assay Cancer cell international Medium 42163235
2026 USP48 associates with YBX1 and removes K48-linked polyubiquitin chains from it, preventing proteasomal degradation. YBX1 stabilization by USP48 drives transcriptional activation of PTK7 and Wnt/β-catenin signaling, forming a positive feedback loop (TCF7L2 directly upregulates USP48 transcription) that sustains stem-like osimertinib resistance in EGFR-mutant NSCLC. CRISPR-Cas9 dropout screening in patient-derived organoids, Co-IP (USP48–YBX1), K48-ubiquitination removal assay, TCF7L2 ChIP/promoter assay, USP48 inhibition with glycyrrhizic acid, orthotopic and PDX mouse models Cancer letters Medium 42142703
2025 USP48 directly interacts with and stabilizes HEG1 by removing K48-linked polyubiquitin chains, preventing its proteasomal degradation and sustaining AKT1 stabilization and AKT signaling in gastric cancer. Co-IP (USP48–HEG1), K48-ubiquitination assay, RNA-seq, pharmacogenomic data analysis, in vivo and in vitro proliferation/clonogenicity assays European journal of medical research Low 41013721
2024 USP48 deubiquitinates and stabilizes SLC1A5, protecting retinal pigment epithelial cells from high-glucose-induced apoptosis, inflammation, ferroptosis, and oxidative stress. Co-IP (USP48–SLC1A5), overexpression/knockdown stability assays, SLC1A5 rescue experiment, ferroptosis and oxidative stress biochemical assays Journal of bioenergetics and biomembranes Low 38427128

Source papers

Stage 0 corpus · 32 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2021 USP48 Is Upregulated by Mettl14 to Attenuate Hepatocellular Carcinoma via Regulating SIRT6 Stabilization. Cancer research 124 33903120
2018 Identification of recurrent USP48 and BRAF mutations in Cushing's disease. Nature communications 115 30093687
2018 USP48 restrains resection by site-specific cleavage of the BRCA1 ubiquitin mark from H2A. Nature communications 87 29335415
2017 Gli1-induced deubiquitinase USP48 aids glioblastoma tumorigenesis by stabilizing Gli1. EMBO reports 72 28623188
2023 USP48 Stabilizes Gasdermin E to Promote Pyroptosis in Cancer. Cancer research 60 36607699
2014 CSN-associated USP48 confers stability to nuclear NF-κB/RelA by trimming K48-linked Ub-chains. Biochimica et biophysica acta 48 25486460
2018 Map of synthetic rescue interactions for the Fanconi anemia DNA repair pathway identifies USP48. Nature communications 37 29891926
2017 The deubiquitinating enzyme USP48 stabilizes TRAF2 and reduces E-cadherin-mediated adherens junctions. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 36 28874458
2021 USP8, USP48, and BRAF mutations differ in their genotype-phenotype correlation in Asian Indian patients with Cushing's disease. Endocrine 22 34664215
2022 USP48 and A20 synergistically promote cell survival in Helicobacter pylori infection. Cellular and molecular life sciences : CMLS 21 35913642
2022 miR-489-3p promotes malignant progression of non-small cell lung cancer through the inactivation of Wnt/β-catenin signaling pathway via regulating USP48. Respiratory research 19 35413838
2024 Blockade of the deubiquitinating enzyme USP48 degrades oncogenic HMGA2 and inhibits colorectal cancer invasion and metastasis. Acta pharmaceutica Sinica. B 16 38572092
2022 Ubiquitin Specific Protease USP48 Destabilizes NF-κB/p65 in Retinal Pigment Epithelium Cells. International journal of molecular sciences 16 36077078
2021 USP48 Governs Cell Cycle Progression by Regulating the Protein Level of Aurora B. International journal of molecular sciences 16 34445214
2020 USP48 Sustains Chemoresistance and Metastasis in Ovarian Cancer. Current cancer drug targets 15 32359336
2019 Catalytic domain of deubiquitinylase USP48 directs interaction with Rel homology domain of nuclear factor kappaB transcription factor RelA. Molecular biology reports 14 30628021
2018 Deubiquitinase USP48 promotes ATRA-induced granulocytic differentiation of acute promyelocytic leukemia cells. International journal of oncology 13 29901102
2024 USP48 deubiquitination stabilizes SLC1A5 to inhibit retinal pigment epithelium cell inflammation, oxidative stress and ferroptosis in the progression of diabetic retinopathy. Journal of bioenergetics and biomembranes 8 38427128
2022 The Deubiquitinating Enzyme USP48 Interacts with the Retinal Degeneration-Associated Proteins UNC119a and ARL3. International journal of molecular sciences 8 36293380
2021 Variants in USP48 encoding ubiquitin hydrolase are associated with autosomal dominant non-syndromic hereditary hearing loss. Human molecular genetics 8 34059922
2024 Baicalin enhances proliferation and reduces inflammatory-oxidative stress effect in H2O2-induced granulosa cells apoptosis via USP48 protein regulation. BMC complementary medicine and therapies 6 38245760
2024 miR-26b-5p Affects the Progression of Acute Myeloid Leukemia by Regulating the USP48-Mediated Wnt/β-Catenin Pathway. Critical reviews in eukaryotic gene expression 3 38505871
2023 USP48/USP31 Is a Nuclear Deubiquitinase that Potently Regulates Synapse Remodeling. bioRxiv : the preprint server for biology 3 37781625
2025 USP48 protects against myocardial ischemia-reperfusion injury by stabilizing and upregulating CNN1 in type 1 diabetes mice. Metabolism: clinical and experimental 2 40513941
2025 USP48 promotes NLRP3-dependent pyroptosis of alveolar macrophages to exacerbate sepsis-induced acute lung injury. International immunopharmacology 2 40580743
2023 USP48 alleviates bone cancer pain and regulates MrgC stabilization in spinal cord neurons of male mice. European journal of pain (London, England) 2 36864656
2025 USP48 inhibits colorectal cancer progression and promotes M1-like macrophage polarization by stabilizing TAK1. Experimental cell research 1 39971179
2025 USP8, USP48, BRAF and TP53 mutations in crooke cell adenoma. Pituitary 1 41047423
2026 Prevalence of germline variants in USP8, USP48, CABLES1 and PAM in patients with pituitary adenomas. European journal of endocrinology 0 42045809
2026 USP48 stabilizes YBX1 to enforce a Wnt-driven stemness circuit and osimertinib resistance in EGFR-mutant NSCLC. Cancer letters 0 42142703
2026 USP48 promotes tumour progression through the deubiquitination and stabilization of DBF4 in clear cell renal carcinoma. Cancer cell international 0 42163235
2025 HEG1 promotes gastric cancer progression by stabilizing AKT1 and is functionally regulated by the deubiquitinase USP48. European journal of medical research 0 41013721

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