Affinage

UBB

Polyubiquitin-B · UniProt P0CG47

Length
229 aa
Mass
25.8 kDa
Annotated
2026-06-10
31 papers in source corpus 17 papers cited in narrative 17 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

UBB encodes a polyubiquitin precursor whose principal cellular role is to supply the free ubiquitin pool required for cell survival, proliferation, and differentiation (PMID:18299572, PMID:25280998). Targeted disruption of Ubb in mice selectively depletes ubiquitin in vulnerable tissues, arresting spermatocytes and oocytes in meiotic prophase I (PMID:18070917) and causing progressive degeneration of hypothalamic arcuate nucleus neurons with adult-onset obesity (PMID:18299572); maintenance of free ubiquitin above a threshold, rather than the conjugated pool, is the cell-autonomous determinant of neuronal vulnerability, as compensatory Ubc upregulation rescues the locus coeruleus but not the hypothalamus, and exogenous free ubiquitin abolishes Ubb-null neuronal apoptosis (PMID:25280998, PMID:22285186). In neural stem cells, Ubb-derived ubiquitin is required during early differentiation to suppress Notch signaling—loss elevates Notch intracellular domain and REST, blocking neurogenesis and promoting premature gliogenesis (PMID:25391618, PMID:28285139, PMID:29422555). Ubb-derived ubiquitin also sustains TNFα-induced NF-κB signaling and p53 turnover in cancer cells (PMID:24022007), and UBB binds the transcription factor SP1 to restrain VEGFA transcription in clear cell renal carcinoma, where DNMT3A epigenetically silences the UBB promoter (PMID:38467852). A distinct branch of UBB biology concerns the frameshift mutant UBB+1: its E2-25K/Hip2-driven incorporation caps polyubiquitin chains and inhibits the 26S proteasome to drive neurotoxicity (PMID:20826778), it is hydrolyzed at its C-terminal extension by UCH-L3 in a manner sensitive to oxidative inactivation (PMID:21762696), and it is cleared by unconventional secretory autophagy in which SQSTM1/p62 recognizes its ubiquitin domain and loads it into autophagosomes that fuse with the plasma membrane via the SEC22B/Syntaxin-4/SNAP23 SNARE machinery (PMID:37075976, PMID:41364760).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2003 Medium

    Established that the frameshift product UBB+1 can act as a pathological seed, driving formation of ubiquitin/cytokeratin protein aggregates resembling Mallory bodies.

    Evidence In vitro immunoprecipitation reconstitution and UBB+1 protein transfection into hepatocytes with immunofluorescence co-localization

    PMID:12710947

    Open questions at the time
    • Does not establish whether aggregation occurs at endogenous UBB+1 levels
    • Mechanism linking UBB+1 to proteasome subunit recruitment not resolved
  2. 2007 High

    Demonstrated that Ubb-derived ubiquitin is consumed during and indispensable for meiotic progression, defining a non-redundant developmental requirement for this polyubiquitin gene.

    Evidence Ubb knockout mouse with histological and cytological analysis of meiosis in both sexes

    PMID:18070917

    Open questions at the time
    • Which ubiquitin-dependent meiotic substrates are limiting is not identified
    • Does not address why meiotic cells are particularly ubiquitin-sensitive
  3. 2008 High

    Showed that adequate ubiquitin supply is essential for neuronal survival, linking Ubb loss to region-selective hypothalamic neurodegeneration and metabolic disease.

    Evidence Ubb knockout mouse with quantitative ubiquitin immunoblot and metabolic/histological phenotyping

    PMID:18299572

    Open questions at the time
    • Molecular basis of arcuate nucleus selectivity not defined
    • Does not separate free vs conjugated ubiquitin contributions
  4. 2010 High

    Provided the structural and biochemical mechanism by which UBB+1 becomes neurotoxic: E2-25K/Hip2 binds UBB+1 to synthesize chain-capping polyubiquitin that inhibits the proteasome.

    Evidence Crystal structures of UBB+1, E2-25K, and their complexes plus polyubiquitylation assays with binding-disrupting mutants

    PMID:20826778

    Open questions at the time
    • In vivo contribution of E2-25K to disease-associated UBB+1 toxicity not established
    • Does not quantify proteasome inhibition thresholds in neurons
  5. 2011 Medium

    Identified UCH-L3 as the deubiquitinase that processes the UBB+1 C-terminal extension and showed oxidative inactivation as a route to UBB+1 accumulation under stress.

    Evidence In vitro deubiquitinating assay with recombinant UCH-L3/YUH1 and oxidative inactivation assay

    PMID:21762696

    Open questions at the time
    • Single in vitro study without cellular confirmation
    • Physiological relevance of oxidative UCH-L3 inhibition in disease not shown
  6. 2012 Medium

    Resolved why neuronal populations differ in vulnerability: free ubiquitin maintenance above a threshold, supported by compensatory Ubc upregulation, determines survival.

    Evidence Ubb knockout mouse with region-resolved immunoblot distinguishing free vs conjugated ubiquitin and histology

    PMID:22285186

    Open questions at the time
    • Mechanism controlling region-specific Ubc compensation unknown
    • Quantitative free-ubiquitin threshold not defined
  7. 2013 Medium

    Placed Ubb-derived ubiquitin as a required component of oncogenic NF-κB signaling and p53 turnover, suggesting therapeutic relevance in cancer.

    Evidence siRNA knockdown with NF-κB reporter, p53 immunoblot, viability assays and xenograft model

    PMID:24022007

    Open questions at the time
    • Does not distinguish direct vs general ubiquitin-pool effects on these pathways
    • Specificity to UBB versus other ubiquitin genes not fully isolated
  8. 2014 Medium

    Mapped how ubiquitin deficiency disrupts neural stem cell fate by elevating NICD/Notch signaling and impairing free-ubiquitin-dependent neuronal survival.

    Evidence Ubb knockout NSC cultures with NICD immunoblot, Notch/proneuronal gene analysis, and lentiviral free-ubiquitin rescue of apoptosis

    PMID:25280998 PMID:25391618

    Open questions at the time
    • Direct ubiquitin-dependent NICD degradation step not biochemically defined
    • Does not establish in vivo developmental consequences
  9. 2014 Medium

    Extended UBB+1 pathology to organelle dynamics, linking its proteasome inhibition to destabilization of mitochondrial fission proteins and altered cell death sensitivity.

    Evidence Ectopic UBB+1 expression in astrocytes with immunoblot, FRAP, proteasome-inhibitor rescue and cell-death assays

    PMID:24941066

    Open questions at the time
    • Direct mechanism of fission-protein loss not resolved
    • Overexpression system may not reflect endogenous UBB+1 levels
  10. 2017 Medium

    Defined the structural consequences of the frameshift extension and identified REST as a downstream mediator of ubiquitin-deficiency-induced neurogenesis failure.

    Evidence NMR relaxation/binding studies of the UBB+1 extension; siRNA REST knockdown rescue in Ubb-null NSCs

    PMID:28285139 PMID:29175520

    Open questions at the time
    • How elevated REST mechanistically connects to ubiquitin shortage not defined
    • Functional relevance of altered UBA2/membrane binding by the extension not established in cells
  11. 2018 Medium

    Demonstrated a stage-specific requirement for Ubb in suppressing Notch during early NSC differentiation, refining when ubiquitin is critical for neurogenesis.

    Evidence Temporal lentiviral Ubb knockdown at defined days in vitro with Notch and differentiation readouts

    PMID:29422555

    Open questions at the time
    • Molecular timer governing the stage-specific dependence unknown
    • Direct ubiquitin substrate within the Notch axis not identified
  12. 2021 Medium

    Showed UBB+1 can act upstream of autophagy activation, reducing amyloid-beta toxicity in an ATG1-dependent manner, indicating context-dependent protective signaling.

    Evidence Yeast expression with transcriptomics, autophagy flux assay, Aβ toxicity/lifespan, and atg1Δ epistasis

    PMID:34751669

    Open questions at the time
    • Yeast model relevance to mammalian neurons uncertain
    • Mechanism by which UBB+1 triggers autophagy not defined
  13. 2023 Medium

    Established that UBB+1 is exported by unconventional secretory autophagy, identifying ATG5-dependent autophagosome routing and SEC22B association as the clearance pathway.

    Evidence Co-IP, 3D-SIM, LC-MS/MS ubiquitination mapping, ATG5 knockout and LC3B conversion assays

    PMID:37075976

    Open questions at the time
    • Whether secretion is protective or pathological in vivo not shown
    • K11/K29/K48 ubiquitination role beyond secretion not resolved
  14. 2024 Medium

    Identified a transcription-factor-binding role for UBB, showing it interacts with SP1 to restrain VEGFA, with DNMT3A epigenetically silencing UBB in renal carcinoma.

    Evidence Co-IP for UBB–SP1, VEGFA reporter/expression assays, ChIP for DNMT3A at the UBB promoter, perturbation in ccRCC cells

    PMID:38467852

    Open questions at the time
    • Whether free ubiquitin or the precursor mediates SP1 binding unclear
    • Single cancer-context study without broader validation
  15. 2025 High

    Completed the secretory route for UBB+1 by defining SQSTM1/p62 as its ubiquitin receptor and the SEC22B/Syntaxin-4/SNAP23 SNARE complex as the fusion machinery for plasma-membrane exocytosis.

    Evidence Reciprocal p62 gain/loss-of-function, SNARE disruptions, Co-IP, vesicle secretion assays and imaging

    PMID:41364760

    Open questions at the time
    • Physiological consequence of secreted UBB+1 on neighboring cells not determined
    • Trigger that diverts UBB+1 to secretion versus degradation unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • How free ubiquitin scarcity is mechanistically translated into selective NICD/REST dysregulation and region-specific neurodegeneration, and whether UBB+1 secretion is protective or disease-propagating in vivo, remain unresolved.
  • No identified rate-limiting ubiquitin substrate in the Notch/REST axis
  • In vivo fate and effect of secreted UBB+1 not established
  • Link between transcriptional UBB regulation and the free-ubiquitin pool not quantified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0031386 protein tag activity 3 GO:0098772 molecular function regulator activity 2 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005829 cytosol 2 GO:0031410 cytoplasmic vesicle 2
Pathway
R-HSA-392499 Metabolism of proteins 3 R-HSA-9612973 Autophagy 3 R-HSA-1266738 Developmental Biology 2 R-HSA-5653656 Vesicle-mediated transport 1
Partners
SEC22BSNAP23SP1SQSTM1STX4UBE2KUCHL3

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2010 E2-25K/Hip2 (ubiquitin-conjugating enzyme) binds UBB+1 (frameshift mutant ubiquitin) via its MGF motif and residues in α9; this interaction drives synthesis of UBB+1-anchored polyubiquitin chains that inhibit the 26S proteasome and cause neuronal cell death. Mutagenesis of E2-25K residues disrupting UBB+1 binding markedly diminished synthesis of neurotoxic polyubiquitin. Crystal structure determination of UBB+1, E2-25K, E2-25K/ubiquitin, and E2-25K/UBB+1 complexes; polyubiquitylation assays with E2-25K mutants; active-site mutagenesis The Journal of biological chemistry High 20826778
2011 The deubiquitinating enzyme UCH-L3 (human ortholog of yeast YUH1) hydrolyzes the C-terminal extension of UBB+1, generating a dysfunctional ubiquitin molecule (UBG76Y). In vitro oxidation of recombinant UCH-L3 impairs its deubiquitinating activity, providing a mechanism for UBB+1 accumulation under oxidative stress. In vitro deubiquitinating enzyme assay with recombinant UCH-L3/YUH1 and UBB+1 substrate; oxidative inactivation assay FEBS letters Medium 21762696
2007 Targeted disruption of the polyubiquitin gene Ubb in mice causes male and female infertility due to arrest of spermatocytes and oocytes during meiotic prophase I, demonstrating that Ubb-derived ubiquitin is consumed during and required for meiotic progression. Targeted gene disruption (knockout mouse); histological and cytological analysis of meiotic progression Molecular and cellular biology High 18070917
2008 Loss of Ubb selectively reduces total ubiquitin levels in the hypothalamus, leading to progressive neurodegeneration of arcuate nucleus neurons and adult-onset obesity with impaired hypothalamic energy balance control, demonstrating that adequate cellular ubiquitin supply is essential for neuronal survival. Ubb knockout mouse; quantitative ubiquitin measurement by immunoblot; histological and metabolic phenotyping Proceedings of the National Academy of Sciences of the United States of America High 18299572
2003 UBB+1 promotes cytokeratin aggresome (Mallory body-like aggregate) formation in vitro: immunoprecipitated cytokeratin-8 incubated with ubiquitin plus UBB+1 (or proteasome inhibitor) formed CK-8/UBB+1/proteasome subunit-positive aggregates, and hepatocytes transfected with UBB+1 protein developed MB-like aggregates co-staining for CK-8 and ubiquitin. In vitro immunoprecipitation reconstitution assay; cell transfection with Chariot-delivered UBB+1 protein; immunofluorescence co-localization Experimental and molecular pathology Medium 12710947
2014 Disruption of Ubb in neural stem cells leads to upregulation of Notch intracellular domain (NICD) steady-state levels and consequent elevation of Notch target gene expression, which suppresses proneuronal gene expression, inhibits neurogenesis, and promotes premature gliogenesis. Ubb knockout mouse; cultured embryonic neural stem cells; immunoblot for NICD; gene expression analysis of Notch target and proneuronal genes Scientific reports Medium 25391618
2014 Restoration of free ubiquitin levels (but not ubiquitin conjugates) in Ubb−/− neurons via lentivirus-mediated exogenous ubiquitin delivery abolished increased apoptosis and improved neuronal and glial phenotypes, establishing that free ubiquitin pool maintenance (above a threshold) is the cell-autonomous requirement for neuronal survival. Lentivirus-mediated ubiquitin rescue in Ubb−/− primary neurons; immunoblot distinguishing free vs. conjugated Ub; apoptosis assay Biochemical and biophysical research communications Medium 25280998
2013 Knockdown of the polyubiquitin gene Ubb (Ubb-KD) with siRNA reduces cellular ubiquitin levels, attenuates TNFα-induced NF-κB activation, stabilizes tumor suppressor p53, and sensitizes cancer cells to stress, placing Ubb-derived ubiquitin as a required component for oncogenic NF-κB signaling and p53 turnover. siRNA knockdown; NF-κB reporter assay; p53 immunoblot; cancer cell viability assays; xenograft mouse model Scientific reports Medium 24022007
2014 UBB+1 expression in astrocytes destabilizes mitochondrial fission-specific proteins Drp1, Fis1, and OPA3 (but not fusion proteins Mfn1, Mfn2, OPA1), inducing mitochondrial elongation/fusion and conferring resistance to H2O2-induced cell death. Proteasome inhibitors prevented the reduction in fission proteins, linking UBB+1-mediated proteasome inhibition to mitochondrial dynamics. Ectopic expression of UBB+1 in astrocytic cells; immunocytochemistry; FRAP; immunoblot with various protease/proteasome inhibitors; cell death assay PloS one Medium 24941066
2017 The C-terminal 19-residue extension of UBB+1 is highly flexible (by NMR relaxation) but contains a short less-solvent-exposed stretch; it does not establish long-lived contacts with the globular ubiquitin domain yet alters binding to the UBA2 domain and membrane mimics, demonstrating that the frameshift extension changes biomolecular recognition without grossly perturbing ubiquitin structure. NMR relaxation and solvent accessibility measurements; thermal stability assay; binding assays with UBA2 domain and membrane mimics International journal of biological macromolecules Medium 29175520
2017 Elevated REST levels in Ubb−/− neural stem cells suppress neuronal differentiation; knockdown of REST in Ubb−/− cells restored expression of neuronal markers (βIII-tubulin, α-internexin) and reduced apoptosis, placing REST as a downstream mediator of Ub-deficiency-induced neurogenesis failure. Ubb knockout cells; siRNA knockdown of REST; immunofluorescence for neuronal markers; apoptosis assay Biochemical and biophysical research communications Medium 28285139
2018 Lentivirus-mediated Ubb knockdown at DIV1 (early differentiation stage) impairs neural stem cell differentiation by activating Notch signaling when it is normally suppressed, whereas Ubb knockdown at DIV7 (after differentiation) has no effect on maturation, demonstrating a stage-specific requirement for Ub in suppressing Notch during NSC differentiation. Temporal lentiviral Ubb knockdown at defined days in vitro; Notch signaling readouts; neuronal differentiation markers Scientific reports Medium 29422555
2023 UBB+1 is secreted via an unconventional autophagosome-mediated pathway: expression of UBB+1 stimulates LC3B-I to LC3B-II conversion (autophagy induction), and ATG5 deficiency inhibits UBB+1 secretion. UBB+1 associates with secretory autophagosome marker SEC22B (by co-IP and SIM microscopy). UBB+1 is ubiquitinated on K11, K29, and K48 in cells (by LC-MS/MS and mutagenesis), but this ubiquitination does not contribute to its secretion. Co-immunoprecipitation; 3D structured illumination microscopy; LC-MS/MS; site-directed mutagenesis; ATG5 knockout; LC3B conversion assay Biochimica et biophysica acta. Gene regulatory mechanisms Medium 37075976
2025 SQSTM1/p62 functions as a ubiquitin receptor for UBB+1, recognizing its ubiquitin domain and loading it into autophagosomes for secretory autophagy. p62 oligomerization prevents UBB+1 aggregation. Both gain- and loss-of-function of p62 suppress UBB+1 secretion; p62 KO causes UBB+1 accumulation in insoluble aggregates. The R-SNARE SEC22B and Q-SNAREs Syntaxin-4 and SNAP23 mediate fusion of UBB+1-containing autophagosomes with the plasma membrane for exocytosis; SEC22B disruption reduces secretion without affecting intracellular turnover. Co-immunoprecipitation; p62 knockout and overexpression; SEC22B/STX4/SNAP23 disruption; vesicle secretion assays; immunofluorescence Proceedings of the National Academy of Sciences of the United States of America High 41364760
2012 In the locus coeruleus of Ubb−/− mice, Ubc is significantly upregulated and maintains free ubiquitin levels (though total Ub decreases), preventing neuronal dysfunction and degeneration, whereas in the hypothalamus both free and total Ub are reduced, correlating with neurodegeneration—establishing that free Ub maintenance above a threshold determines neuronal vulnerability. Ubb knockout mouse; quantitative immunoblot distinguishing free vs. conjugated Ub in dissected brain regions; histological neurodegeneration assessment Biochemical and biophysical research communications Medium 22285186
2021 Low-level UBB+1 expression in yeast activates the autophagy pathway (increased ATG8p transport to vacuole, enhanced vacuolar activity) and reduces intracellular Aβ42/Aβ40 levels, ameliorating amyloid toxicity in an ATG1-dependent manner, placing UBB+1 upstream of autophagy activation. Yeast expression system; genome-wide transcriptional analysis; autophagy flux assay (ATG8p-GFP); Aβ toxicity and lifespan assay; atg1Δ epistasis Aging Medium 34751669
2024 UBB directly interacts with SP1 (specificity protein 1) and thereby controls VEGFA transcription; UBB downregulation in ccRCC releases SP1-dependent VEGFA upregulation. DNMT3A is recruited to the UBB promoter to epigenetically suppress UBB transcription. Co-immunoprecipitation (UBB–SP1 interaction); VEGFA reporter/expression assays; chromatin immunoprecipitation for DNMT3A at UBB promoter; siRNA/overexpression in ccRCC cells Oncogene Medium 38467852

Source papers

Stage 0 corpus · 31 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 The mouse polyubiquitin gene Ubb is essential for meiotic progression. Molecular and cellular biology 89 18070917
2008 Hypothalamic neurodegeneration and adult-onset obesity in mice lacking the Ubb polyubiquitin gene. Proceedings of the National Academy of Sciences of the United States of America 82 18299572
2010 Structural basis of E2-25K/UBB+1 interaction leading to proteasome inhibition and neurotoxicity. The Journal of biological chemistry 48 20826778
2020 UBB pseudogene 4 encodes functional ubiquitin variants. Nature communications 47 32161257
2013 Downregulation of ubiquitin level via knockdown of polyubiquitin gene Ubb as potential cancer therapeutic intervention. Scientific reports 44 24022007
2007 Expression of mutant ubiquitin (UBB+1) and p62 in myotilinopathies and desminopathies. Neuropathology and applied neurobiology 41 17931355
2011 Mutant ubiquitin (UBB+1) associated with neurodegenerative disorders is hydrolyzed by ubiquitin C-terminal hydrolase L3 (UCH-L3). FEBS letters 40 21762696
2014 Disruption of polyubiquitin gene Ubb causes dysregulation of neural stem cell differentiation with premature gliogenesis. Scientific reports 29 25391618
2003 The mechanism of cytokeratin aggresome formation: the role of mutant ubiquitin (UBB+1). Experimental and molecular pathology 29 12710947
2012 Long-term proteasomal inhibition in transgenic mice by UBB(+1) expression results in dysfunction of central respiration control reminiscent of brainstem neuropathology in Alzheimer patients. Acta neuropathologica 25 22730000
2024 Downregulation of UBB potentiates SP1/VEGFA-dependent angiogenesis in clear cell renal cell carcinoma. Oncogene 22 38467852
1990 Localization of the human UbB polyubiquitin gene to chromosome band 17p11.1-17p12. American journal of human genetics 20 2154095
2014 Restoration of cellular ubiquitin reverses impairments in neuronal development caused by disruption of the polyubiquitin gene Ubb. Biochemical and biophysical research communications 17 25280998
2012 Review: unchained maladie - a reassessment of the role of Ubb(+1) -capped polyubiquitin chains in Alzheimer's disease. Neuropathology and applied neurobiology 17 22082077
2009 Loss of polyubiquitin gene Ubb leads to metabolic and sleep abnormalities in mice. Neuropathology and applied neurobiology 17 20002312
2021 Polyubiquitin gene Ubb is required for upregulation of Piwi protein level during mouse testis development. Cell death discovery 16 34312369
2019 The Molecular Misreading of APP and UBB Induces a Humoral Immune Response in Alzheimer's Disease Patients with Diagnostic Ability. Molecular neurobiology 16 31654319
2018 Temporal downregulation of the polyubiquitin gene Ubb affects neuronal differentiation, but not maturation, in cells cultured in vitro. Scientific reports 16 29422555
2012 Locus coeruleus neurons are resistant to dysfunction and degeneration by maintaining free ubiquitin levels although total ubiquitin levels decrease upon disruption of polyubiquitin gene Ubb. Biochemical and biophysical research communications 14 22285186
2017 Alzheimer's disease-associated ubiquitin mutant Ubb+1: Properties of the carboxy-terminal domain and its influence on biomolecular interactions. International journal of biological macromolecules 11 29175520
2019 Disruption of the polyubiquitin gene Ubb causes retinal degeneration in mice. Biochemical and biophysical research communications 10 30935687
2014 Mutant ubiquitin UBB+1 induces mitochondrial fusion by destabilizing mitochondrial fission-specific proteins and confers resistance to oxidative stress-induced cell death in astrocytic cells. PloS one 10 24941066
1988 Human ubiquitin genes: one member of the UbB gene subfamily is a tetrameric non-processed pseudogene. FEBS letters 10 2834222
2020 Disruption of the polyubiquitin gene Ubb reduces the self-renewal capacity of neural stem cells. Biochemical and biophysical research communications 8 32321641
2023 Alzheimer's disease-associated mutant ubiquitin (UBB+1) is secreted through an autophagosome-like vesicle-mediated unconventional pathway. Biochimica et biophysica acta. Gene regulatory mechanisms 6 37075976
2021 The Dose-Dependent Pleiotropic Effects of the UBB+1 Ubiquitin Mutant. Frontiers in molecular biosciences 5 33842548
2021 UBB+1 reduces amyloid-β cytotoxicity by activation of autophagy in yeast. Aging 5 34751669
2025 Molecular mechanisms underlying p62-dependent secretion of the Alzheimer-associated ubiquitin variant UBB+1. Proceedings of the National Academy of Sciences of the United States of America 2 41364760
2017 Regulation of REST levels overcomes dysregulation of neural stem cell differentiation caused by disruption of polyubiquitin gene Ubb. Biochemical and biophysical research communications 1 28285139
2026 UBB as an early-stage potential biomarker for breast cancer via modulation of the ubiquitination pathway. Scientific reports 0 42120939
2025 A Potential Link Between Early Onset Reactive Astrogliosis and Adult-Onset Dysfunction of Leptin Signaling in Polyubiquitin Gene Ubb Knockout Mice. Discovery medicine 0 40287809

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