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Showing UPF3B — UPF3X is a alias.

UPF3B

Regulator of nonsense transcripts 3B · UniProt Q9BZI7

Length
483 aa
Mass
57.8 kDa
Annotated
2026-06-10
33 papers in source corpus 20 papers cited in narrative 20 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

UPF3B is a core nonsense-mediated mRNA decay (NMD) factor that couples the exon junction complex (EJC) to the UPF surveillance machinery and contributes directly to translation termination quality control (PMID:12718880, PMID:28899899). Through its conserved C-terminal domain it binds the EJC, docking across a composite surface formed by eIF4AIII, MAGO, and Y14 as resolved by crystallography, with NMD-impairing mutations mapping to the core interface (PMID:12718880, PMID:20479275). Its middle region (RRM-L plus NOPS-L) engages UPF2 via a hydrophobic cleft on the MIF4GIII domain and is the critical functional unit for RNA/ribosome binding and NMD activity; the EJC-binding domain itself is dispensable when the middle domain is intact, and combined disruption of both modules synergistically abolishes decay (PMID:35640974, PMID:35451102, PMID:35451084). Beyond its adaptor role, UPF3B directly interacts with eukaryotic release factors, UPF1, and the ribosome, delaying premature translation termination and dissociating post-termination ribosomal complexes in a reconstituted system (PMID:28899899). UPF3B activity is controlled by its paralog UPF3A: UPF3A binds UPF2 with higher affinity, competes with UPF3B for this interaction, is unstable when free, and functions as a redundant NMD activator (and context-dependent repressor) such that loss of UPF3B stabilizes UPF3A and is partially compensated (PMID:27040500, PMID:35640974, PMID:22182939). UPF3B also binds and inhibits the ER stress sensor IRE1α, suppressing its kinase activity, autophosphorylation, and clustering (PMID:39138189). Loss of UPF3B impairs neural stem cell differentiation and dendritic spine maturation and produces learning and sensorimotor-gating deficits in mice, consistent with its causal role in X-linked intellectual disability, where missense mutations such as Y160D reduce NMD activity and weaken UPF2 binding ~40-fold (PMID:35640974, PMID:26012578, PMID:28948974).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2003 High

    Established that UPF3B physically links the EJC to NMD, defining which of its protein contacts are essential for decay.

    Evidence Co-IP and lambdaN/boxB tethered-function NMD assays with RNAi rescue in human cells

    PMID:12718880

    Open questions at the time
    • Did not resolve the structural basis of the Y14 interaction
    • Roles of the middle domain and UPF2 contact in unmodified contexts unaddressed
  2. 2006 High

    Separated UPF3B's NMD-promoting activity from a distinct translation-stimulatory activity, showing the two map to different protein regions.

    Evidence Tethered-function assays with domain-swap and truncation mutants comparing UPF3a and UPF3b

    PMID:16601204

    Open questions at the time
    • Molecular basis of translation stimulation not identified
    • Did not test endogenous targets
  3. 2010 High

    Provided the atomic-resolution picture of how UPF3B's C-terminal domain docks onto the EJC, explaining NMD-impairing mutations.

    Evidence X-ray structure (3.4 Å) of UPF3b C-terminal domain with eIF4AIII/MAGO/Y14/Barentsz/RNA plus interface mutagenesis

    PMID:20479275

    Open questions at the time
    • Structure limited to C-terminal domain; middle/UPF2 interface not captured
    • Did not address full-length conformational dynamics
  4. 2016 High

    Reframed UPF3A versus UPF3B as functionally divergent paralogs, with UPF3A acting largely as an NMD inhibitor due to a weakened EJC-interaction domain.

    Evidence Conditional UPF3A knockout mice, in vitro NMD reporters, and transcriptome profiling

    PMID:27040500

    Open questions at the time
    • Tension with later evidence that UPF3A activates NMD in UPF3B-null cells
    • Context-dependence of repressor versus activator role not fully resolved
  5. 2017 High

    Demonstrated a direct biochemical role for UPF3B at the ribosome, distinct from its EJC-adaptor function.

    Evidence Fully reconstituted in vitro translation/termination system with release-factor and ribosome binding assays

    PMID:28899899

    Open questions at the time
    • In-cell contribution of termination delay to NMD target selection not quantified
    • Structural basis of eRF/ribosome contacts undetermined
  6. 2022 High

    Defined the UPF3B/UPF3A–UPF2 interface structurally and quantitatively, explaining how the disease mutation Y160D weakens UPF2 binding and how UPF3A out-competes UPF3B.

    Evidence Crystal structures of UPF2 MIF4GIII with UPF3B or UPF3A, ITC affinity measurements, interface mutagenesis

    PMID:35640974

    Open questions at the time
    • Did not directly link affinity changes to in-cell NMD output across substrates
    • Functional role of RNA-induced oligomerization not fully resolved
  7. 2022 High

    Established that the middle domain, not the EJC-binding domain, is the essential functional unit of UPF3 paralogs and that UPF3A and UPF3B are functionally redundant for NMD.

    Evidence CRISPR single and double knockouts in HCT116/human cells with domain-deletion and point-mutant complementation, NMD reporters and RNA-seq (two convergent EMBO J studies)

    PMID:35451084 PMID:35451102

    Open questions at the time
    • Residual EJC-independent NMD mechanism in double knockouts not fully defined
    • Precise biochemical activity of the middle domain in decay unclear
  8. 2004 Medium

    Localized UPF3B-mediated decay to the cytoplasm and showed nuclear mRNA export is a prerequisite despite the protein's predominantly nuclear steady-state localization.

    Evidence Tethered UPF3B with Rev/RRE-regulated export plus fluorescence localization

    PMID:17194930

    Open questions at the time
    • Single-lab, single-study
    • Did not define the trigger for cytoplasmic decay onset
  9. 2013 Medium

    Placed UPF3B downstream of a defined transcriptional activator, SATB2, linking NMD-factor dosage to a developmental regulator.

    Evidence ChIP, luciferase reporter, siRNA knockdown in HEK293, and Satb2-knockout mouse tissue

    PMID:23925499

    Open questions at the time
    • Single lab
    • Physiological impact of SATB2-driven UPF3B levels on NMD output untested
  10. 2011 Medium

    Showed that UPF3A protein stability is governed by competition with UPF3B for UPF2, providing a buffering mechanism for UPF3B loss.

    Evidence Western blot and qRT-PCR in UPF3B-null patient lymphoblastoid lines across multiple families

    PMID:22182939

    Open questions at the time
    • No direct in vitro binding-competition assay in this study
    • Correlation with phenotype severity not mechanistically dissected
  11. 2013 Medium

    Connected UPF3B-dependent NMD to neural progenitor fate, showing its loss expands progenitors at the expense of differentiation.

    Evidence siRNA knockdown in neural progenitors and hippocampal neurons with proliferation/differentiation and localization assays

    PMID:23821644

    Open questions at the time
    • Knockdown rather than complete loss
    • Direct NMD targets driving the phenotype not identified here
  12. 2015 Medium

    Linked disease-associated UPF3B missense mutations to reduced NMD activity and impaired neuronal differentiation, and showed NMD is downregulated during neural differentiation.

    Evidence Tethered-function NMD assays with mutant constructs, neurite complexity assays, and pharmacological NMD inhibition in neural stem cells

    PMID:26012578

    Open questions at the time
    • Single lab
    • Causal NMD targets for neurite phenotype not defined
  13. 2017 High

    Provided in vivo evidence that UPF3B loss causes dendritic spine immaturity, impaired neural stem cell differentiation, and behavioral deficits modeling the human disorder.

    Evidence Upf3b-null mice with behavioral testing, in vivo spine morphology, NSC differentiation, and frontal cortex RNA-seq

    PMID:28948974

    Open questions at the time
    • Which dysregulated NMD targets are causal for each behavioral phenotype unresolved
    • Cell-type-specific contributions not dissected
  14. 2024 Medium

    Identified a non-NMD function for UPF3B as a direct inhibitor of the ER stress sensor IRE1α, and a phospho-switch (Thr169) controlling UPF2 binding.

    Evidence Co-IP, kinase and autophosphorylation assays, clustering assays, and Y160D/T169 mutagenesis

    PMID:39138189

    Open questions at the time
    • No structural validation of the UPF3B–IRE1α interface
    • Single lab; physiological relevance of the T169 phospho-switch untested in vivo
  15. 2024 Low

    Reported UPF3B (and a truncated UPF3B-S variant) acting on specific cancer-relevant transcripts to modulate Hippo and PI3K/AKT/mTOR signaling.

    Evidence RIP, mRNA stability assays, reporter assays, and HCC models for CDH1/PPP2R2C regulation

    PMID:38402949 PMID:38889220

    Open questions at the time
    • Mechanisms partly attributed to a truncated variant rather than canonical UPF3B; limited orthogonal validation
    • Generality beyond cancer context unknown
  16. 2025 Low

    Reported UPF3B partnering with RBM8A to regulate BBC3/PUMA mRNA stability in gastric cancer.

    Evidence Co-IP, RIP-seq, RNA pulldown, and Actinomycin D mRNA stability assay

    PMID:40613240

    Open questions at the time
    • Single Co-IP without domain-level dissection of UPF3B's role
    • Functional consequence attributed to the complex, not UPF3B specifically

Open questions

Synthesis pass · forward-looking unresolved questions
  • How UPF3B's reconstituted termination/ribosome-dissociation activity, its EJC-independent middle-domain function, and its non-NMD interactions (IRE1α, tissue-specific localization) are integrated into substrate-specific decay in vivo remains unresolved.
  • No integrated model linking termination delay to in-cell target selection
  • Structural basis of non-EJC interactions undefined
  • Tissue-specific roles (e.g., cardiac Z-disc localization) functionally untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 2 GO:0060090 molecular adaptor activity 2 GO:0045182 translation regulator activity 1 GO:0098772 molecular function regulator activity 1
Localization
GO:0005634 nucleus 1 GO:0005829 cytosol 1
Pathway
R-HSA-8953854 Metabolism of RNA 3 R-HSA-8953897 Cellular responses to stimuli 1
Partners
EIF4A3IRE1ΑMAGOHRBM8AUPF1UPF2UPF3AY14
Complex memberships
exon junction complex (EJC)

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 hUpf3b contains a conserved C-terminal domain that mediates direct interaction with the EJC protein Y14; tethered function analysis showed the Y14/hUpf3b interaction is essential for NMD, while the hUpf3b–hUpf2 interaction is not strictly required for NMD activity when hUpf3b is tethered, though hUpf2 is still necessary for NMD induced by tethered Y14. Co-immunoprecipitation, tethered function (lambdaN/boxB) assay, RNAi knockdown and siRNA-rescue experiments Molecular cell High 12718880
2006 Induction of NMD by hUpf3b requires interaction with EJC components Y14, Magoh, BTZ, and eIF4AIII via the C-terminal domain; stimulation of translation by hUpf3b is independent of this EJC interaction and is determined by other protein regions, indicating distinct downstream pathways for NMD versus translation stimulation. LambdaN/boxB tethered function assay, domain-swap and truncation analysis of hUpf3a vs hUpf3b RNA (New York, N.Y.) High 16601204
2010 Crystal structure (3.4 Å) of a minimal UPF3b–EJC assembly (UPF3b C-terminal domain + MAGO + Y14 + eIF4AIII + Barentsz + RNA + AMP-PNP) showed that UPF3b binds with its C-terminal domain stretched over a composite surface formed by eIF4AIII, MAGO, and Y14; NMD-impairing mutations map to the core interacting surfaces, and differences between UPF3b and UPF3a map to peripheral interacting residues. X-ray crystallography at 3.4 Å resolution with functional validation by mutagenesis of interface residues Proceedings of the National Academy of Sciences of the United States of America High 20479275
2016 UPF3A acts primarily as a potent NMD inhibitor that stabilizes hundreds of transcripts, while UPF3B is the critical NMD activator; UPF3A acquired repressor activity through impairment of a critical EJC-interaction domain present in UPF3B; mice conditionally lacking UPF3A exhibit hyper-NMD with defects in embryogenesis and gametogenesis. Loss-of-function mouse genetics (conditional knockout), in vitro NMD reporter assays, transcriptome profiling Cell High 27040500
2017 Using a fully reconstituted in vitro translation system, UPF3B was found to (i) directly interact with eukaryotic release factors (eRFs), (ii) delay translation termination under conditions mimicking premature termination, and (iii) dissociate post-termination ribosomal complexes lacking nascent peptide; UPF1 and ribosomes were identified as new interaction partners of UPF3B. Fully reconstituted in vitro translation/termination assay, direct binding assays with release factors and ribosomes The EMBO journal High 28899899
2022 Crystal structures of UPF2's MIF4GIII domain in complex with either UPF3B or UPF3A revealed intimate binding interfaces; UPF3B's disease-causing mutation Y160D displaces Y160 from a hydrophobic cleft in UPF2, reducing binding affinity ~40-fold; UPF3A (upregulated in UPF3B-Y160D patients) binds UPF2 with ~10-fold higher affinity than UPF3B via NOPS-L residues; the middle domain (RRM-L and NOPS-L) is essential for RNA/ribosome-binding, RNA-induced oligomerization, and UPF2 interaction. X-ray crystallography of UPF3B–UPF2 and UPF3A–UPF2 complexes, isothermal titration calorimetry (binding affinity measurements), mutagenesis of interface residues Nucleic acids research High 35640974
2022 NMD remains partially active in human HCT116 cells lacking both UPF3 paralogs; the EJC-binding domain of UPF3 paralogs is dispensable for NMD activation; instead, the conserved 'mid' domain of UPF3 paralogs is consequential for NMD activity; UPF3A strongly activates NMD in cells lacking UPF3B, demonstrating functional redundancy. CRISPR/Cas9 knockout of UPF3A, UPF3B, or both; complementation with domain-deletion and EJC-binding-deficient mutants; NMD reporter assays and RNA-seq The EMBO journal High 35451084 35451102
2022 Co-depletion of UPF3A and UPF3B markedly inhibits global NMD with transcriptome-wide upregulation of NMD substrates; EJC-binding-deficient or UPF2-binding-deficient UPF3B largely retains NMD activity when tested alone, but combinations of middle-domain deletions with these mutations show additive/synergistic NMD loss, indicating the middle domain is a critical functional unit. CRISPR/Cas9 knockout; NMD reporter assays; domain-deletion and point-mutant rescue experiments; transcriptome-wide RNA-seq The EMBO journal High 35451084
2004 UPF3B-mediated mRNA degradation occurs exclusively in the cytoplasm; nuclear mRNA export is required for UPF3B-mediated NMD even though the UPF3B fusion protein used is a nucleocytoplasmic shuttling protein predominantly localized to the nucleus. Tethered UPF3B combined with retroviral Rev/RRE-based nuclear export regulation; subcellular localization by fluorescence microscopy RNA biology Medium 17194930
2013 SATB2 directly binds the UPF3B promoter (shown by ChIP) and activates UPF3B transcription (shown by luciferase reporter assay); siRNA knockdown of SATB2 in HEK293 cells and Satb2-knockout mouse embryonic tissue both showed significantly decreased UPF3B expression, placing SATB2 as a transcriptional activator upstream of UPF3B. Chromatin immunoprecipitation (ChIP), luciferase reporter assay, siRNA knockdown in HEK293 cells, Satb2-knockout mouse embryonic tissue analysis Human genetics Medium 23925499
2011 In UPF3B-null patient lymphoblastoid cells, UPF3A protein (but not mRNA) is stabilized in proportion inversely correlated with phenotype severity, demonstrating that UPF3B normally competes with UPF3A for UPF2 binding and that free UPF3A is unstable; UPF3A partially compensates for loss of UPF3B function. Western blot and qRT-PCR from patient-derived lymphoblastoid cell lines with UPF3B loss-of-function mutations; correlation analysis across multiple patients Molecular psychiatry Medium 22182939
2009 UPF3B protein is expressed in neurons and localizes to dendritic spines in mouse primary hippocampal neurons as determined by immunofluorescence. Immunofluorescence/immunolocalization in mouse primary hippocampal neurons Molecular psychiatry Low 19238151
2013 Loss of Upf3b-NMD in neural progenitor cells results in expansion of cell numbers at the expense of differentiation; in primary hippocampal neurons, loss of Upf3b-NMD causes subtle neurite growth defects; Upf3b subcellular localization is regulated during development. siRNA knockdown of Upf3b in neural progenitor cells and primary hippocampal neurons; cell proliferation and differentiation assays; immunocytochemistry for subcellular localization Human molecular genetics Medium 23821644
2015 UPF3B missense mutations associated with neurodevelopmental disorders reduce NMD activity in tethered function assays; expression of missense mutant UPF3B disturbs neuronal differentiation and reduces neurite branching complexity; NMD is downregulated during neural stem cell differentiation with concurrent downregulation of UPF3B and UPF1. Tethered function NMD assay with mutant UPF3B constructs; GFP-tagged UPF3B localization in neural stem cells and neurons; neurite complexity assay; NMD inhibitor (Amlexanox) treatment Molecular brain Medium 26012578
2017 Upf3b-null mice display deficits in fear-conditioned learning, profound impairment in prepulse inhibition, and deficient dendritic spine maturation in cortical pyramidal neurons in vivo; neural stem cells from Upf3b-null mice have impaired differentiation capacity. Upf3b-null mouse generation; behavioral testing (fear conditioning, Morris water maze, PPI); in vivo dendritic spine morphology; neural stem cell differentiation assay; RNA-seq of frontal cortex Molecular psychiatry High 28948974
2024 UPF3B directly interacts with IRE1α (the ER stress sensor); this interaction inhibits IRE1α kinase activity, abolishes autophosphorylation, and reduces IRE1α clustering; the disease-causing mutation UPF3BY160D abolishes the UPF3B–IRE1α interaction; phosphorylation of UPF3B at Thr169 abolishes its interaction with UPF2. Co-immunoprecipitation, kinase activity assay, autophosphorylation assay, IRE1α clustering assay, site-directed mutagenesis (Y160D, T169 phosphomimetic) Cell death & disease Medium 39138189
2024 UPF3B binds the 3'-UTR of CDH1 mRNA to promote its degradation (via the truncated splice variant UPF3B-S generated by HnRNPR-dependent exon 8 exclusion); UPF3B-S overexpression enhances dephosphorylation of LATS1 and nuclear accumulation of YAP1, activating Hippo signaling. RNA immunoprecipitation (RIP), in vitro and in vivo HCC models with UPF3B-S knockdown/overexpression, Basescope assay Journal of advanced research Low 38402949
2024 UPF3B binds to PPP2R2C mRNA (a regulatory subunit of PP2A) and promotes its degradation, activating the PI3K/AKT/mTOR pathway; E2F6 transcription factor directly binds the UPF3B promoter and activates its transcription. Co-immunoprecipitation, RNA-binding/pulldown assays, mRNA stability assays, luciferase reporter assay for E2F6-UPF3B promoter, in vivo and in vitro HCC proliferation assays Cancer science Low 38889220
2025 RBM8A interacts with UPF3B (shown by co-immunoprecipitation) to jointly regulate the stability of BBC3 (PUMA) mRNA, promoting its degradation in gastric cancer cells. Co-immunoprecipitation; RNA immunoprecipitation-seq; RNA pulldown; Actinomycin D mRNA stability assay International journal of molecular medicine Low 40613240
2023 In cardiac sarcomeres, UPF3B (but not UPF1 or UPF2) localizes specifically to Z-discs, the presumed site of sarcomeric protein translation, suggesting a role for UPF3B-dependent NMD at the site of initial translation. Immunofluorescence localization in cardiac tissue from HCM patients and controls; RNA-seq gene set enrichment analysis Journal of molecular and cellular cardiology Low 37797718

Source papers

Stage 0 corpus · 33 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 Y14 and hUpf3b form an NMD-activating complex. Molecular cell 251 12718880
2007 Mutations in UPF3B, a member of the nonsense-mediated mRNA decay complex, cause syndromic and nonsyndromic mental retardation. Nature genetics 219 17704778
2016 The Antagonistic Gene Paralogs Upf3a and Upf3b Govern Nonsense-Mediated RNA Decay. Cell 133 27040500
2006 Functions of hUpf3a and hUpf3b in nonsense-mediated mRNA decay and translation. RNA (New York, N.Y.) 110 16601204
2010 Insights into the recruitment of the NMD machinery from the crystal structure of a core EJC-UPF3b complex. Proceedings of the National Academy of Sciences of the United States of America 108 20479275
2013 The UPF3B gene, implicated in intellectual disability, autism, ADHD and childhood onset schizophrenia regulates neural progenitor cell behaviour and neuronal outgrowth. Human molecular genetics 105 23821644
2009 Mutations of the UPF3B gene, which encodes a protein widely expressed in neurons, are associated with nonspecific mental retardation with or without autism. Molecular psychiatry 101 19238151
2011 Transcriptome profiling of UPF3B/NMD-deficient lymphoblastoid cells from patients with various forms of intellectual disability. Molecular psychiatry 96 22182939
2017 Dual function of UPF3B in early and late translation termination. The EMBO journal 87 28899899
2017 A Upf3b-mutant mouse model with behavioral and neurogenesis defects. Molecular psychiatry 61 28948974
2015 Full UPF3B function is critical for neuronal differentiation of neural stem cells. Molecular brain 49 26012578
2018 Antisense suppression of the nonsense mediated decay factor Upf3b as a potential treatment for diseases caused by nonsense mutations. Genome biology 45 29334995
2022 Mammalian UPF3A and UPF3B can activate nonsense-mediated mRNA decay independently of their exon junction complex binding. The EMBO journal 43 35451102
2022 Human UPF3A and UPF3B enable fault-tolerant activation of nonsense-mediated mRNA decay. The EMBO journal 36 35451084
2012 Exome sequencing identifies UPF3B as the causative gene for a Chinese non-syndrome mental retardation pedigree. Clinical genetics 34 22957832
2012 Broadening the phenotype associated with mutations in UPF3B: two further cases with renal dysplasia and variable developmental delay. European journal of medical genetics 32 22609145
2020 The role of the NMD factor UPF3B in olfactory sensory neurons. eLife 29 32773035
2013 Disorders with similar clinical phenotypes reveal underlying genetic interaction: SATB2 acts as an activator of the UPF3B gene. Human genetics 26 23925499
2022 Structures of nonsense-mediated mRNA decay factors UPF3B and UPF3A in complex with UPF2 reveal molecular basis for competitive binding and for neurodevelopmental disorder-causing mutation. Nucleic acids research 17 35640974
2020 A synonymous UPF3B variant causing a speech disorder implicates NMD as a regulator of neurodevelopmental disorder gene networks. Human molecular genetics 17 32667670
2024 HnRNPR-mediated UPF3B mRNA splicing drives hepatocellular carcinoma metastasis. Journal of advanced research 16 38402949
2019 Molecular and Clinical Characterization of a Novel Nonsense Variant in Exon 1 of the UPF3B Gene Found in a Large Spanish Basque Family (MRX82). Frontiers in genetics 16 31737052
2017 An RNA decay factor wears a new coat: UPF3B modulates translation termination. F1000Research 9 29333258
2024 Unveiling the role of UPF3B in hepatocellular carcinoma: Potential therapeutic target. Cancer science 6 38889220
2024 UPF3B modulates endoplasmic reticulum stress through interaction with inositol-requiring enzyme-1α. Cell death & disease 5 39138189
2023 Nonsense mediated decay factor UPF3B is associated with cMyBP-C haploinsufficiency in hypertrophic cardiomyopathy patients. Journal of molecular and cellular cardiology 5 37797718
2017 New functions in translation termination uncovered for NMD factor UPF3B. The EMBO journal 5 28935685
2004 Localization of MRX82: a new nonsyndromic X-linked mental retardation locus to Xq24-q25 in a Basque family. American journal of medical genetics. Part A 5 15526294
2024 Expanding the phenotype of UPF3B-related disorder: Case reports and literature review. American journal of medical genetics. Part A 4 38318947
2023 Spatial expression of the nonsense-mediated mRNA decay factors UPF3A and UPF3B among mouse tissues. Journal of Zhejiang University. Science. B 2 37961809
2004 Nonsense mediated decay induced by tethered human UPF3B is restricted to the cytoplasm. RNA biology 1 17194930
2025 RBM8A promotes gastric cancer progression by binding with UPF3B to induce BBC3 mRNA degradation. International journal of molecular medicine 0 40613240
2025 UPF3B Accelerates the Growth of Liver Cancer Cells by Enhancing Autophagy via CDK12. Cell biology international 0 40637141

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