GO:2000623 negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay: RNA Stability Control, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:2000623 describes any process that stops, prevents, or reduces the frequency, rate, or extent of nonsense-mediated mRNA decay (NMD), a translation-dependent RNA surveillance pathway.
• NMD is best known for degrading transcripts with premature termination codons, but it also tunes the abundance of many normal mRNAs, so its negative regulation directly shapes the expressed proteome.
• Core NMD factors include UPF1, UPF2, UPF3A/UPF3B, SMG1, SMG5, SMG6, SMG7, and the exon-junction complex, while CCR4-NOT and decapping machinery execute transcript degradation.
• Negative regulation of NMD occurs through mechanisms such as UPF1 phosphorylation status, methylation of UPF1, availability of UPF2/UPF3, and transcript-intrinsic features that make mRNAs poor NMD substrates.
• Dysregulated NMD is implicated in tumorigenesis, neurodevelopmental delay, and immune regulation, making this GO term relevant to cancer, neuroscience, and immunotherapy research.
• CRISPR knockout, point-mutation, knock-in, and overexpression models allow causal testing of NMD regulators and their target transcripts in disease-relevant cell systems.
Description
GO:2000623, negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay, is a Gene Ontology biological process term that captures the cellular mechanisms which suppress or dampen nonsense-mediated mRNA decay (NMD). NMD is a conserved translation-dependent surveillance pathway that recognizes and degrades nuclear-transcribed mRNAs harboring premature termination codons, thereby protecting cells from truncated proteins and regulating the steady-state levels of many physiological transcripts. Because NMD can eliminate a large fraction of the transcriptome, its negative regulation is a critical layer of post-transcriptional control that adjusts gene expression without changing transcription. Researchers study GO:2000623 to understand how cells fine-tune RNA stability during development, differentiation, stress, and disease. In lymphocytes, for example, NMD and nonsense-associated altered splicing are tightly regulated to support immune cell function, and perturbations in this balance can alter antigen receptor diversity and immune responses. In cancer, NMD activity can be modulated to favor tumor-promoting transcripts or to limit immunogenic non-canonical proteins, and inhibiting NMD has been proposed as a strategy to enhance immunotherapy sensitivity. This article synthesizes authoritative QuickGO annotation and verified PubMed literature to describe the definition, mechanism, key genes, disease links, and experimental models relevant to GO:2000623. It is intended for researchers designing CRISPR-based studies of NMD regulators and for those interpreting transcriptomic and proteomic data in the context of RNA surveillance.
negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay At A Glance
| GO ID | GO:2000623 |
|---|---|
| GO term | negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay |
| Ontology | biological_process |
| Synonym | negative regulation of nonsense-mediated mRNA decay; negative regulation of mRNA degradation, nonsense-mediated decay; negative regulation of mRNA catabolic process, nonsense-mediated |
| Major function | Suppression or dampening of NMD-mediated degradation of nuclear-transcribed mRNAs, thereby stabilizing NMD-target transcripts and modulating the expressed proteome |
| Core NMD machinery | UPF1, UPF2, UPF3A/UPF3B, SMG1, SMG5, SMG6, SMG7, exon-junction complex components, decapping and CCR4-NOT deadenylation complexes |
| Regulatory inputs | UPF1 phosphorylation and methylation status, UPF2/UPF3 availability, transcript-intrinsic NMD features, and cellular stress or immune signaling |
| Disease relevance | Cancer, neurodevelopmental delay, immune regulation, and non-canonical protein expression |
| Experimental models | CRISPR knockout, point mutation, knock-in, and overexpression cell models combined with RNA-seq, Ribo-seq, and proteomics |
What Is GO:2000623?
GO:2000623 is defined by QuickGO as any process that stops, prevents, or reduces the frequency, rate, or extent of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay. In other words, it is the negative regulation of NMD, the pathway that degrades nuclear-transcribed mRNAs containing premature termination codons or other NMD-triggering features. This term does not describe NMD itself, but rather the upstream or intrinsic mechanisms that suppress NMD activity, such as limiting the availability or activity of core NMD factors, modifying their post-translational state, or producing transcripts that evade NMD recognition.
Why Is negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay Important in Cell Biology?
Negative regulation of NMD is important because NMD controls the stability of a large portion of the transcriptome, and altering its activity can rapidly reprogram gene expression without transcriptional changes. This regulation influences diverse processes including tumorigenesis, immune cell function, neurodevelopment, and the expression of non-canonical proteins from diverse origins. Understanding GO:2000623 therefore provides mechanistic insight into how cells balance RNA quality control with physiological gene regulation, and it offers therapeutic opportunities in cancer immunotherapy and genetic disease.
• NMD is a translation-dependent RNA surveillance pathway, and its negative regulation directly determines the half-life of many normal and aberrant transcripts.
• Negative regulation of NMD can stabilize NMD-target mRNAs that encode tumor-promoting or immune-modulatory proteins, linking this GO term to cancer biology.
• In lymphocytes, regulated NMD and nonsense-associated altered splicing support immune receptor diversity and lymphocyte homeostasis.
• De novo variants in CNOT1, a component of the CCR4-NOT complex involved in RNA and protein stability, cause neurodevelopmental delay, highlighting the importance of NMD-related regulation in the brain.
• NMD shapes the expression of non-canonical proteins from diverse origins, so its negative regulation can expand the antigenic landscape relevant to immunotherapy.
• Inhibiting UPF1 methylation reduces NMD and enhances tumor immunotherapy sensitivity, demonstrating that negative regulation of NMD can be therapeutically exploited.
• Plant NMD has unique aspects, indicating that negative regulation of NMD is evolutionarily relevant beyond animals.
• NMD regulation is critical for physiological significance across tissues, and its dysregulation is associated with multiple disease states.
• CRISPR-based models enable causal testing of whether a candidate regulator negatively controls NMD in a specific cell type.
What Happens During negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay?
Recognition of NMD-triggering features and the default decay pathway
In simple terms: NMD normally spots faulty mRNAs and destroys them; negative regulation means slowing or blocking that destruction.
NMD is triggered when translating ribosomes encounter a premature termination codon or other signals such as long 3' UTRs or upstream open reading frames, leading to recruitment of UPF1 and its associated factors. The exon-junction complex deposited during splicing can enhance NMD efficiency for transcripts with premature termination codons, and the pathway ultimately recruits decapping and deadenylation activities to degrade the mRNA. Negative regulation of GO:2000623 can occur when these recognition or execution steps are suppressed, for example by limiting UPF1 activity or by transcript features that prevent efficient NMD targeting.
UPF1 phosphorylation, methylation, and post-translational control
In simple terms: Chemical tags on the NMD machinery can switch the pathway on or off.
UPF1 is a central ATP-dependent RNA helicase in NMD, and its phosphorylation by SMG1 is a key activation step that recruits SMG5, SMG6, and SMG7 to promote decay. Methylation of UPF1 has been shown to regulate NMD activity, and inhibiting UPF1 methylation reduces NMD, thereby enhancing tumor immunotherapy sensitivity. These post-translational modifications provide direct mechanisms for negative regulation of NMD, because altering the modification state of UPF1 can reduce the frequency or extent of transcript degradation.
Availability and stoichiometry of UPF2, UPF3A, and UPF3B
In simple terms: The NMD machine needs several parts; if some parts are scarce, decay slows down.
UPF2 and UPF3A/UPF3B are core NMD factors that interact with UPF1 and the exon-junction complex to promote decay. Changes in the abundance or isoform balance of these factors can negatively regulate NMD by limiting the formation of productive decay complexes. In lymphocytes, regulated expression of NMD factors and nonsense-associated altered splicing contributes to immune-specific control of transcript fate, illustrating how factor availability can tune NMD activity.
Transcript-intrinsic features that evade or suppress NMD
In simple terms: Some mRNAs are built in a way that makes them hard for NMD to catch.
NMD efficiency depends on transcript architecture, including the position of the premature termination codon relative to exon-junction complexes, 3' UTR length, and upstream open reading frames. Transcripts with features that poorly trigger NMD are effectively protected from decay, which represents a transcript-intrinsic form of negative regulation of GO:2000623. Large-scale analyses in human cancers have revealed rules that predict which transcripts are sensitive or resistant to NMD, providing a framework for understanding negative regulation at the substrate level.
Cellular contexts that suppress NMD: stress, immune signaling, and disease
In simple terms: Under certain conditions, cells deliberately turn down NMD to change which proteins are made.
NMD activity can be modulated by cellular state, including stress responses and immune signaling, allowing cells to stabilize specific transcripts when needed. In cancer, altered NMD can favor the expression of tumor-promoting isoforms or non-canonical proteins, and NMD has been proposed as a mediator of tumorigenesis. In neurodevelopment, disruption of CCR4-NOT components such as CNOT1 affects RNA and protein stability and causes neurodevelopmental delay, underscoring the physiological importance of negative regulation of NMD-related processes.
Key Genes Involved in GO:2000623 negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay
The following genes and proteins are central to NMD and its negative regulation, based on verified literature and QuickGO annotation.
| Gene | Major Role | Research Relevance |
|---|---|---|
| UPF1 | Core ATP-dependent RNA helicase required for NMD; phosphorylation and methylation regulate its activity | Target for negative regulation studies; methylation inhibition reduces NMD and enhances immunotherapy sensitivity |
| UPF2 | Essential NMD factor that interacts with UPF1 and the exon-junction complex | Modulating UPF2 levels can negatively regulate NMD and alter transcript stability |
| UPF3A | NMD factor with regulatory roles in decay complex formation | Isoform balance affects NMD efficiency and transcript fate |
| UPF3B | NMD factor involved in recognition of premature termination codons | Mutations or altered expression can influence NMD activity and disease phenotypes |
| SMG1 | Phosphatidylinositol 3-kinase-related kinase that phosphorylates UPF1 to activate NMD | Key upstream regulator whose inhibition can suppress NMD |
| SMG5 | Component of the NMD decay complex recruited by phosphorylated UPF1 | Participates in execution of NMD and can be targeted to modulate decay |
| SMG6 | Endonuclease that cleaves NMD target mRNAs | Direct decay effector; its activity determines NMD extent |
| SMG7 | Adaptor protein that promotes NMD-mediated degradation | Modulating SMG7 affects NMD efficiency and transcript levels |
| CNOT1 | Central component of the CCR4-NOT complex involved in RNA and protein stability | De novo variants cause neurodevelopmental delay, linking NMD-related regulation to brain development |
| CNOT2 | Subunit of the CCR4-NOT deadenylation complex | Contributes to mRNA stability and NMD-related decay |
| CNOT3 | Subunit of the CCR4-NOT complex | Involved in RNA stability and potential negative regulation of NMD |
| EJC components (e.g., RBM8A, MAGOH) | Exon-junction complex proteins that enhance NMD of premature termination codon-containing transcripts | Modulating EJC components can alter NMD sensitivity |
| DCP1A | Decapping enzyme subunit involved in mRNA degradation | Execution step of NMD that can be regulated |
| DCP2 | Catalytic subunit of the decapping complex | Target for understanding decay execution in NMD |
| XRN1 | 5'-3' exoribonuclease that degrades decapped mRNAs | Final step of NMD-mediated decay |
| EXOSC3 | Exosome component involved in 3'-5' RNA degradation | Contributes to NMD-related RNA turnover |
| NMD-associated non-canonical protein regulators | Proteins from diverse origins whose expression is controlled by NMD | Relevant to immunotherapy and antigen presentation |
How Is negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay Regulated?
Negative regulation of NMD is controlled at multiple levels. UPF1 phosphorylation by SMG1 is required for NMD activation, and phosphatases or methylation events can reverse or dampen this activation, thereby negatively regulating the pathway. Methylation of UPF1 has been shown to modulate NMD activity, and inhibiting this methylation reduces NMD and enhances tumor immunotherapy sensitivity. The availability of UPF2 and UPF3A/UPF3B, as well as the stoichiometry of the exon-junction complex, can limit decay complex formation and thus suppress NMD. Transcript-intrinsic features such as premature termination codon position, 3' UTR length, and upstream open reading frames determine whether an mRNA is efficiently targeted, providing a substrate-level layer of negative regulation. In lymphocytes, immune signaling and regulated splicing further tune NMD and nonsense-associated altered splicing, illustrating cell-type-specific control. In cancer, oncogenic signaling and tumor microenvironment cues can alter NMD activity, and NMD has been proposed as a mediator of tumorigenesis. Plant NMD also exhibits unique regulatory aspects, indicating evolutionary diversification of negative regulation.
negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| UPF1 | Cancer immunotherapy sensitivity; NMD activity modulation | CRISPR knockout or point-mutation of methylation sites in cancer cell lines followed by immunotherapy assays |
| CNOT1 | Neurodevelopmental delay | Knock-in of patient variants in iPSC-derived neurons |
| UPF2 | NMD regulation and transcript stability | Knockout and overexpression in lymphocyte models |
| UPF3B | NMD and immune cell function | Point mutation and knockout in immune cell lines |
| SMG1 | NMD activation and cancer | Knockout or kinase-dead knock-in in tumor models |
Cancer and tumorigenesis
NMD is a mediator of tumorigenesis, and its negative regulation can stabilize transcripts that promote tumor growth or immune evasion. Large-scale analyses in human cancers have defined rules by which NMD shapes the transcriptome, revealing that many oncogenic and tumor-suppressive transcripts are NMD-sensitive. Inhibiting UPF1 methylation reduces NMD and enhances tumor immunotherapy sensitivity, demonstrating that negative regulation of NMD can be therapeutically beneficial in oncology. NMD also controls the expression of non-canonical proteins from diverse origins, which can serve as tumor antigens and influence immune recognition.
Neurodevelopmental delay and neurological disease
De novo variants in CNOT1, a central component of the CCR4-NOT complex involved in gene expression and RNA and protein stability, cause neurodevelopmental delay. Because CCR4-NOT participates in mRNA deadenylation and decay, disruption of this complex can perturb NMD-related regulation and transcript stability in the developing brain. This link highlights the importance of negative regulation of NMD for normal neurodevelopment and suggests that NMD-related pathways should be considered in neurodevelopmental disorders.
Immune regulation and immunotherapy
In lymphocytes, NMD and nonsense-associated altered splicing are tightly regulated to support immune cell function and receptor diversity. Modulating NMD activity can alter the presentation of non-canonical proteins and affect tumor immunotherapy sensitivity. Inhibiting UPF1 methylation to reduce NMD has been shown to enhance immunotherapy sensitivity, indicating that negative regulation of NMD is a druggable node in immuno-oncology.
Physiological significance and broader disease relevance
NMD has broad physiological significance, and its dysregulation is associated with multiple disease states beyond cancer and neurodevelopment. The pathway controls the stability of many normal transcripts, so negative regulation of NMD can influence metabolism, differentiation, and stress responses. Understanding these roles is essential for interpreting disease-associated transcriptomic changes and for designing safe therapeutic strategies that target NMD.
From negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of a candidate gene negatively regulate NMD? | CRISPR knockout cell line followed by RNA-seq and NMD reporter assays |
| Does a specific phosphorylation or methylation site on UPF1 control NMD? | Point-mutation knock-in of phospho- or methylation-deficient UPF1 |
| Does a disease-associated variant in CNOT1 alter NMD-related transcript stability? | Knock-in of the patient variant in iPSC-derived neurons |
| Where and when does an NMD regulator localize in cells? | Tagged knock-in with fluorescent or epitope tag followed by imaging |
| Does overexpression of an NMD suppressor stabilize target transcripts? | Overexpression cell model combined with RNA-seq and proteomics |
| Can modulating NMD enhance immunotherapy sensitivity? | CRISPR knockout or point mutation in cancer cells co-cultured with immune cells |
How to Study the negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay Process
| Method | What It Measures | Typical Application |
|---|---|---|
| RNA-seq | Transcript abundance and stability changes | Identifying NMD-sensitive transcripts after regulator perturbation |
| Ribo-seq | Ribosome occupancy and translation efficiency | Detecting translation-dependent NMD and upstream open reading frame usage |
| Proteomics | Protein abundance, including non-canonical proteins | Discovering NMD-regulated antigens and validating targets |
| NMD reporter assays | NMD activity in live cells | Screening for negative regulators of NMD |
| CRISPR knockout screens | Gene requirement for NMD regulation | Identifying novel NMD suppressors |
| CRISPR point-mutation knock-in | Effect of specific post-translational modification sites | Testing UPF1 methylation or phosphorylation mutants |
| Imaging of tagged NMD factors | Localization and dynamics of NMD machinery | Studying assembly and regulation of decay complexes |
| Immunotherapy co-culture assays | Immune-mediated killing after NMD modulation | Evaluating therapeutic potential of NMD inhibition |
RNA-seq and transcriptome-wide NMD profiling
RNA-seq can quantify changes in transcript abundance after manipulating candidate NMD regulators, revealing which mRNAs are stabilized when NMD is negatively regulated. Comparing wild-type and knockout cells allows identification of NMD-sensitive transcripts and validation of predicted NMD rules. In cancer studies, transcriptome profiling has been used to define the impact of NMD on oncogenic and tumor-suppressive networks.
Ribo-seq and translation-dependent NMD analysis
Because NMD is translation-dependent, ribosome profiling (Ribo-seq) can measure ribosome occupancy and identify transcripts whose translation triggers NMD. Combining Ribo-seq with RNA-seq distinguishes changes in transcription from changes in mRNA stability, which is essential for studying negative regulation of NMD. This approach can also reveal upstream open reading frame usage and premature termination codon readthrough events.
Proteomics and non-canonical protein detection
Mass spectrometry-based proteomics can detect proteins whose expression changes when NMD is suppressed, including non-canonical proteins from diverse origins. Because NMD controls the abundance of many proteins, proteomic profiling complements transcriptomic data and can identify immunogenic antigens relevant to immunotherapy. Targeted proteomics can validate candidate NMD targets identified by RNA-seq.
Imaging and reporter assays for NMD activity
Fluorescent or luminescent NMD reporters can measure NMD activity in live cells and are useful for screening regulators of GO:2000623. Imaging of tagged NMD factors, such as UPF1 or SMG proteins, can reveal their localization and dynamics during negative regulation. These assays are compatible with high-content screening and CRISPR-based perturbation.
How CRISPR Can Be Used to Study GO:2000623 negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay
Knockout
CRISPR knockout of candidate NMD regulators such as UPF1, UPF2, SMG1, or CNOT1 can test whether loss of the gene reduces NMD activity, thereby demonstrating negative regulation. Knockout cell lines are typically validated by RNA-seq and NMD reporter assays to confirm stabilization of known NMD targets. In cancer models, knockout of NMD factors can enhance immunotherapy sensitivity, providing functional evidence for therapeutic targeting.
Point Mutation
Point-mutation knock-in can dissect the role of specific residues in NMD regulation, such as phosphorylation or methylation sites on UPF1. For example, methylation-deficient UPF1 mutants can be used to test whether reduced methylation negatively regulates NMD and enhances immunotherapy sensitivity. Point mutations in CNOT1 can model patient variants associated with neurodevelopmental delay and assess their impact on RNA stability.
Knock-in
Knock-in of disease-associated variants, such as CNOT1 mutations, allows study of how specific alleles affect NMD-related transcript stability in relevant cell types like iPSC-derived neurons. Tagged knock-in of NMD factors with fluorescent or epitope tags enables imaging and biochemical analysis of the decay machinery. Knock-in of NMD reporter cassettes can provide sensitive readouts of NMD activity in a physiological context.
Overexpression
Overexpression of NMD suppressors or dominant-negative NMD factors can negatively regulate NMD and stabilize target transcripts, which is useful for identifying downstream effects on the proteome. Overexpression models combined with RNA-seq and proteomics can reveal non-canonical proteins whose expression depends on NMD suppression. Overexpression of UPF3A or other regulatory isoforms can shift the balance of NMD activity and provide insight into isoform-specific regulation.
How EDITGENE Supports negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay Research
Researchers studying negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay-related genes often need to determine whether a candidate gene is causally involved in suppressing NMD, stabilizing specific transcripts, or modulating disease-relevant phenotypes. EDITGENE provides CRISPR-based cell model services that enable precise, reproducible testing of these hypotheses in relevant cell types.
Contact EDITGENE today to design your custom CRISPR model for negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay research.
Frequently Asked Questions About negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay
What is GO:2000623?
GO:2000623 is the Gene Ontology biological process term for negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay, meaning any process that stops, prevents, or reduces the frequency, rate, or extent of NMD.
What is negative regulation of nonsense-mediated mRNA decay?
It is the suppression or dampening of NMD, the pathway that degrades nuclear-transcribed mRNAs with premature termination codons or other NMD-triggering features, thereby stabilizing target transcripts.
What genes are involved in negative regulation of NMD?
Key genes include UPF1, UPF2, UPF3A, UPF3B, SMG1, SMG5, SMG6, SMG7, and CCR4-NOT components such as CNOT1, all of which can influence NMD activity when their levels or modifications change.
How is NMD negatively regulated?
NMD can be negatively regulated by limiting UPF1 phosphorylation or methylation, reducing UPF2/UPF3 availability, altering exon-junction complex stoichiometry, or through transcript-intrinsic features that make mRNAs poor NMD substrates.
Why is negative regulation of NMD important in cancer?
NMD is a mediator of tumorigenesis, and its negative regulation can stabilize oncogenic transcripts or non-canonical proteins; inhibiting NMD has been shown to enhance tumor immunotherapy sensitivity.
What diseases are linked to NMD regulation?
Diseases include cancer, neurodevelopmental delay caused by CNOT1 variants, and immune-related conditions, reflecting the broad physiological significance of NMD.
How can I study negative regulation of NMD with CRISPR?
CRISPR knockout, point-mutation knock-in, tagged knock-in, and overexpression models can be combined with RNA-seq, Ribo-seq, proteomics, and NMD reporter assays to test causal roles of candidate regulators.
What methods measure NMD activity?
RNA-seq, Ribo-seq, proteomics, fluorescent or luminescent NMD reporters, and imaging of tagged NMD factors are commonly used to measure NMD activity and its negative regulation.
Is NMD regulation relevant in plants?
Yes, plant NMD has unique aspects, indicating that negative regulation of NMD is evolutionarily relevant beyond animals.
What cell models are suitable for NMD research?
Cancer cell lines, lymphocyte models, iPSC-derived neurons, and other disease-relevant cells can be engineered with CRISPR to study negative regulation of NMD.
Conclusion
GO:2000623, negative regulation of nuclear-transcribed mRNA catabolic process, nonsense-mediated decay, represents a critical layer of post-transcriptional control that determines the stability of many nuclear-transcribed mRNAs. Its mechanisms involve post-translational modification of UPF1, availability of core NMD factors, transcript-intrinsic features, and cell-type-specific signaling, with broad implications for cancer, neurodevelopment, and immunity. CRISPR-based cell models combined with transcriptomic, translatomic, and proteomic methods provide powerful tools to dissect this process and identify therapeutic opportunities.
References
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- 3. Lambert JM et al.. 2020. Mechanisms and Regulation of Nonsense-Mediated mRNA Decay and Nonsense-Associated Altered Splicing in Lymphocytes.. Int J Mol Sci 21(4) PMID: 32079193
- 4. Vissers LELM et al.. 2020. De Novo Variants in CNOT1, a Central Component of the CCR4-NOT Complex Involved in Gene Expression and RNA and Protein Stability, Cause Neurodevelopmental Delay.. Am J Hum Genet 107(1):164-172 PMID: 32553196
- 5. Shaul O. 2015. Unique Aspects of Plant Nonsense-Mediated mRNA Decay.. Trends Plant Sci 20(11):767-779 PMID: 26442679
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