GO:1901222 regulation of non-canonical NF-kappaB signal transduction: Signaling Pathway, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:1901222 describes any process that modulates the frequency, rate or extent of the non-canonical NF-kappaB signaling cascade, a pathway centered on NIK, IKKalpha and p100 processing to p52.
• The non-canonical NF-kappaB pathway is activated by a defined set of TNF receptor superfamily members such as LTbetaR, BAFFR, CD40 and RANK, and is tightly controlled by TRAF3 degradation and NIK stabilization.
• Dysregulation of this pathway is linked to immune disorders, autoimmunity, lymphoid malignancies and solid tumors, making it a therapeutic target.
• Key regulatory nodes include NIK, TRAF2, TRAF3, cIAP1/2, IKKalpha, p100/p52, RelB and TBK1, which together determine pathway output.
• Experimental dissection of GO:1901222 relies on knockout, point-mutation, knock-in and overexpression models combined with phospho-protein analysis, p100 processing assays and NF-kappaB reporter systems.
• Emerging evidence implicates non-canonical NF-kappaB signaling in tumor microenvironment remodeling, tertiary lymphoid structure formation and immunotherapy response.
Description
GO:1901222, regulation of non-canonical NF-kappaB signal transduction, is a Gene Ontology biological process term that captures any process modulating the frequency, rate or extent of the non-canonical NF-kappaB signaling cascade. Unlike the canonical NF-kappaB pathway, which depends on IKKbeta-mediated IkappaBalpha degradation and rapid nuclear translocation of RelA-containing dimers, the non-canonical pathway proceeds through NIK-dependent activation of IKKalpha, which in turn triggers partial proteasomal processing of p100 (NFKB2) to p52 and nuclear accumulation of RelB:p52 dimers. This slower, post-translational mechanism allows cells to respond to specific TNF receptor superfamily ligands with sustained rather than transient NF-kappaB activity. Because the non-canonical cascade controls lymphoid organogenesis, B-cell maturation, osteoclastogenesis and inflammatory gene programs, its regulation is central to immunology and cancer biology. Genetic and pharmacological studies have shown that excessive or defective non-canonical NF-kappaB activity contributes to autoimmunity, chronic inflammation and lymphoid malignancies, while pathway modulation can influence tissue regeneration and anti-tumor immunity. Consequently, researchers need precise tools to interrogate the regulators that set the threshold, duration and amplitude of this pathway. This article integrates the QuickGO definition of GO:1901222 with verified PubMed literature to summarize the molecular logic, key genes, disease relevance and experimental strategies used to study regulation of non-canonical NF-kappaB signal transduction.
regulation of non-canonical NF-kappaB signal transduction At A Glance
| GO ID | GO:1901222 |
|---|---|
| GO term | regulation of non-canonical NF-kappaB signal transduction |
| Ontology | biological_process |
| Definition | Any process that modulates the frequency, rate or extent of the non-canonical NF-kappaB signaling cascade. |
| Synonym | regulation of NIK/NF-kappaB signaling; regulation of noncanonical NF-kappaB signaling; regulation of p52-dependent NF-kappaB signaling; NF-kappaB import into nucleus |
| Major function | Controls the amplitude, duration and threshold of non-canonical NF-kappaB activation, primarily through NIK, TRAF2/3, cIAP1/2, IKKalpha and p100 processing. |
| Key upstream inducers | TNF receptor superfamily members including LTbetaR, BAFFR, CD40, RANK and TWEAK. |
| Key downstream effectors | RelB:p52 dimers and target genes involved in lymphoid organogenesis, B-cell survival and inflammation. |
| Disease relevance | Autoimmunity, chronic inflammation, lymphoid malignancies and solid tumors. |
What Is GO:1901222?
In practical terms, GO:1901222 refers to any biological process that changes how often, how fast or how strongly the non-canonical NF-kappaB signaling cascade operates. This includes mechanisms that promote or inhibit NIK stabilization, IKKalpha activation, p100 processing to p52, RelB:p52 nuclear import and downstream target gene transcription. The term is therefore a regulatory umbrella: it does not describe the core cascade itself, but the modulatory inputs that tune its activity in response to ligands, cellular stress or developmental cues.
Why Is regulation of non-canonical NF-kappaB signal transduction Important in Cell Biology?
Regulation of non-canonical NF-kappaB signal transduction is important because it determines whether cells mount a sustained, RelB-dependent transcriptional response that shapes immune organ development, B-cell survival and inflammatory output. Unlike the canonical pathway, which is often transient, the non-canonical cascade is controlled by the steady-state balance of NIK versus TRAF3 and cIAP1/2, so small changes in regulator abundance or activity can produce large shifts in pathway output. This sensitivity makes GO:1901222 a focal point for understanding how tumors, immune cells and stromal compartments interpret environmental signals.
• Controls lymphoid organogenesis and B-cell maturation through LTbetaR- and BAFFR-dependent NIK activation.
• Regulates osteoclastogenesis and bone homeostasis via RANK-induced non-canonical NF-kappaB signaling.
• Drives inflammatory gene programs in autoimmune and chronic inflammatory diseases.
• Is constitutively active in several lymphoid malignancies, including multiple myeloma and Hodgkin lymphoma.
• Modulates tumor microenvironment remodeling and immune cell recruitment in glioblastoma and other solid tumors.
• Influences tertiary lymphoid structure formation and anti-tumor immunity.
• Provides a therapeutic target for small-molecule NIK inhibitors and IKKalpha modulators.
• Interacts with TBK1 and other kinases that fine-tune NF-kappaB-dependent cancer immunity.
• Can be modulated to promote tissue regeneration, as shown for LTbetaR inhibition in lung.
• Serves as a paradigm for studying how post-translational regulators set signaling thresholds.
What Happens During regulation of non-canonical NF-kappaB signal transduction?
Ligand-induced receptor activation and TRAF3 degradation
In simple terms: A signal arrives at the cell surface and starts a chain reaction that removes a brake from the pathway.
Non-canonical NF-kappaB signaling is initiated when ligands such as lymphotoxin-beta, BAFF, CD40L or RANK bind their cognate TNF receptor superfamily receptors. This engagement recruits TRAF3, TRAF2 and cIAP1/2 to the receptor complex, leading to cIAP-mediated ubiquitination and proteasomal degradation of TRAF3. Because TRAF3 normally scaffolds NIK for degradation, its removal allows NIK to accumulate, which is the first committed regulatory step of GO:1901222.
NIK stabilization and IKKalpha activation
In simple terms: The accumulated NIK protein then switches on a kinase that prepares the pathway for gene activation.
Stabilized NIK phosphorylates and activates IKKalpha, a kinase that is distinct from the canonical IKKbeta arm. IKKalpha activation is a key regulatory node because it couples NIK abundance to downstream p100 processing. Regulatory inputs that alter NIK stability, such as TRAF2/TRAF3 availability or cIAP activity, therefore directly modulate the frequency and extent of non-canonical NF-kappaB signal transduction.
p100 processing to p52 and RelB:p52 nuclear import
In simple terms: A larger precursor protein is trimmed into its active form, which then moves into the nucleus to turn on genes.
Activated IKKalpha phosphorylates the C-terminal region of p100 (NFKB2), triggering partial proteasomal processing that removes the inhibitory domain and generates p52. p52 then dimerizes with RelB and translocates to the nucleus, where it binds kappaB sites and activates target genes. Regulation of this step determines the duration and magnitude of the transcriptional response and is a central feature of GO:1901222.
Negative feedback and pathway termination
In simple terms: The cell also has built-in brakes that prevent the signal from running out of control.
Non-canonical NF-kappaB signaling is restrained by negative regulators including TRAF3, cIAP1/2, A20 and deubiquitinases that promote NIK degradation or limit IKKalpha activity. These feedback mechanisms ensure that pathway output is transient and context-appropriate. Loss of such brakes can lead to constitutive p52-dependent transcription, which is observed in lymphoid malignancies and inflammatory disorders.
Crosstalk with other signaling modules
In simple terms: This pathway does not work alone; it talks to other signaling systems that adjust its strength.
Non-canonical NF-kappaB signaling intersects with canonical NF-kappaB, MAPK, PI3K-AKT and TBK1-dependent modules, which can either potentiate or dampen pathway output. For example, TBK1 has been implicated in modulating NF-kappaB activity in cancer cells and immune cells, influencing the balance between pro-survival and anti-tumor responses. Such crosstalk expands the set of processes that can regulate GO:1901222.
Key Genes Involved in GO:1901222 regulation of non-canonical NF-kappaB signal transduction
The following genes and proteins are central to the regulation and execution of non-canonical NF-kappaB signal transduction and are frequently studied in this context.
| Gene | Major Role | Research Relevance |
|---|---|---|
| NIK (MAP3K14) | Central kinase that activates IKKalpha upon stabilization | Key regulatory node; target for knockout and point-mutation studies |
| TRAF3 | Scaffold that promotes NIK degradation; degraded upon receptor activation | Negative regulator; loss causes constitutive pathway activation |
| TRAF2 | Adaptor that recruits cIAP1/2 to degrade TRAF3 and NIK | Modulates pathway threshold; studied in KO models |
| cIAP1/2 (BIRC2/BIRC3) | E3 ligases that ubiquitinate TRAF3 and NIK | Regulate NIK stability; targets for inhibitor studies |
| IKKalpha (CHUK) | Kinase that phosphorylates p100 to trigger processing | Essential effector; point mutations used to dissect catalytic activity |
| NFKB2 (p100/p52) | Precursor processed to p52; forms RelB:p52 dimers | Readout of pathway activity; knockout and knock-in models |
| RELB | Transcription factor partner of p52 | Determines target gene specificity; KO models show immune defects |
| LTBR | Receptor for lymphotoxin-beta; activates non-canonical pathway | Target for pathway modulation in lung regeneration |
| TNFRSF13C (BAFFR) | B-cell receptor that activates NIK-dependent signaling | Critical for B-cell survival; studied in autoimmune models |
| CD40 | Receptor that can activate non-canonical NF-kappaB in B cells | Links adaptive immunity to pathway regulation |
| TNFRSF11A (RANK) | Receptor that drives osteoclastogenesis via NIK | Bone biology and cancer metastasis models |
| TBK1 | Kinase that modulates NF-kappaB and interferon signaling | Cancer immunity and therapy response studies |
| IFI35 | Regulator of non-canonical NF-kappaB in glioblastoma stem cells | Tumor microenvironment and stemness studies |
| A20 (TNFAIP3) | Negative regulator that limits NF-kappaB activity | Autoimmunity and lymphoma models |
| CYLD | Deubiquitinase that restrains NIK and IKKalpha | Tumor suppressor context; KO and mutation studies |
| NFKB1 | Canonical NF-kappaB subunit with crosstalk to non-canonical pathway | Comparative studies of canonical vs non-canonical signaling |
| BCL3 | Atypical IkappaB family member that modulates NF-kappaB dimers | Regulatory crosstalk and lymphoid biology |
| RELA | Canonical NF-kappaB subunit; crosstalk partner | Comparative pathway analysis |
How Is regulation of non-canonical NF-kappaB signal transduction Regulated?
Regulation of non-canonical NF-kappaB signal transduction is itself controlled at multiple levels. Upstream, ligand availability and receptor expression determine whether the pathway is engaged. Intracellularly, the balance between NIK and its negative regulators TRAF3, TRAF2, cIAP1/2, A20 and CYLD sets the activation threshold. Post-translational modifications, including phosphorylation, ubiquitination and deubiquitination, control the stability and activity of NIK, IKKalpha and p100. Crosstalk with TBK1 and other kinases can further tune pathway output in cancer and immune cells. In addition, transcriptional and epigenetic mechanisms can alter the expression of pathway components, thereby changing cellular responsiveness over longer timescales.
regulation of non-canonical NF-kappaB signal transduction and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| NIK (MAP3K14) | Lymphoid malignancies, autoimmunity | Knockout and point-mutation cell lines; xenograft models |
| TRAF3 | B-cell lymphoma, immune dysregulation | Knockout models to study constitutive pathway activation |
| NFKB2 | Immunodeficiency and autoimmunity | Knock-in of patient mutations; p100 processing assays |
| IFI35 | Glioblastoma stem cell maintenance | Knockdown/knockout in glioblastoma stem cell models |
| LTBR | Lung regeneration and fibrosis | Inhibitor studies and conditional knockout in lung models |
Non-canonical NF-kappaB signaling in lymphoid malignancies
Constitutive activation of non-canonical NF-kappaB signaling is a hallmark of several lymphoid malignancies, including multiple myeloma and Hodgkin lymphoma, where mutations or copy-number changes affecting NIK, TRAF3, TRAF2 or cIAP1/2 lead to persistent p100 processing and RelB:p52 activity. These alterations promote tumor cell survival, proliferation and resistance to apoptosis, making the pathway an attractive therapeutic target. Small-molecule NIK inhibitors and IKKalpha modulators are being explored to disrupt this oncogenic signaling.
Autoimmunity and chronic inflammation
Dysregulated non-canonical NF-kappaB signaling contributes to autoimmune and chronic inflammatory conditions by sustaining pro-inflammatory gene expression and promoting aberrant immune cell survival. Loss-of-function mutations in negative regulators such as A20 or CYLD can unleash pathway activity, while excessive BAFFR or CD40 signaling can amplify B-cell responses. Understanding how GO:1901222 is controlled in immune cells may inform therapies for lupus, rheumatoid arthritis and related disorders.
Solid tumors and the tumor microenvironment
In solid tumors such as glioblastoma, non-canonical NF-kappaB signaling can support cancer stem cell maintenance and recruit tumor-associated macrophages, thereby shaping an immunosuppressive microenvironment. Pathway activity has also been linked to tertiary lymphoid structure formation and immunotherapy response, where fibroblast and B-cell subsets influence immune-hot versus immune-cold phenotypes. These findings suggest that modulating GO:1901222 could alter tumor-immune interactions and treatment outcomes.
Tissue regeneration and repair
Inhibition of LTbetaR signaling, which feeds into non-canonical NF-kappaB, has been shown to activate WNT-induced regeneration in lung tissue. This illustrates that regulated suppression of the pathway can be beneficial in regenerative contexts, highlighting the need for precise control over GO:1901222. Such findings expand the disease relevance of this GO term beyond oncology and immunology.
From regulation of non-canonical NF-kappaB signal transduction-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is a candidate gene required for non-canonical NF-kappaB activation? | CRISPR knockout in immune or cancer cell lines followed by p100 processing assays |
| Does a specific phosphorylation site regulate NIK or IKKalpha activity? | Point-mutation knock-in of phospho-dead or phospho-mimetic variants |
| How does a disease-associated mutation affect pathway output? | Knock-in of the patient mutation and comparison with wild-type cells |
| Where and when is a pathway component expressed? | Tagged knock-in with fluorescent or epitope tags for imaging and proteomics |
| Can overexpression drive constitutive pathway activation? | Dox-inducible overexpression of NIK, RelB or p52 in reporter cell lines |
| Which regulators control pathway strength in a specific tissue? | Conditional knockout or overexpression in organoid or mouse models |
How to Study the regulation of non-canonical NF-kappaB signal transduction Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Western blot for p100/p52 | Processing of p100 to p52 | Pathway activation status after stimulation |
| Phospho-IKKalpha immunoblot | IKKalpha activation | Upstream kinase activity in KO or mutant cells |
| NF-kappaB luciferase reporter | Transcriptional output | Comparing pathway activity across conditions |
| Immunofluorescence for RelB | Nuclear translocation | Spatial readout of pathway activation |
| RNA-seq | Global gene expression changes | Identifying pathway target genes and signatures |
| Proteomics / immunoprecipitation | Protein interactions and stability | Mapping NIK, TRAF3 and IKKalpha complexes |
| Single-cell RNA-seq | Cell-type-specific pathway activity | Tumor microenvironment studies |
| Spatial transcriptomics | In situ pathway and niche context | Immunotherapy response analysis |
Phospho-protein and processing assays
Because non-canonical NF-kappaB signaling depends on NIK stabilization, IKKalpha phosphorylation and p100 processing to p52, western blotting with phospho-specific and processing-specific antibodies is a standard approach. Researchers typically monitor NIK levels, phospho-IKKalpha, p100/p52 ratios and RelB nuclear translocation after ligand stimulation or genetic perturbation. These assays provide direct biochemical readouts of GO:1901222 activity.
NF-kappaB reporter and nuclear translocation assays
Luciferase reporters driven by kappaB sites, combined with immunofluorescence or subcellular fractionation, allow quantification of pathway output and RelB:p52 nuclear import. Such assays are useful for comparing wild-type and mutant cells and for testing small-molecule inhibitors. They can be adapted to high-throughput screening formats.
Transcriptomic and proteomic profiling
RNA-seq and proteomics can identify gene expression and protein interaction changes that accompany pathway activation or inhibition. In glioblastoma stem cells, for example, IFI35-dependent regulation of non-canonical NF-kappaB signaling was linked to distinct transcriptional programs and macrophage recruitment. These approaches help place GO:1901222 in a broader cellular context.
Single-cell and spatial analysis
Single-cell and spatial transcriptomics have been used to identify fibroblast subtypes and immune niches associated with immunotherapy response, some of which relate to NF-kappaB-dependent signaling. Such methods can reveal how non-canonical NF-kappaB activity varies across cell types within a tumor or tissue. They are increasingly used to study pathway regulation in situ.
How CRISPR Can Be Used to Study GO:1901222 regulation of non-canonical NF-kappaB signal transduction
Knockout
CRISPR knockout of genes such as NIK, TRAF3, TRAF2, IKKalpha or NFKB2 is widely used to test their requirement for non-canonical NF-kappaB signaling. Loss of negative regulators like TRAF3 or A20 can produce constitutive pathway activation, while loss of NIK or IKKalpha abolishes p100 processing. Knockout cell lines therefore provide clean genetic backgrounds for dissecting GO:1901222.
Point Mutation
Point mutations can be introduced to dissect phosphorylation sites, ubiquitination sites or catalytic residues in NIK, IKKalpha or p100. For example, phospho-dead or phospho-mimetic variants help determine which residues are required for pathway activation or termination. Such models are valuable for linking specific molecular events to pathway output.
Knock-in
Knock-in of disease-associated mutations, epitope tags or fluorescent reporters allows researchers to study pathway regulation in a physiologically relevant context. Tagged knock-in of NIK or RelB can facilitate imaging and proteomic analysis of endogenous complexes. Knock-in models are also used to validate patient-derived mutations in immune or cancer cells.
Overexpression
Overexpression of NIK, RelB, p52 or upstream ligands can drive constitutive non-canonical NF-kappaB activation and is useful for gain-of-function studies. Inducible overexpression systems allow temporal control of pathway activation, which helps distinguish direct from indirect effects. These models complement knockout and knock-in approaches in building a complete picture of GO:1901222.
How EDITGENE Supports regulation of non-canonical NF-kappaB signal transduction Research
Researchers studying regulation of non-canonical NF-kappaB signal transduction-related genes often need to determine whether a candidate gene is causally involved in pathway control or is merely correlated with pathway activity. Rigorous causal inference requires well-controlled genetic models, such as knockout, point-mutation, knock-in and overexpression cell lines, combined with functional readouts like p100 processing and NF-kappaB reporter assays. EDITGENE provides these models and associated screening services to accelerate discovery in this pathway.
Contact EDITGENE today to design your custom CRISPR model for regulation of non-canonical NF-kappaB signal transduction research.
Related Products
| Product name | Cat.No. | Species | Gene ID | |
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| EDA Knockout HEK293 Cell Line | EDJ-KQ561 | Human | 1896 | Details Get a Quote |
| AGER Knockout HEK293 Cell Line | EDJ-KQ1094 | Human | 177 | Details Get a Quote |
| DLG1 Knockout HEK293 Cell Line | EDJ-KQ1386 | Human | 1739 | Details Get a Quote |
| BCL3 Knockout HEK293 Cell Line | EDJ-KQ1481 | Human | 602 | Details Get a Quote |
| AKIP1 Knockout HEK293 Cell Line | EDJ-KQ2142 | Human | 56672 | Details Get a Quote |
| EZR Knockout HEK293 Cell Line | EDJ-KQ3384 | Human | 7430 | Details Get a Quote |
| PTPN22 Knockout HEK293 Cell Line | EDJ-KQ3809 | Human | 26191 | Details Get a Quote |
| RASSF2 Knockout HEK293 Cell Line | EDJ-KQ6739 | Human | 9770 | Details Get a Quote |
| TRIM6 Knockout HEK293 Cell Line | EDJ-KQ7614 | Human | 117854 | Details Get a Quote |
| EDA Knockout HCT 116 Cell Line | EDJ-KQ18942 | Human | 1896 | Details Get a Quote |
| BCL3 Knockout A-549 Cell Line | EDJ-KQ21066 | Human | 602 | Details Get a Quote |
| BCL3 Knockout HeLa Cell Line | EDJ-KQ21068 | Human | 602 | Details Get a Quote |
| EZR Knockout A-549 Cell Line | EDJ-KQ25070 | Human | 7430 | Details Get a Quote |
| EZR Knockout HCT 116 Cell Line | EDJ-KQ25071 | Human | 7430 | Details Get a Quote |
| EZR Knockout HeLa Cell Line | EDJ-KQ25072 | Human | 7430 | Details Get a Quote |
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Frequently Asked Questions About regulation of non-canonical NF-kappaB signal transduction
What is GO:1901222?
GO:1901222 is the Gene Ontology term for regulation of non-canonical NF-kappaB signal transduction, describing any process that modulates the frequency, rate or extent of the non-canonical NF-kappaB cascade.
What genes are involved in regulation of non-canonical NF-kappaB signal transduction?
Key genes include NIK (MAP3K14), TRAF3, TRAF2, cIAP1/2, IKKalpha (CHUK), NFKB2, RELB, LTBR, BAFFR, CD40, RANK, TBK1 and IFI35.
How is the non-canonical NF-kappaB pathway activated?
It is activated by TNF receptor superfamily ligands that trigger TRAF3 degradation, NIK stabilization, IKKalpha activation and p100 processing to p52.
What is the difference between canonical and non-canonical NF-kappaB signaling?
The canonical pathway relies on IKKbeta and IkappaBalpha degradation for rapid RelA nuclear import, whereas the non-canonical pathway depends on NIK, IKKalpha and p100 processing to generate RelB:p52 dimers.
Which diseases are linked to non-canonical NF-kappaB signaling?
It is linked to lymphoid malignancies, autoimmune and inflammatory diseases, glioblastoma and other solid tumors, as well as tissue regeneration contexts.
How can I study regulation of non-canonical NF-kappaB signaling in the lab?
Common approaches include knockout, point-mutation, knock-in and overexpression models combined with p100 processing assays, NF-kappaB reporters, RNA-seq and proteomics.
What is the role of NIK in non-canonical NF-kappaB signaling?
NIK is the central kinase that, upon stabilization, activates IKKalpha and drives p100 processing, making it a key regulatory node.
How does TRAF3 regulate non-canonical NF-kappaB signaling?
TRAF3 normally promotes NIK degradation; its ligand-induced degradation relieves this brake and allows pathway activation.
Can CRISPR be used to study non-canonical NF-kappaB signaling?
Yes, CRISPR knockout, point mutation, knock-in and overexpression models are widely used to dissect pathway regulators and their causal roles.
What readouts are used to measure non-canonical NF-kappaB activity?
Typical readouts include p100/p52 processing by western blot, phospho-IKKalpha levels, RelB nuclear translocation and NF-kappaB luciferase reporters.
Conclusion
GO:1901222, regulation of non-canonical NF-kappaB signal transduction, captures the diverse mechanisms that tune a central immune and inflammatory pathway. Its core logic revolves around NIK stabilization, IKKalpha activation and p100 processing to p52, with multiple positive and negative regulators setting the threshold and duration of signaling. Dysregulation of this pathway contributes to lymphoid malignancies, autoimmunity, chronic inflammation and tumor microenvironment remodeling, making it a high-value target for basic and translational research. Advances in CRISPR-based models, combined with phospho-protein assays, transcriptomics and single-cell/spatial methods, now allow researchers to dissect GO:1901222 with unprecedented precision. EDITGENE supports these efforts by providing knockout, point-mutation, knock-in, overexpression and CRISPR screening services tailored to non-canonical NF-kappaB research.
References
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- 2. Sun SC. 2011. Non-canonical NF-κB signaling pathway.. Cell Res 21(1):71-85 PMID: 21173796
- 3. Yu H et al.. 2020. Targeting NF-κB pathway for the therapy of diseases: mechanism and clinical study.. Signal Transduct Target Ther 5(1):209 PMID: 32958760
- 4. Li D et al.. 2024. IFI35 regulates non-canonical NF-κB signaling to maintain glioblastoma stem cells and recruit tumor-associated macrophages.. Cell Death Differ 31(6):738-752 PMID: 38594444
- 5. Conlon TM et al.. 2020. Inhibition of LTβR signalling activates WNT-induced regeneration in lung.. Nature 588(7836):151-156 PMID: 33149305
- 6. Chen C et al.. 2026. B cells disrupt tertiary lymphoid structure formation and suppress anti-tumor immunity.. Cancer Cell 44(3):551-566.e17 PMID: 41512868
- 7. Runde AP et al.. 2022. The role of TBK1 in cancer pathogenesis and anticancer immunity.. J Exp Clin Cancer Res 41(1):135 PMID: 35395857
- 8. Jenkins BH et al.. 2025. Single cell and spatial analysis of immune-hot and immune-cold tumours identifies fibroblast subtypes associated with distinct immunological niches and positive immunotherapy response.. Mol Cancer 24(1):3 PMID: 39757146
