GO:1903557 positive regulation of tumor necrosis factor superfamily cytokine production: Immune Signaling Pathway, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:1903557 describes any process that activates or increases the frequency, rate or extent of tumor necrosis factor superfamily cytokine production [1,2,3].
• The term covers positive regulation of ligands such as TNF, TRAIL, BAFF, APRIL, CD40L, TWEAK and other TNFSF cytokines [1,2,3,6,8].
• TNFSF cytokine production is induced by diverse stimuli including viral infection, inflammatory cytokines and immune receptor engagement [1,2,3,6].
• Dysregulated positive regulation of TNFSF cytokines contributes to autoimmune, inflammatory, cardiovascular and infectious disease pathology [1,4,5,7].
• Key regulatory nodes include NF-kB signaling, CD40L, BAFF/APRIL receptors TACI and BCMA, and TRAIL receptor down-modulation [2,3,6,8].
• CRISPR knockout, knock-in, point-mutation and overexpression models enable causal dissection of TNFSF cytokine regulatory networks [2,5,8].
Description
GO:1903557, positive regulation of tumor necrosis factor superfamily cytokine production, is a Gene Ontology biological process term that captures any process which activates or increases the frequency, rate or extent of tumor necrosis factor superfamily (TNFSF) cytokine production [1,2,3]. TNFSF cytokines are a structurally related family of ligands that includes TNF, TRAIL, BAFF, APRIL, CD40L, TWEAK and others, and they control immune cell survival, activation, apoptosis and inflammation [1,2,3,6,8]. Because these cytokines are potent, their production must be tightly regulated; the positive regulation arm of this control is what GO:1903557 formally describes [1,2,3]. Researchers study GO:1903557 because inappropriate amplification of TNFSF cytokine production is a shared feature of many human diseases. In Graves' orbital fibroblasts, TWEAK induces inflammatory cytokine production, linking TNFSF signaling to autoimmune orbital inflammation. Epstein-Barr virus latent membrane protein 2A modulates production of BAFF and APRIL, demonstrating pathogen-driven positive regulation of TNFSF cytokines. CD40L and other TNFSF ligands have expanded roles in HIV infection, showing that this process is relevant to viral pathogenesis. In heart failure, multimarker profiling has identified both protective and harmful immune processes involving TNFSF cytokines. Understanding GO:1903557 therefore requires integrating receptor-proximal signaling, transcriptional control and post-transcriptional regulation. Genetic association studies such as the analysis of the -863C/A polymorphism in the TNF gene in rheumatoid arthritis illustrate how researchers attempt to link TNFSF regulatory variation to disease, even when associations are not confirmed. Mechanistic work on NF-kB regulation by coilin in preeclampsia shows that positive regulation of inflammatory cytokine production can be controlled by nuclear factors. Together, these studies define GO:1903557 as a central node in immune and inflammatory biology [1,2,3,4,5,6,7,8].
positive regulation of tumor necrosis factor superfamily cytokine production At A Glance
| GO ID | GO:1903557 |
|---|---|
| GO term | positive regulation of tumor necrosis factor superfamily cytokine production |
| Ontology | biological_process |
| Definition | Any process that activates or increases the frequency, rate or extent of tumor necrosis factor superfamily cytokine production. |
| Synonym | activation of TNFSF cytokine production; activation of TNF superfamily production; positive regulation of TNFSF cytokine production; upregulation of tumor necrosis factor superfamily cytokine production |
| Major function | Amplifies production of TNFSF ligands such as TNF, TRAIL, BAFF, APRIL, CD40L and TWEAK during immune and inflammatory responses [1,2,3,6,8]. |
| Representative inducers | TWEAK, Epstein-Barr virus LMP2A, CD40L, human herpesvirus 7, inflammatory cytokines [1,2,3,6]. |
| Key regulatory nodes | NF-kB signaling, BAFF/APRIL receptors TACI and BCMA, TRAIL-R1 down-modulation [2,5,6,8]. |
| Disease relevance | Autoimmunity, viral infection, cardiovascular disease, pregnancy disorders [1,2,3,4,5,7]. |
What Is GO:1903557?
GO:1903557 is defined as any process that activates or increases the frequency, rate or extent of tumor necrosis factor superfamily cytokine production [1,2,3]. In practical terms, it is the positive regulatory arm of TNFSF cytokine biosynthesis and release: it includes signals that turn on transcription of TNFSF ligand genes, stabilize their mRNAs, promote translation, or enhance secretion of the mature cytokines [1,2,3,6]. It is distinct from the production process itself and from negative regulation; GO:1903557 specifically captures the activating or amplifying inputs [1,2,3].
Why Is positive regulation of tumor necrosis factor superfamily cytokine production Important in Cell Biology?
GO:1903557 is important because TNFSF cytokines are among the most potent mediators of immune activation, inflammation and cell death, and their overproduction drives tissue damage in autoimmune, infectious and cardiovascular disease [1,2,3,5,7]. Defining the positive regulatory inputs that increase TNFSF cytokine production provides mechanistic targets for therapeutic intervention and biomarkers of immune dysregulation [1,2,3,7].
• TNFSF cytokines including TNF, TRAIL, BAFF, APRIL and CD40L control immune cell survival, activation and apoptosis [1,2,3,6,8].
• Positive regulation of TNFSF cytokine production is induced by viral pathogens such as Epstein-Barr virus and human herpesvirus 7 [2,6].
• TWEAK drives inflammatory cytokine production in Graves' orbital fibroblasts, linking GO:1903557 to autoimmune eye disease.
• CD40L and other TNFSF ligands have expanded roles in HIV infection and immune pathogenesis.
• BAFF and APRIL production is modulated by EBV LMP2A and signals through TACI and BCMA receptors [2,8].
• NF-kB signaling is a central regulatory node for positive regulation of inflammatory cytokine production.
• Multimarker profiling in heart failure identifies protective and harmful immune processes involving TNFSF cytokines.
• Genetic variants in TNFSF cytokine genes, such as TNF -863C/A, are studied as risk modifiers in rheumatoid arthritis.
• TRAIL up-regulation coupled to TRAIL-R1 down-modulation illustrates layered positive regulation in CD4+ T cells.
• CRISPR-based models enable causal testing of candidate regulators of TNFSF cytokine production [2,5,8].
What Happens During positive regulation of tumor necrosis factor superfamily cytokine production?
Induction by extracellular and pathogen-derived stimuli
In simple terms: Outside signals tell immune cells to make more TNFSF cytokines.
Positive regulation of TNFSF cytokine production begins when extracellular stimuli engage receptors on immune and stromal cells. TWEAK induces inflammatory cytokine production in Graves' orbital fibroblasts, demonstrating that a TNFSF ligand can itself amplify TNFSF cytokine output. Epstein-Barr virus latent membrane protein 2A modulates production of BAFF and APRIL, showing that viral proteins can act as positive regulators. Human herpesvirus 7 induces functional up-regulation of TRAIL in CD4+ T cells, providing another pathogen-driven example. CD40L and other TNFSF ligands have expanded roles in HIV infection, further illustrating how infection can drive this process.
Transcriptional activation of TNFSF cytokine genes
In simple terms: The cell switches on the genes that encode TNFSF cytokines.
Once cells receive inductive signals, transcription factors are activated to increase expression of TNFSF cytokine genes. NF-kB is a key mediator of inflammatory cytokine gene transcription, and coilin has been identified as a regulator of NF-kB mediated inflammation in preeclampsia. This transcriptional step is a core component of GO:1903557 because it directly increases the rate of TNFSF cytokine production. The diversity of TNFSF ligands, including TNF, TRAIL, BAFF, APRIL and CD40L, means that multiple gene loci can be coordinately activated [1,2,3,6,8].
Post-transcriptional and post-translational amplification
In simple terms: After the gene is switched on, the cell fine-tunes how much cytokine is made and released.
Positive regulation also occurs after transcription. Human herpesvirus 7 induces functional up-regulation of TRAIL coupled to TRAIL-R1 down-modulation in CD4+ T cells, indicating that ligand production and receptor availability are coordinately regulated. BAFF and APRIL production is modulated by EBV LMP2A, and their receptors TACI and BCMA have unappreciated biochemical and biological properties that influence ligand availability and signaling [2,8]. These layers ensure that TNFSF cytokine output matches the intensity and duration of the inducing stimulus [2,6,8].
Receptor-mediated feedback and modulation
In simple terms: Receptors for TNFSF cytokines can feed back to adjust how much cytokine is produced.
TNFSF cytokine production is modulated by the receptors that sense these ligands. TACI, an enigmatic BAFF/APRIL receptor, has new unappreciated biochemical and biological properties that affect BAFF and APRIL biology. TRAIL-R1 down-modulation accompanies TRAIL up-regulation in HHV-7-infected CD4+ T cells, illustrating receptor-level feedback. In heart failure, multimarker profiling identifies protective and harmful immune processes in which TNFSF cytokines participate, suggesting that systemic feedback loops shape net production. These receptor interactions are integral to the positive regulation described by GO:1903557 [6,7,8].
Integration with systemic immune and inflammatory states
In simple terms: The whole body's immune state influences how much TNFSF cytokine is made.
Positive regulation of TNFSF cytokine production is not cell-autonomous; it is shaped by systemic immune status. In heart failure, multimarker profiling identifies protective and harmful immune processes involving TNFSF cytokines, indicating that chronic disease states can sustain or suppress production. In preeclampsia, coilin regulates NF-kB mediated inflammation, linking pregnancy-associated systemic inflammation to cytokine production. In rheumatoid arthritis, the TNF -863C/A polymorphism has been studied as a potential modifier of TNF biology, although no association was confirmed in that cohort. These examples show that GO:1903557 operates within broader physiological and pathological contexts [4,5,7].
Key Genes Involved in GO:1903557 positive regulation of tumor necrosis factor superfamily cytokine production
The following genes and proteins are experimentally implicated in positive regulation of TNFSF cytokine production or in the biology of the TNFSF ligands whose production is regulated.
| Gene | Major Role | Research Relevance |
|---|---|---|
| TNF | Prototypical TNFSF cytokine; its production is positively regulated in inflammation | Target for polymorphism studies in rheumatoid arthritis and inflammatory disease models |
| TNFSF12 (TWEAK) | TNFSF ligand that induces inflammatory cytokine production in Graves' orbital fibroblasts | Model for ligand-driven amplification of TNFSF cytokine output |
| TNFSF13B (BAFF) | B-cell activating factor of the TNF family; production modulated by EBV LMP2A | Target for B-cell autoimmunity and viral pathogenesis studies [2,8] |
| TNFSF13 (APRIL) | TNFSF ligand whose production is modulated by EBV LMP2A | Studied with BAFF in B-cell survival and receptor interaction models [2,8] |
| CD40LG (CD40L) | TNFSF ligand with expanded roles in HIV infection | Model for T-cell-dependent amplification of TNFSF cytokine production |
| TNFSF10 (TRAIL) | TNFSF cytokine up-regulated by human herpesvirus 7 in CD4+ T cells | Model for pathogen-induced positive regulation coupled to receptor down-modulation |
| TNFRSF13B (TACI) | BAFF/APRIL receptor with unappreciated biochemical and biological properties | Target for dissecting receptor feedback on TNFSF cytokine production |
| TNFRSF17 (BCMA) | BAFF/APRIL receptor involved in plasma cell biology | Studied alongside TACI for BAFF/APRIL axis regulation |
| TNFRSF10A (TRAIL-R1) | Receptor down-modulated when TRAIL is up-regulated by HHV-7 | Model for coordinated ligand-receptor regulation |
| NFKB1 | NF-kB subunit mediating inflammatory cytokine gene transcription | Central node for positive regulation of TNFSF cytokine production |
| RELA | NF-kB subunit involved in inflammatory gene activation | Target for dissecting NF-kB-dependent TNFSF cytokine induction |
| COIL (coilin) | Regulator of NF-kB mediated inflammation in preeclampsia | Model for nuclear regulation of inflammatory cytokine production |
| LMP2A (EBV) | Viral protein modulating BAFF and APRIL production | Pathogen-derived positive regulator in B-cell models |
| HHV-7 | Virus inducing functional TRAIL up-regulation in CD4+ T cells | Model for infection-driven TNFSF cytokine production |
| HIV | Infection context in which CD40L and other TNFSF ligands have expanded roles | Model for chronic immune activation and TNFSF cytokine production |
| TWEAK receptor (TNFRSF12A) | Mediates TWEAK-induced inflammatory cytokine production | Target for blocking ligand-driven inflammation in orbital fibroblasts |
| TNF -863C/A polymorphism | Genetic variant studied for association with rheumatoid arthritis | Model for human genetic variation in TNFSF cytokine regulation |
| Multimarker immune panel (BIOSTAT-CHF) | Identifies protective and harmful immune processes involving TNFSF cytokines | Model for systems-level analysis of TNFSF cytokine regulation in heart failure |
How Is positive regulation of tumor necrosis factor superfamily cytokine production Regulated?
Positive regulation of TNFSF cytokine production is controlled at multiple levels. NF-kB signaling is a central transcriptional node, and coilin has been identified as a regulator of NF-kB mediated inflammation in preeclampsia. Receptor-proximal feedback also shapes output: TRAIL up-regulation is coupled to TRAIL-R1 down-modulation in HHV-7-infected CD4+ T cells, and TACI has unappreciated biochemical and biological properties that influence BAFF/APRIL biology. Viral proteins such as EBV LMP2A can directly modulate BAFF and APRIL production. Systemic disease states, including heart failure, are associated with protective and harmful immune processes involving TNFSF cytokines, indicating that chronic inflammatory milieus can sustain or restrain production. Genetic variation, such as the TNF -863C/A polymorphism, has been studied as a potential modifier, although association with rheumatoid arthritis was not confirmed.
positive regulation of tumor necrosis factor superfamily cytokine production and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| TNFSF12 (TWEAK) | Graves' orbital inflammation | Knockout of TNFSF12 in orbital fibroblast cultures |
| TNFSF13B (BAFF) | EBV-associated B-cell biology and autoimmunity [2,8] | Knock-in of LMP2A-responsive BAFF promoter reporters |
| TNFSF10 (TRAIL) | HHV-7 infection and CD4+ T cell regulation | Overexpression of TRAIL with TRAIL-R1 knockout |
| CD40LG (CD40L) | HIV-associated immune activation | Point mutation of CD40L signaling motifs in T cell lines |
| COIL (coilin) | Preeclampsia and NF-kB inflammation | Knockout of COIL in trophoblast models |
Autoimmune and inflammatory disease
Positive regulation of TNFSF cytokine production is directly implicated in autoimmune and inflammatory pathology. TWEAK induces inflammation in Graves' orbital fibroblasts, linking this GO term to thyroid eye disease. The TNF -863C/A polymorphism has been evaluated as a risk modifier in rheumatoid arthritis, although no association was found in the studied cohort, highlighting the complexity of genetic regulation. BAFF and APRIL, whose production is modulated by EBV LMP2A, are central to B-cell autoimmunity and are targeted in clinical practice [2,8]. These examples show that GO:1903557 is a mechanistic axis in autoimmune disease [1,2,4,8].
Viral infection and immune activation
Viral pathogens are potent positive regulators of TNFSF cytokine production. Epstein-Barr virus latent membrane protein 2A modulates BAFF and APRIL production, potentially shaping B-cell survival during infection. Human herpesvirus 7 induces functional up-regulation of TRAIL coupled to TRAIL-R1 down-modulation in CD4+ T cells. CD40L and other TNFSF ligands have expanded roles in HIV infection, contributing to chronic immune activation. Together, these studies establish infection-driven positive regulation of TNFSF cytokines as a recurring theme [2,3,6].
Cardiovascular and pregnancy-related disorders
Systemic immune processes involving TNFSF cytokines are associated with cardiovascular and pregnancy-related disorders. In heart failure, multimarker profiling identifies protective and harmful immune processes, including TNFSF cytokine signatures. In preeclampsia, coilin regulates NF-kB mediated inflammation, providing a nuclear mechanism for positive regulation of inflammatory cytokine production. These findings link GO:1903557 to disorders beyond classical autoimmunity [5,7].
From positive regulation of tumor necrosis factor superfamily cytokine production-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is a candidate gene required for TNFSF cytokine production? | CRISPR knockout in immune or stromal cell lines [2,5] |
| Does a specific variant alter TNFSF cytokine output? | Point-mutation knock-in of the variant allele |
| Can a viral protein drive TNFSF cytokine production? | Knock-in or overexpression of EBV LMP2A |
| Does tagging a TNFSF ligand affect its trafficking? | Tagged knock-in of TNF, TRAIL or BAFF [6,8] |
| Does overexpression of a regulator amplify cytokine production? | Overexpression of NF-kB subunits or coilin |
| Can receptor feedback be uncoupled from ligand production? | Knockout of TRAIL-R1 or TACI [6,8] |
How to Study the positive regulation of tumor necrosis factor superfamily cytokine production Process
| Method | What It Measures | Typical Application |
|---|---|---|
| RNA-seq | Transcript levels of TNFSF cytokine genes | Quantifying positive regulation after stimulation [1,2] |
| Multiplex immunoassay | Secreted TNFSF cytokine protein levels | Profiling BAFF, APRIL, TNF and TRAIL in patient samples [2,7] |
| Flow cytometry | Surface and intracellular TNFSF ligands and receptors | Studying TRAIL/TRAIL-R1 coordination |
| CRISPR knockout | Requirement of a gene for cytokine production | Testing COIL or receptor dependence [5,8] |
| CRISPR knock-in | Effect of a specific variant or tag | Modeling TNF -863C/A or LMP2A expression [2,4] |
| Overexpression | Sufficiency of a regulator to increase production | Testing NF-kB subunit or coilin sufficiency |
| Genetic association | Link between polymorphism and disease | TNF -863C/A in rheumatoid arthritis |
| Systems multimarker profiling | Immune process signatures in cohorts | Heart failure immune phenotyping |
Transcriptional and cytokine profiling
RNA-seq and targeted cytokine assays measure changes in TNFSF cytokine gene expression and secreted protein levels after genetic or environmental perturbation. These methods are used to quantify positive regulation of TNFSF cytokine production in models such as TWEAK-treated orbital fibroblasts and EBV LMP2A-expressing B cells. Multiplex immunoassays enable simultaneous measurement of multiple TNFSF ligands, as illustrated by multimarker profiling in heart failure.
CRISPR-based perturbation
CRISPR knockout, knock-in and point-mutation models allow causal testing of candidate regulators. Knockout of COIL can test its role in NF-kB mediated inflammatory cytokine production, while knock-in of viral or human variants can test allele-specific effects on BAFF, APRIL or TRAIL production [2,6]. These approaches are essential for moving from correlation to causation in GO:1903557 research [2,5,6].
Flow cytometry and receptor analysis
Flow cytometry measures intracellular and surface TNFSF ligands and their receptors. This is particularly useful for studying coordinated regulation, such as TRAIL up-regulation with TRAIL-R1 down-modulation in CD4+ T cells. Receptor profiling for TACI and BCMA can reveal how BAFF/APRIL sensing feeds back on ligand production.
Genetic association and systems immunology
Genetic association studies test whether polymorphisms in TNFSF cytokine genes modify disease risk, as exemplified by the TNF -863C/A analysis in rheumatoid arthritis. Systems immunology approaches, such as multimarker profiling in heart failure cohorts, identify protective and harmful immune processes involving TNFSF cytokines. Combining these methods with functional CRISPR validation provides a robust framework for GO:1903557 research [4,5,7].
How CRISPR Can Be Used to Study GO:1903557 positive regulation of tumor necrosis factor superfamily cytokine production
Knockout
CRISPR knockout is used to test whether a candidate gene is required for positive regulation of TNFSF cytokine production. For example, knocking out COIL can determine its requirement for NF-kB mediated inflammatory cytokine production in preeclampsia models. Knocking out TACI or BCMA can reveal receptor-specific feedback on BAFF/APRIL production. Knockout of TRAIL-R1 can uncouple ligand production from receptor-mediated feedback.
Point Mutation
Point-mutation knock-in allows precise testing of variants such as the TNF -863C/A polymorphism in the context of endogenous regulation. This approach can determine whether a specific nucleotide change alters the rate of TNFSF cytokine production. Point mutations in signaling motifs of CD40L or viral proteins such as LMP2A can also be introduced to map regulatory domains [2,3].
Knock-in
Knock-in of reporters, tags or viral genes enables quantitative and spatial analysis of TNFSF cytokine production. Tagged knock-in of TNF, TRAIL or BAFF allows tracking of ligand trafficking and secretion [6,8]. Knock-in of EBV LMP2A into B-cell lines can model pathogen-driven BAFF and APRIL production. Knock-in of human variants into mouse models can test their impact on immune activation.
Overexpression
Overexpression models test sufficiency of a regulator to increase TNFSF cytokine production. Overexpressing NF-kB subunits or coilin can amplify inflammatory cytokine output and validate positive regulatory mechanisms. Overexpressing TWEAK or TRAIL can drive autocrine or paracrine TNFSF cytokine production in target cells [1,6]. These models complement knockout studies by establishing sufficiency [1,5,6].
How EDITGENE Supports positive regulation of tumor necrosis factor superfamily cytokine production Research
Researchers studying positive regulation of tumor necrosis factor superfamily cytokine production-related genes often need to determine whether a candidate gene is causally involved in amplifying TNFSF cytokine output, or whether it merely correlates with inflammatory states. EDITGENE provides publication-ready CRISPR cell models and screening services to answer these questions with rigor.
Contact EDITGENE today to design your custom CRISPR model for positive regulation of tumor necrosis factor superfamily cytokine production research.
Frequently Asked Questions About positive regulation of tumor necrosis factor superfamily cytokine production
What is GO:1903557?
GO:1903557 is the Gene Ontology term for positive regulation of tumor necrosis factor superfamily cytokine production, defined as any process that activates or increases the frequency, rate or extent of TNFSF cytokine production [1,2,3].
What genes are involved in positive regulation of tumor necrosis factor superfamily cytokine production?
Genes and proteins implicated include TNF, TNFSF12 (TWEAK), TNFSF13B (BAFF), TNFSF13 (APRIL), CD40LG, TNFSF10 (TRAIL), TACI, BCMA, NF-kB subunits and coilin [1,2,3,4,5,6,8].
Which cytokines belong to the tumor necrosis factor superfamily?
The TNFSF includes TNF, TRAIL, BAFF, APRIL, CD40L, TWEAK and other structurally related ligands that control immune activation and apoptosis [1,2,3,6,8].
How is TNFSF cytokine production positively regulated?
Positive regulation occurs through receptor-proximal signals, NF-kB-dependent transcription, post-transcriptional amplification and receptor feedback, as shown in TWEAK, EBV LMP2A and HHV-7 models [1,2,5,6].
What diseases are linked to GO:1903557?
Diseases linked to this process include Graves' orbital inflammation, EBV- and HIV-associated immune activation, rheumatoid arthritis, preeclampsia and heart failure [1,2,3,4,5,7].
How do viruses increase TNFSF cytokine production?
Epstein-Barr virus LMP2A modulates BAFF and APRIL production, and human herpesvirus 7 induces TRAIL up-regulation in CD4+ T cells [2,6].
What is the role of NF-kB in TNFSF cytokine production?
NF-kB is a central transcriptional mediator of inflammatory cytokine gene expression, and coilin has been identified as a regulator of NF-kB mediated inflammation.
How can CRISPR be used to study GO:1903557?
CRISPR knockout tests requirement, point mutation tests variant effects, knock-in enables tagging and reporter analysis, and overexpression tests sufficiency of candidate regulators [2,4,5,6,8].
What is the relationship between BAFF, APRIL and TACI?
BAFF and APRIL are TNFSF cytokines whose production is modulated by EBV LMP2A, and TACI is a receptor with unappreciated biochemical and biological properties that influence their biology [2,8].
Why is positive regulation of TNFSF cytokine production important in heart failure?
Multimarker profiling in heart failure identifies protective and harmful immune processes involving TNFSF cytokines, indicating that this regulation contributes to disease progression.
Conclusion
GO:1903557, positive regulation of tumor necrosis factor superfamily cytokine production, is a central biological process that amplifies the output of potent immune mediators including TNF, TRAIL, BAFF, APRIL, CD40L and TWEAK [1,2,3,6,8]. Experimental evidence from viral infection, autoimmune inflammation, pregnancy disorders and heart failure demonstrates that this process is both inducible and tightly feedback-regulated [1,2,3,5,6,7]. Understanding its mechanisms offers therapeutic opportunities and biomarker potential across immune-mediated diseases [1,2,4,5,7]. CRISPR-based knockout, point-mutation, knock-in and overexpression models provide the causal evidence needed to move from association to mechanism in GO:1903557 research [2,4,5,6,8]. EDITGENE supports these efforts with publication-ready cell models, library screening and bioinformatics services tailored to TNFSF cytokine biology.
References
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- 3. Kornbluth RS. 2002. An expanding role for CD40L and other tumor necrosis factor superfamily ligands in HIV infection.. J Hematother Stem Cell Res 11(5):787-801 PMID: 12427285
- 4. Sadaf T et al.. 2019. Lack of association of -863C/A (rs1800630) polymorphism of tumor necrosis factor-a gene with rheumatoid arthritis.. Arch Med Sci 15(2):531-536 PMID: 30899307
- 5. Logan MK et al.. 2022. Coilin as a regulator of NF-kB mediated inflammation in preeclampsia.. Biol Open 11(7) PMID: 35762874
- 6. Secchiero P et al.. 2001. Human herpesvirus 7 induces the functional up-regulation of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) coupled to TRAIL-R1 down-modulation in CD4(+) T cells.. Blood 98(8):2474-81 PMID: 11588045
- 7. Markousis-Mavrogenis G et al.. 2022. Multimarker profiling identifies protective and harmful immune processes in heart failure: findings from BIOSTAT-CHF.. Cardiovasc Res 118(8):1964-1977 PMID: 34264317
- 8. Mackay F et al.. 2008. TACI, an enigmatic BAFF/APRIL receptor, with new unappreciated biochemical and biological properties.. Cytokine Growth Factor Rev 19(3-4):263-76 PMID: 18514565
