GO:0071635 negative regulation of transforming growth factor beta production: Regulatory Mechanism, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0071635 describes any process that stops, prevents, or reduces the frequency, rate, or extent of production of transforming growth factor-beta (TGF-beta).
• TGF-beta is a pleiotropic cytokine whose overproduction drives fibrosis, immune evasion, and tumor progression, making its negative regulation a central therapeutic node [3,5].
• AMPK activation is a well-documented negative regulator of TGF-beta production and signaling, linking cellular energy status to fibrotic and inflammatory programs.
• Interleukin-12 (IL-12) suppresses TGF-beta production, providing an immunological brake on TGF-beta-mediated immune suppression.
• Dysregulated negative regulation of TGF-beta production contributes to idiopathic pulmonary fibrosis, atherosclerosis, glioblastoma, and chronic inflammatory disorders [1,5,7].
• CRISPR knockout, point-mutation, knock-in, and overexpression models are essential to dissect causal roles of candidate regulators within GO:0071635 [3,8].
Description
Transforming growth factor-beta (TGF-beta) is a multifunctional cytokine that controls cell proliferation, differentiation, apoptosis, immune surveillance, and extracellular matrix remodeling [3,6]. Because excessive or sustained TGF-beta production underlies a broad spectrum of pathological states, cells have evolved dedicated mechanisms to restrain its synthesis and secretion. The Gene Ontology term GO:0071635, negative regulation of transforming growth factor beta production, captures any biological process that stops, prevents, or reduces the frequency, rate, or extent of TGF-beta production. This term is distinct from negative regulation of TGF-beta signaling; it specifically concerns the upstream events that limit the amount of mature TGF-beta available for receptor engagement [3,8]. Researchers study GO:0071635 because TGF-beta overproduction is a common denominator in fibrosis, cancer, and immune dysfunction [1,5,7]. For example, in idiopathic pulmonary fibrosis, persistent TGF-beta release from alveolar epithelial cells and macrophages drives fibroblast activation and collagen deposition, and strategies that reduce TGF-beta production attenuate disease in preclinical models. In glioblastoma, TGF-beta superfamily signaling promotes stemness and immune evasion, and negative regulators of its production are considered candidate therapeutic entry points. In atherosclerosis, the balance between atherogenic and atheroprotective TGF-beta effects is tightly linked to local production rates. Mechanistically, negative regulation of TGF-beta production can occur at transcriptional, post-transcriptional, and secretory levels. AMPK activation reduces TGF-beta production and downstream signaling, coupling metabolic stress to anti-fibrotic and anti-inflammatory outcomes. Interleukin-12 (IL-12) suppresses TGF-beta production in immune cells, illustrating cytokine cross-talk that limits TGF-beta-driven tolerance. Additional layers of control involve prostaglandin-dependent pathways and redox-sensitive transcription factors such as Nrf2 [1,2]. Understanding these layers requires precise genetic models, which is why CRISPR-based knockout, point-mutation, knock-in, and overexpression platforms are increasingly used to interrogate GO:0071635 [3,8].
negative regulation of transforming growth factor beta production At A Glance
| GO ID | GO:0071635 |
|---|---|
| GO term | negative regulation of transforming growth factor beta production |
| Ontology | biological_process |
| Synonym | negative regulation of TGF-beta production; negative regulation of TGFbeta production; negative regulation of TGF-B production; negative regulation of TGFB production; negative regulation of transforming growth factor-beta secretion |
| Major function | Reduces the frequency, rate, or extent of TGF-beta production, limiting the amount of bioactive TGF-beta available for downstream signaling. |
| Biological context | Operates in fibrosis, cancer, immune regulation, and cardiovascular biology where TGF-beta overproduction is pathogenic [1,5,7]. |
| Key regulatory inputs | AMPK activation, IL-12 signaling, prostaglandin/COX-2 pathways, and redox-sensitive transcription factors such as Nrf2 [1,2,3,8]. |
| Representative cell types | Fibroblasts, macrophages, alveolar epithelial cells, glioblastoma cells, and vascular cells [1,2,5,7]. |
| Therapeutic relevance | Enhancing negative regulation of TGF-beta production is a strategy to attenuate fibrosis, tumor progression, and chronic inflammation [1,3,5]. |
What Is GO:0071635?
GO:0071635 (negative regulation of transforming growth factor beta production) is a biological process term defined as any process that stops, prevents, or reduces the frequency, rate, or extent of production of transforming growth factor-beta. It encompasses molecular events that lower the synthesis, processing, or secretion of TGF-beta ligands, thereby reducing the amount of bioactive TGF-beta available to bind cell-surface receptors. The term is not limited to a single cell type or stimulus; it applies whenever a regulatory input diminishes TGF-beta output relative to a baseline state [3,8].
Why Is negative regulation of transforming growth factor beta production Important in Cell Biology?
GO:0071635 is important because TGF-beta is one of the most potent drivers of fibrosis, immune suppression, and tumor progression, and its production must be tightly restrained to maintain tissue homeostasis [3,5,7]. When negative regulatory mechanisms fail, sustained TGF-beta output promotes extracellular matrix deposition, epithelial-to-mesenchymal transition, and immune evasion, contributing to diseases such as idiopathic pulmonary fibrosis, glioblastoma, and atherosclerosis [1,5,7]. Conversely, augmenting negative regulation of TGF-beta production can reduce pathological fibrosis and restore anti-tumor immunity in preclinical models [1,3]. Thus, understanding the genes and pathways that execute GO:0071635 provides a rational basis for therapeutic intervention and for designing CRISPR-based experiments that test causality [3,8].
• TGF-beta overproduction is a hallmark of fibrotic diseases, including idiopathic pulmonary fibrosis, where reducing TGF-beta output attenuates fibroblast activation and collagen deposition.
• In glioblastoma, TGF-beta superfamily signaling promotes tumor initiation and progression, making negative regulators of TGF-beta production candidate therapeutic targets.
• Atherosclerosis involves interwoven atherogenic and atheroprotective TGF-beta effects, and local production rates influence plaque stability.
• IL-12-mediated suppression of TGF-beta production illustrates how immune cytokines can brake TGF-beta-driven tolerance.
• AMPK activation negatively regulates TGF-beta, linking metabolic stress and energy sensing to anti-fibrotic and anti-inflammatory outcomes.
• COX-2-dependent prostaglandin signaling modulates TGF-beta-dependent gene expression in fibroblasts, revealing intersection between inflammatory and fibrotic pathways.
• Redox-sensitive Nrf2 signaling can reduce TGF-beta-driven pathology, as shown in ROS-responsive drug delivery models for pulmonary fibrosis.
• Dysregulated TGF-beta production contributes to impaired immune surveillance in chronic infections and cancer.
• Negative regulation of TGF-beta production is relevant to megakaryocytopoiesis and hematopoietic regulation, where TGF-beta is a key cytokine.
• CRISPR-based genetic models enable causal testing of candidate negative regulators within GO:0071635 [3,8].
What Happens During negative regulation of transforming growth factor beta production?
Integration of Negative Regulatory Signals at the TGF-beta Locus
In simple terms: Cells receive signals that tell them to make less TGF-beta.
Negative regulation of TGF-beta production begins when extracellular or intracellular cues activate transcription factors and signaling cascades that repress TGF-beta gene expression or processing. AMPK activation is a well-characterized example: it reduces TGF-beta production and downstream signaling, coupling energy stress to diminished TGF-beta output. IL-12 provides an immunological signal that suppresses TGF-beta production in immune cells, demonstrating cytokine-mediated negative control. These inputs converge on the TGF-beta promoter and enhancer regions, as well as on post-transcriptional machinery, to lower the steady-state level of TGF-beta mRNA and protein [3,8].
Transcriptional and Post-Transcriptional Repression of TGF-beta Synthesis
In simple terms: The cell turns down the instructions for making TGF-beta.
Once negative regulatory signals are integrated, transcriptional repressors and co-repressor complexes reduce TGF-beta gene transcription. Post-transcriptional mechanisms, including mRNA destabilization and translational inhibition, further decrease TGF-beta protein synthesis. AMPK-dependent pathways have been shown to negatively regulate TGF-beta at these levels, contributing to reduced TGF-beta bioavailability. In fibroblasts, COX-2-dependent prostaglandin signaling modulates TGF-beta-dependent responses, indicating that inflammatory mediators can intersect with TGF-beta production control.
Regulation of TGF-beta Processing and Secretion
In simple terms: Even if some TGF-beta is made, the cell can limit how much is released.
TGF-beta is synthesized as a precursor that undergoes proteolytic processing and is secreted in a latent complex. Negative regulation of TGF-beta production includes mechanisms that reduce the efficiency of this processing or secretion, thereby lowering the amount of bioactive TGF-beta released. The GO synonym 'negative regulation of transforming growth factor-beta secretion' explicitly captures this secretory control. Redox-sensitive pathways, such as Nrf2 signaling, can influence the secretory and inflammatory milieu that governs TGF-beta release.
Feedback and Cross-Talk with Inflammatory and Metabolic Pathways
In simple terms: Other pathways can step in to keep TGF-beta levels in check.
Negative regulation of TGF-beta production is embedded in a network of feedback loops. IL-12 suppresses TGF-beta production, providing an immune-mediated brake that limits TGF-beta-driven tolerance. AMPK acts as a metabolic checkpoint that restrains TGF-beta production and signaling, with implications for treating associated disorders. In fibrotic lung disease, Nrf2 activation via ROS-responsive nanoplatforms reduces TGF-beta-related pathology, illustrating redox-inflammatory cross-talk. These interconnected pathways ensure that TGF-beta production is tuned to the physiological state of the cell and tissue [1,3,8].
Cell-Type-Specific Execution of Negative Regulation
In simple terms: Different cells use different tools to reduce TGF-beta.
The mechanisms executing GO:0071635 vary by cell type. In fibroblasts, COX-2 and prostaglandin pathways modulate TGF-beta-dependent responses. In immune cells, IL-12 drives suppression of TGF-beta production. In alveolar epithelial cells and macrophages during pulmonary fibrosis, Nrf2-linked antioxidant responses reduce TGF-beta-driven injury. In glioblastoma cells, TGF-beta superfamily signaling is context-dependent, and negative regulators may be overridden during tumor progression. This cell-type specificity means that experimental models must match the biological context to accurately study GO:0071635 [1,2,5,8].
Key Genes Involved in GO:0071635 negative regulation of transforming growth factor beta production
The following genes and proteins are experimentally implicated in negative regulation of TGF-beta production or in the broader control of TGF-beta bioavailability, based on the verified literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| PRKAA1/AMPK | Energy sensor that negatively regulates TGF-beta production and signaling | Target for anti-fibrotic and anti-inflammatory interventions; AMPK activation reduces TGF-beta output |
| IL12A/IL-12 | Cytokine that suppresses TGF-beta production in immune cells | Provides an immunological brake on TGF-beta-mediated tolerance; relevant to infection and cancer immunity |
| PTGS2/COX-2 | Modulates TGF-beta-dependent gene expression in fibroblasts | Links prostaglandin signaling to TGF-beta production control; relevant to fibrosis and inflammation |
| NFE2L2/Nrf2 | Redox-sensitive transcription factor that reduces TGF-beta-driven pathology | Targeted by ROS-responsive drug delivery in pulmonary fibrosis models |
| TGFB1 | Major TGF-beta isoform whose production is the target of negative regulation | Central ligand in fibrosis, cancer, and immune regulation; production must be tightly controlled [3,5] |
| TGFB2 | TGF-beta isoform contributing to TGF-beta superfamily signaling | Implicated in glioblastoma initiation and progression; negative regulation is context-dependent |
| TGFB3 | TGF-beta isoform with context-dependent roles | Part of the TGF-beta superfamily involved in tumor and developmental biology |
| TGFBR1 | Type I TGF-beta receptor mediating downstream signaling | Receptor-level control intersects with production-level negative regulation |
| TGFBR2 | Type II TGF-beta receptor that binds TGF-beta ligands | Defines cellular responsiveness to TGF-beta; relevant to feedback regulation |
| SMAD2 | Downstream effector of TGF-beta signaling | Mediates transcriptional responses that can feed back on TGF-beta production |
| SMAD3 | Downstream effector of TGF-beta signaling | Participates in feedback loops controlling TGF-beta output |
| SMAD4 | Common SMAD co-mediator of TGF-beta signaling | Central node in TGF-beta transcriptional responses |
| IFNG | Interferon-gamma, an immune cytokine that counter-regulates TGF-beta | Modulates immune responses by opposing TGF-beta-mediated suppression |
| IL10 | Anti-inflammatory cytokine that intersects with TGF-beta regulation | Part of the cytokine network controlling TGF-beta production and immune tolerance |
| CD36 | Scavenger receptor implicated in TGF-beta-related vascular biology | Relevant to atherosclerosis where TGF-beta has atherogenic and atheroprotective roles |
| MMP9 | Matrix metalloproteinase linked to TGF-beta activation and remodeling | Contributes to extracellular matrix turnover in atherosclerosis and fibrosis |
| PF4 | Platelet factor 4 involved in megakaryocytopoiesis regulation | TGF-beta is a key cytokine in megakaryocytopoiesis; PF4 illustrates hematopoietic context |
| THBS1 | Thrombospondin-1, a TGF-beta activator | Links platelet and matrix biology to TGF-beta bioavailability |
How Is negative regulation of transforming growth factor beta production Regulated?
Negative regulation of TGF-beta production is itself regulated by multiple upstream pathways. AMPK acts as a metabolic checkpoint: its activation reduces TGF-beta production and signaling, and this axis has therapeutic implications for fibrosis and related disorders. IL-12 provides an immune-mediated suppressive signal that lowers TGF-beta production. COX-2-dependent prostaglandin synthesis modulates TGF-beta-dependent responses in fibroblasts, indicating that inflammatory mediators can tune TGF-beta output. Redox-sensitive Nrf2 signaling reduces TGF-beta-driven pathology in pulmonary fibrosis models, linking oxidative stress responses to negative regulation of TGF-beta production. These regulatory inputs form a network that adjusts TGF-beta production according to metabolic, immune, and redox status [1,2,3,8].
negative regulation of transforming growth factor beta production and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| NFE2L2/Nrf2 | Idiopathic pulmonary fibrosis; redox-sensitive reduction of TGF-beta pathology | Lung fibroblast or alveolar epithelial cell lines with Nrf2 overexpression or knockout; bleomycin-induced fibrosis models |
| PRKAA1/AMPK | Fibrosis and metabolic disorders; AMPK negatively regulates TGF-beta | AMPK knockout or constitutively active knock-in in fibroblasts; TGF-beta production assays |
| IL12A/IL-12 | Immune regulation; IL-12 suppresses TGF-beta production | Immune cell lines or primary macrophages with IL-12 receptor knockout; cytokine production assays |
| PTGS2/COX-2 | Fibrosis and inflammation; COX-2 modulates TGF-beta responses | Fibroblast lines with COX-2 knockout or overexpression; prostaglandin and TGF-beta assays |
| TGFB1 | Glioblastoma and fibrosis; TGF-beta production drives pathology | Glioblastoma cell lines with TGFB1 knockout or overexpression; invasion and stemness assays |
Idiopathic Pulmonary Fibrosis
Idiopathic pulmonary fibrosis is characterized by excessive TGF-beta production and fibroblast activation. ROS-responsive liposomes delivering drugs via Nrf2 signaling reduce TGF-beta-related pathology in preclinical models, demonstrating that enhancing negative regulation of TGF-beta production can attenuate fibrosis. AMPK activation also negatively regulates TGF-beta and is considered a therapeutic strategy for fibrotic disorders.
Glioblastoma
In glioblastoma, TGF-beta superfamily signaling promotes tumor initiation and progression, and negative regulators of TGF-beta production may be overridden to sustain a pro-tumorigenic microenvironment. Targeting pathways that restore negative regulation of TGF-beta production is a potential strategy to limit glioblastoma stemness and immune evasion.
Atherosclerosis
TGF-beta has interwoven atherogenic and atheroprotective aspects in atherosclerosis, and local production rates influence plaque biology. Negative regulation of TGF-beta production is therefore context-dependent: too little TGF-beta can promote inflammation, while too much can drive fibrosis and matrix remodeling. Understanding these balances is essential for therapeutic targeting.
Immune Dysregulation and Chronic Inflammation
TGF-beta modulates the immune response and can promote tolerance and immune evasion. IL-12 suppresses TGF-beta production, providing an immunological counterweight. Dysregulated negative regulation of TGF-beta production can therefore contribute to chronic infections, autoimmunity, and tumor immune escape [6,8].
From negative regulation of transforming growth factor beta production-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of a candidate gene increase TGF-beta production? | CRISPR knockout of the candidate gene in a relevant cell line, followed by TGF-beta ELISA and qPCR |
| Does a specific point mutation in a regulator alter its ability to suppress TGF-beta? | CRISPR point-mutation knock-in of the mutation, followed by TGF-beta production assays |
| Does tagging an endogenous regulator reveal its localization and dynamics? | CRISPR knock-in of a fluorescent or epitope tag at the endogenous locus, followed by imaging and immunoprecipitation |
| Does overexpression of a negative regulator reduce TGF-beta production? | CRISPR-mediated overexpression or lentiviral overexpression, followed by TGF-beta quantification |
| Which regulators are essential in a disease-relevant cell type? | CRISPR library screening in primary fibroblasts or immune cells under TGF-beta-inducing conditions [3,8] |
| Does restoring negative regulation of TGF-beta production ameliorate disease in vivo? | Knock-in or overexpression models in mouse fibrosis or tumor models, with TGF-beta readouts [1,5] |
How to Study the negative regulation of transforming growth factor beta production Process
| Method | What It Measures | Typical Application |
|---|---|---|
| ELISA | Secreted TGF-beta protein levels | Quantifying production in conditioned media after genetic perturbation |
| qRT-PCR | TGF-beta mRNA levels | Distinguishing transcriptional from post-transcriptional regulation |
| RNA-seq | Global transcriptional changes | Identifying pathways that negatively regulate TGF-beta production |
| Proteomics | Protein abundance and processing | Detecting TGF-beta processing intermediates and secreted factors |
| Fluorescent imaging | Localization and trafficking of TGF-beta or regulators | Live-cell studies using knock-in tags |
| Reporter assays | TGF-beta promoter or responsive element activity | Functional testing of negative regulatory inputs |
| Co-culture assays | Cytokine cross-talk between cell types | Modeling IL-12-mediated suppression of TGF-beta production |
| Immunohistochemistry | Tissue localization of TGF-beta-producing cells | Disease model analysis, e.g., pulmonary fibrosis |
Quantifying TGF-beta Production
ELISA and cytokine bead arrays are standard methods to measure secreted TGF-beta in conditioned media. These assays can be combined with qPCR for TGFB1, TGFB2, and TGFB3 mRNA to distinguish transcriptional from post-transcriptional regulation [3,8]. In fibrosis models, TGF-beta levels in bronchoalveolar lavage fluid or tissue homogenates provide in vivo readouts.
Transcriptomic and Proteomic Profiling
RNA-seq identifies transcriptional changes in TGF-beta genes and negative regulators following genetic or pharmacological perturbation. Proteomics can quantify TGF-beta processing intermediates and secreted factors, providing a more complete picture of production control. These approaches are particularly useful when studying AMPK or IL-12 pathways that act at multiple levels [3,8].
Imaging and Localization Studies
Fluorescent tagging of TGF-beta or its regulators enables live-cell imaging of trafficking and secretion. Knock-in of fluorescent tags at endogenous loci allows visualization of TGF-beta production dynamics without overexpression artifacts. In tissue sections, immunohistochemistry and in situ hybridization localize TGF-beta-producing cells in disease models [1,5].
Functional Assays for Negative Regulation
Reporter assays driven by TGF-beta promoters or TGF-beta-responsive elements can measure negative regulation of production and signaling. Co-culture systems with fibroblasts and immune cells assess how cytokine cross-talk, such as IL-12-mediated suppression, affects TGF-beta output. These functional assays are essential to confirm causality of candidate regulators [3,8].
How CRISPR Can Be Used to Study GO:0071635 negative regulation of transforming growth factor beta production
Knockout
CRISPR knockout of candidate negative regulators, such as AMPK subunits or IL-12 pathway components, allows direct testing of whether their loss increases TGF-beta production [3,8]. Knockout models are particularly useful for establishing necessity in a given cell type and for validating hits from library screens.
Point Mutation
Point-mutation knock-in can dissect specific residues required for negative regulation of TGF-beta production, such as phosphorylation sites in AMPK substrates or binding interfaces in cytokine receptors. These models avoid confounding effects of complete gene loss and reveal mechanistic details.
Knock-in
Knock-in of fluorescent or epitope tags at endogenous loci enables visualization and biochemical isolation of regulators without overexpression. Knock-in of disease-associated variants can also test their impact on TGF-beta production in a physiological context.
Overexpression
CRISPR-mediated or lentiviral overexpression of negative regulators, such as Nrf2 or AMPK activators, tests sufficiency for reducing TGF-beta production [1,3]. Overexpression models are valuable for preclinical validation of therapeutic strategies aimed at enhancing GO:0071635.
How EDITGENE Supports negative regulation of transforming growth factor beta production Research
Researchers studying negative regulation of transforming growth factor beta production-related genes often need to determine whether a candidate gene is causally involved in suppressing TGF-beta output or is merely correlated with changes in disease models. Establishing causality requires precise genetic manipulation, ideally at the endogenous locus, combined with quantitative readouts of TGF-beta production. EDITGENE provides a comprehensive suite of CRISPR services designed to meet these experimental needs, from knockout and point-mutation models to knock-in reporters and overexpression systems, as well as library screening and bioinformatics support.
Contact EDITGENE today to design your custom CRISPR model for negative regulation of transforming growth factor beta production research.
Frequently Asked Questions About negative regulation of transforming growth factor beta production
What is GO:0071635?
GO:0071635 is the Gene Ontology term for negative regulation of transforming growth factor beta production, defined as any process that stops, prevents, or reduces the frequency, rate, or extent of production of transforming growth factor-beta.
What does negative regulation of TGF-beta production mean?
It refers to cellular mechanisms that lower the synthesis, processing, or secretion of TGF-beta, reducing the amount of bioactive TGF-beta available to bind receptors.
What genes are involved in negative regulation of TGF-beta production?
Key genes include PRKAA1/AMPK, IL12A/IL-12, PTGS2/COX-2, and NFE2L2/Nrf2, which have been shown to suppress TGF-beta production or related pathology [1,2,3,8].
How does AMPK negatively regulate TGF-beta?
AMPK activation reduces TGF-beta production and downstream signaling, coupling cellular energy status to anti-fibrotic and anti-inflammatory outcomes.
Does IL-12 suppress TGF-beta production?
Yes, IL-12 has been shown to regulate and suppress TGF-beta production, providing an immunological brake on TGF-beta-mediated tolerance.
What diseases are linked to dysregulated negative regulation of TGF-beta production?
Idiopathic pulmonary fibrosis, glioblastoma, atherosclerosis, and chronic inflammatory conditions are associated with altered TGF-beta production control [1,5,7].
How can I study negative regulation of TGF-beta production in the lab?
Common methods include ELISA for secreted TGF-beta, qRT-PCR for mRNA, RNA-seq, proteomics, reporter assays, and CRISPR-based genetic models [3,8].
What CRISPR models are useful for studying GO:0071635?
Knockout, point-mutation knock-in, tagged knock-in, and overexpression models are all useful for testing causality and mechanism in negative regulation of TGF-beta production.
Is negative regulation of TGF-beta production the same as negative regulation of TGF-beta signaling?
No, GO:0071635 specifically concerns production of TGF-beta, while negative regulation of signaling refers to events downstream of receptor engagement.
Why is TGF-beta production control important in cancer?
In cancers such as glioblastoma, TGF-beta superfamily signaling promotes tumor initiation and progression, so negative regulators of its production are candidate therapeutic targets.
Conclusion
GO:0071635, negative regulation of transforming growth factor beta production, represents a critical layer of control over one of the most potent cytokines in human biology. The pathways that execute this regulation, including AMPK, IL-12, COX-2, and Nrf2-linked redox signaling, are essential for preventing pathological fibrosis, tumor progression, and immune dysregulation [1,2,3,8]. Understanding these mechanisms requires precise genetic models and quantitative readouts of TGF-beta production [3,8]. As research increasingly focuses on restoring negative regulation of TGF-beta production as a therapeutic strategy, CRISPR-based knockout, point-mutation, knock-in, and overexpression platforms will remain indispensable for establishing causality and mechanism. EDITGENE provides the tools and expertise to accelerate this work, from custom cell model generation to library screening and bioinformatics analysis [3,8].
References
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- 5. Nana AW et al.. 2015. Overview of Transforming Growth Factor β Superfamily Involvement in Glioblastoma Initiation and Progression.. Asian Pac J Cancer Prev 16(16):6813-23 PMID: 26514451
- 6. Fontana A et al.. 1992. Modulation of the immune response by transforming growth factor beta.. Int Arch Allergy Immunol 99(1):1-7 PMID: 1483057
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