GO:0032000 positive regulation of fatty acid beta-oxidation: Metabolic Pathway, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0032000 describes any process that activates or increases the frequency, rate or extent of fatty acid beta-oxidation, the mitochondrial and peroxisomal catabolic pathway that breaks down fatty acids into acetyl-CoA.
• The term is a biological_process ontology node and is distinct from the beta-oxidation pathway itself; it captures upstream activating inputs such as PPAR signaling, SIRT1/PGC-1alpha activity, and nutrient-sensing cues.
• Positive regulation of fatty acid beta-oxidation is central to energy homeostasis, and its dysregulation is linked to non-alcoholic steatohepatitis, obesity, leukemia stem cell self-renewal, and viral replication.
• Key molecular activators include PPARalpha, PGC-1alpha, SIRT1, SMYD3, and pSTAT4-OX40 signaling, which converge on transcriptional and post-translational control of beta-oxidation enzymes.
• Experimental dissection of GO:0032000 relies on CRISPR knockout, point-mutation, knock-in, and overexpression models combined with metabolomics, RNA-seq, and functional assays.
• The term is highly relevant to metabolic disease, immuno-metabolism, and cancer metabolism, making it a tractable target for therapeutic and diagnostic research.
Description
GO:0032000, positive regulation of fatty acid beta-oxidation, is a Gene Ontology biological_process term that defines any process which activates or increases the frequency, rate or extent of fatty acid beta-oxidation. Fatty acid beta-oxidation is the catabolic spiral that shortens fatty acyl-CoA molecules by two carbons per cycle, generating acetyl-CoA, NADH, and FADH2, and it occurs primarily in mitochondria and peroxisomes. The positive regulation term therefore captures the upstream signals, transcription factors, and post-translational events that switch this pathway on or turn up its flux. Researchers study GO:0032000 because it sits at the intersection of energy balance, inflammation, and cell-fate control. Activation of peroxisome proliferator-activated receptors by fatty acids was among the earliest described mechanisms positively regulating peroxisomal beta-oxidation. More recent work has shown that formononetin promotes fatty acid beta-oxidation through the SIRT1/PGC-1alpha/PPARalpha axis to treat non-alcoholic steatohepatitis, and that SMYD3 activates fatty acid beta-oxidation to promote self-renewal of leukemia stem cells. These findings illustrate that positive regulation of beta-oxidation is not merely a metabolic housekeeping function but a process with disease-modifying consequences. The term is also relevant to host-pathogen interactions and immune regulation. African swine fever virus hijacks lipolysis induced by chaperone-mediated autophagy to upregulate fatty acid beta-oxidation and promote viral replication, while fatty acid beta-oxidation enhances the immune regulatory function of double-negative T cells through pSTAT4-OX40 signaling. In cattle, rumen microbiota-host interactions regulate intramuscular fat deposition via an alpha-linolenic acid-fatty acid beta-oxidation/L-carnitine-MPO axis. Together, these studies establish GO:0032000 as a broadly important regulatory node in metabolism, immunity, and infection.
positive regulation of fatty acid beta-oxidation At A Glance
| GO ID | GO:0032000 |
|---|---|
| GO term | positive regulation of fatty acid beta-oxidation |
| Ontology | biological_process |
| Definition | Any process that activates or increases the frequency, rate or extent of fatty acid beta-oxidation. |
| Synonym | activation of fatty acid beta-oxidation; stimulation of fatty acid beta-oxidation; up regulation of fatty acid beta-oxidation; up-regulation of fatty acid beta-oxidation; upregulation of fatty acid beta-oxidation |
| Major function | Upregulation of mitochondrial and peroxisomal fatty acid catabolism in response to metabolic, hormonal, or immune signals. |
| Key regulators | PPARalpha, PGC-1alpha, SIRT1, SMYD3, pSTAT4-OX40 signaling. |
| Disease relevance | Non-alcoholic steatohepatitis, obesity, leukemia stem cell self-renewal, viral infection, immune regulation. |
| Research methods | CRISPR knockout/knock-in/overexpression, RNA-seq, metabolomics, functional metabolic assays. |
What Is GO:0032000?
In our own words, GO:0032000 (positive regulation of fatty acid beta-oxidation) refers to any biological process that activates or increases the frequency, rate, or extent of fatty acid beta-oxidation. It is a regulatory biological_process term, meaning it does not describe the enzymatic steps of beta-oxidation itself but rather the upstream or concurrent events that enhance flux through that pathway. Such events can include transcriptional activation of beta-oxidation genes by nuclear receptors, post-translational modification of beta-oxidation enzymes, changes in substrate availability, or signaling cascades that increase mitochondrial fatty acid uptake and oxidation.
Why Is positive regulation of fatty acid beta-oxidation Important in Cell Biology?
Positive regulation of fatty acid beta-oxidation is important because it determines how cells and organisms switch between lipid storage and lipid burning, a decision with direct consequences for metabolic health, immune function, and disease progression. Activation of this process can ameliorate hepatic steatosis and inflammation in non-alcoholic steatohepatitis, but it can also support pathological states such as leukemia stem cell self-renewal and viral replication. Understanding GO:0032000 therefore provides a mechanistic handle on both therapeutic opportunities and disease liabilities.
• Controls energy homeostasis by increasing mitochondrial and peroxisomal fatty acid catabolism.
• Protects against hepatic steatosis and non-alcoholic steatohepatitis when appropriately activated.
• Supports leukemia stem cell self-renewal, linking metabolism to cancer stemness.
• Enhances immune regulatory function of double-negative T cells via pSTAT4-OX40 signaling.
• Can be hijacked by pathogens such as African swine fever virus to promote replication.
• Regulates intramuscular fat deposition in cattle through microbiota-host interactions.
• Is a target of natural compounds such as formononetin and Polygonatum sibiricum extracts.
• Provides a mechanistic link between vitamin B12/folate status and NASH inflammation/fibrosis.
• Offers a tractable node for CRISPR-based functional genomics and drug discovery.
What Happens During positive regulation of fatty acid beta-oxidation?
Signal reception and nuclear receptor activation
In simple terms: The cell first senses a signal that says more fat should be burned, often through nuclear receptors that turn on fat-burning genes.
Positive regulation of fatty acid beta-oxidation begins when extracellular or intracellular signals activate transcription factors such as peroxisome proliferator-activated receptors (PPARs). Fatty acids themselves can act as activating ligands for PPARs, leading to increased expression of peroxisomal beta-oxidation enzymes. In non-alcoholic steatohepatitis models, formononetin promotes fatty acid beta-oxidation through the SIRT1/PGC-1alpha/PPARalpha pathway, illustrating how a small molecule can initiate this regulatory cascade.
Transcriptional upregulation of beta-oxidation genes
In simple terms: Once the signal is received, the cell makes more copies of the enzymes that actually break down fat.
Activated PPARalpha and its coactivator PGC-1alpha drive transcription of genes encoding mitochondrial and peroxisomal beta-oxidation enzymes, including acyl-CoA dehydrogenases and thiolases. This transcriptional program increases the capacity of the cell to oxidize fatty acids. SMYD3 has also been shown to activate fatty acid beta-oxidation, promoting self-renewal of leukemia stem cells, indicating that epigenetic or methyltransferase-dependent mechanisms can contribute to transcriptional upregulation.
Post-translational and signaling amplification
In simple terms: The cell can also flip chemical switches on existing enzymes to make them work faster without making new ones.
Beyond transcription, positive regulation of beta-oxidation involves post-translational modifications and signaling pathways that enhance enzyme activity or substrate delivery. Fatty acid beta-oxidation enhances immune regulatory function of double-negative T cells through the pSTAT4-OX40 signaling pathway, demonstrating that beta-oxidation flux can feed back into immune signaling. In African swine fever virus infection, chaperone-mediated autophagy-induced lipolysis upregulates fatty acid beta-oxidation to promote viral replication, showing that post-translational degradation and lipolysis can amplify this process.
Metabolic flux and physiological output
In simple terms: The end result is that the cell burns more fat, producing energy and changing its behavior.
The ultimate output of positive regulation of fatty acid beta-oxidation is increased flux through the beta-oxidation spiral, yielding acetyl-CoA, NADH, and FADH2. This supports ATP production, alters acetyl-CoA pools for biosynthesis, and can influence cell fate. In leukemia stem cells, this increased flux supports self-renewal; in hepatocytes, it reduces fat accumulation and inflammation in NASH; and in cattle, it contributes to intramuscular fat deposition via an alpha-linolenic acid-fatty acid beta-oxidation/L-carnitine-MPO axis.
Integration with systemic metabolism
In simple terms: What happens in one tissue can affect the whole body, linking diet, gut microbes, and fat storage.
Positive regulation of fatty acid beta-oxidation is integrated with systemic metabolic signals. Rumen microbiota-host interactions regulate intramuscular fat deposition in cattle via the alpha-linolenic acid-fatty acid beta-oxidation/L-carnitine-MPO axis, showing that microbial metabolites can influence host beta-oxidation. Aqueous extracts of Polygonatum sibiricum rhizome ameliorate obesity and liver fat accumulation in high-fat diet-fed mice, with multiomics revealing effects on fatty acid oxidation pathways. Vitamin B12 and folate decrease inflammation and fibrosis in NASH by preventing syntaxin 17 homocysteinylation, indirectly supporting healthy beta-oxidation.
Key Genes Involved in GO:0032000 positive regulation of fatty acid beta-oxidation
The following genes and proteins are experimentally implicated in the positive regulation of fatty acid beta-oxidation, based on the verified literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| PPARalpha | Nuclear receptor that transcriptionally activates beta-oxidation genes upon fatty acid binding | Central regulator of peroxisomal and mitochondrial beta-oxidation; target of formononetin and other compounds |
| PGC-1alpha | Transcriptional coactivator that partners with PPARalpha to drive beta-oxidation gene expression | Key node in SIRT1/PGC-1alpha/PPARalpha axis; studied in NASH and metabolic disease |
| SIRT1 | Deacetylase that activates PGC-1alpha and promotes fatty acid beta-oxidation | Upstream regulator targeted by formononetin in NASH models |
| SMYD3 | Methyltransferase that activates fatty acid beta-oxidation | Promotes leukemia stem cell self-renewal; potential cancer metabolism target |
| STAT4 | Transcription factor phosphorylated (pSTAT4) in response to beta-oxidation | Links beta-oxidation to OX40 signaling and immune regulatory function of double-negative T cells |
| OX40 | Costimulatory receptor involved in pSTAT4-OX40 signaling | Mediates immune regulatory effects downstream of fatty acid beta-oxidation |
| Syntaxin 17 | Autophagosomal SNARE protein protected by vitamin B12/folate from homocysteinylation | Links autophagy, lipid metabolism, and NASH inflammation/fibrosis |
| L-carnitine | Carrier molecule required for mitochondrial fatty acid import | Part of the alpha-linolenic acid-fatty acid beta-oxidation/L-carnitine-MPO axis in cattle |
| MPO | Myeloperoxidase, an enzyme linked to oxidative stress and inflammation | Component of the microbiota-host axis regulating intramuscular fat deposition |
| Chaperone-mediated autophagy components | Mediate lipolysis that upregulates beta-oxidation during viral infection | Host factors hijacked by African swine fever virus |
| PPARgamma | Nuclear receptor family member with roles in lipid metabolism | Implicated in Polygonatum sibiricum extract effects on obesity and liver fat |
| CPT1A | Rate-limiting enzyme for mitochondrial fatty acid import | Downstream target of PPARalpha/PGC-1alpha activation |
| ACOX1 | Peroxisomal acyl-CoA oxidase, first enzyme of peroxisomal beta-oxidation | Classic marker of PPAR-mediated peroxisomal beta-oxidation activation |
| HADHA | Mitochondrial trifunctional protein subunit in beta-oxidation | Represents mitochondrial beta-oxidation capacity in NASH studies |
| UCP2 | Uncoupling protein linked to fatty acid oxidation and energy dissipation | Modulated by Polygonatum sibiricum extracts in obesity models |
| FGF21 | Hormone induced by fatty acid oxidation and PPARalpha activation | Biomarker and mediator of metabolic stress responses |
How Is positive regulation of fatty acid beta-oxidation Regulated?
Positive regulation of fatty acid beta-oxidation is controlled at multiple levels. Transcriptional regulation is dominated by the PPARalpha/PGC-1alpha axis, which is activated by fatty acids and by compounds such as formononetin through SIRT1. SMYD3 provides an additional layer of activation, potentially through epigenetic mechanisms, in leukemia stem cells. Post-translational regulation includes phosphorylation events such as pSTAT4 in double-negative T cells and chaperone-mediated autophagy-driven lipolysis during viral infection. Systemic factors, including gut microbiota-derived metabolites and vitamin B12/folate status, also modulate the pathway. Together, these mechanisms ensure that beta-oxidation is tuned to nutrient availability, immune signals, and cellular stress.
positive regulation of fatty acid beta-oxidation and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| SIRT1/PGC-1alpha/PPARalpha | Non-alcoholic steatohepatitis | Hepatocyte-specific knockout or overexpression in high-fat diet mouse models |
| SMYD3 | Leukemia stem cell self-renewal | CRISPR knockout or point-mutation in leukemia cell lines and xenografts |
| STAT4/OX40 | Immune regulation by double-negative T cells | Knockout or knock-in of STAT4 phosphorylation sites in T cell models |
| Syntaxin 17 | NASH inflammation and fibrosis | Point-mutation of homocysteinylation sites in hepatocyte models |
| Chaperone-mediated autophagy components | African swine fever virus replication | Knockout of LAMP2A or other CMA genes in porcine macrophage models |
Non-alcoholic steatohepatitis and metabolic liver disease
Positive regulation of fatty acid beta-oxidation is protective in non-alcoholic steatohepatitis (NASH). Formononetin promotes fatty acid beta-oxidation through the SIRT1/PGC-1alpha/PPARalpha pathway to treat NASH in experimental models. Vitamin B12 and folate decrease inflammation and fibrosis in NASH by preventing syntaxin 17 homocysteinylation, a mechanism that supports autophagic and metabolic homeostasis. Aqueous extracts of Polygonatum sibiricum rhizome ameliorate obesity and liver fat accumulation in high-fat diet-fed mice, with multiomics implicating fatty acid oxidation pathways. These studies suggest that enhancing GO:0032000 activity could be therapeutically beneficial in metabolic liver disease.
Leukemia and cancer stem cell metabolism
In leukemia, positive regulation of fatty acid beta-oxidation can be pathogenic. SMYD3 activates fatty acid beta-oxidation to promote self-renewal of leukemia stem cells, indicating that this GO term can support cancer stemness. This contrasts with the protective role in NASH and highlights context-dependent effects of beta-oxidation activation. Targeting the regulatory mechanisms of GO:0032000 may therefore offer a strategy to disrupt leukemia stem cell maintenance.
Immune regulation and infection
Fatty acid beta-oxidation enhances the immune regulatory function of double-negative T cells through the pSTAT4-OX40 signaling pathway, linking GO:0032000 to immune tolerance and inflammation resolution. Conversely, African swine fever virus hijacks lipolysis induced by chaperone-mediated autophagy to upregulate fatty acid beta-oxidation and promote viral replication, showing that pathogens can exploit this process. These findings position positive regulation of beta-oxidation as a double-edged sword in host defense and immune homeostasis.
Obesity and adipose biology
In obesity models, activation of fatty acid beta-oxidation is associated with reduced fat accumulation. Polygonatum sibiricum rhizome extracts ameliorate obesity and liver fat accumulation in high-fat diet-fed mice, with multiomics revealing effects on fatty acid oxidation. In cattle, rumen microbiota-host interactions regulate intramuscular fat deposition via the alpha-linolenic acid-fatty acid beta-oxidation/L-carnitine-MPO axis, demonstrating that GO:0032000 influences fat deposition in agricultural species as well.
From positive regulation of fatty acid beta-oxidation-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is PPARalpha required for formononetin-induced beta-oxidation? | PPARalpha knockout hepatocytes or mice |
| Does SMYD3 methyltransferase activity drive leukemia stem cell self-renewal? | SMYD3 point-mutation (catalytic dead) knock-in in leukemia cells |
| How does pSTAT4-OX40 signaling link beta-oxidation to immune regulation? | STAT4 phospho-mutant knock-in in double-negative T cells |
| Can syntaxin 17 homocysteinylation be prevented to reduce NASH fibrosis? | Syntaxin 17 point-mutation knock-in in hepatocytes |
| Does overexpression of PGC-1alpha enhance beta-oxidation and reduce steatosis? | PGC-1alpha overexpression in hepatocyte cell lines or mouse liver |
| What is the role of chaperone-mediated autophagy in virus-induced beta-oxidation? | LAMP2A knockout in porcine macrophages |
How to Study the positive regulation of fatty acid beta-oxidation Process
| Method | What It Measures | Typical Application |
|---|---|---|
| RNA-seq | Global transcriptome changes | Identifying beta-oxidation gene programs activated by PPARalpha/PGC-1alpha |
| Seahorse extracellular flux | Real-time oxygen consumption and fatty acid oxidation | Functional assessment of beta-oxidation flux in cells |
| Targeted metabolomics | Levels of acyl-carnitines and fatty acid intermediates | Quantifying pathway activity in NASH and obesity models |
| Western blot | Protein expression and post-translational modifications | Detecting pSTAT4, acetylated PGC-1alpha, or homocysteinylated syntaxin 17 |
| Co-immunoprecipitation | Protein-protein interactions | Validating SIRT1/PGC-1alpha complex formation |
| CRISPR knockout | Loss-of-function phenotypes | Testing requirement of PPARalpha, SMYD3, or STAT4 for beta-oxidation |
| CRISPR knock-in | Precise mutation or tag introduction | Modeling point mutations in STAT4 or syntaxin 17 |
| Overexpression | Gain-of-function effects | Testing PGC-1alpha or PPARalpha sufficiency for beta-oxidation activation |
Transcriptomic profiling of beta-oxidation gene programs
RNA-seq and quantitative PCR are used to measure expression of PPARalpha, PGC-1alpha, CPT1A, ACOX1, HADHA, and other beta-oxidation genes following genetic or pharmacological perturbation. In NASH studies, formononetin treatment increased expression of beta-oxidation genes in a SIRT1/PGC-1alpha/PPARalpha-dependent manner. Multiomics approaches have also been used to reveal effects of Polygonatum sibiricum extracts on fatty acid oxidation pathways in obese mice.
Metabolic flux and substrate oxidation assays
Seahorse extracellular flux analysis, radiolabeled fatty acid oxidation assays, and targeted metabolomics measure actual flux through beta-oxidation. These methods complement gene expression data by quantifying functional changes in fatty acid catabolism. In leukemia stem cells, SMYD3-dependent activation of beta-oxidation was linked to functional self-renewal capacity. In double-negative T cells, beta-oxidation supported pSTAT4-OX40 signaling and immune regulatory function.
Protein interaction and post-translational modification analysis
Co-immunoprecipitation, Western blotting, and mass spectrometry are used to detect interactions and modifications such as acetylation, phosphorylation, and homocysteinylation. The SIRT1/PGC-1alpha interaction is central to formononetin action, while pSTAT4 is a key phosphorylation event downstream of beta-oxidation in T cells. Syntaxin 17 homocysteinylation is a post-translational modification relevant to NASH.
In vivo and disease model validation
High-fat diet mouse models, NASH models, leukemia xenografts, and viral infection models are used to validate findings from cell culture. Formononetin was tested in NASH models, SMYD3 in leukemia stem cell models, and African swine fever virus in porcine infection models. These in vivo systems are essential for translating mechanistic insights about GO:0032000 into disease relevance.
How CRISPR Can Be Used to Study GO:0032000 positive regulation of fatty acid beta-oxidation
Knockout
CRISPR knockout is used to delete genes such as PPARalpha, SIRT1, SMYD3, or STAT4 to test their requirement for positive regulation of fatty acid beta-oxidation. For example, knockout of PPARalpha would be expected to blunt formononetin-induced beta-oxidation, while SMYD3 knockout would reduce leukemia stem cell self-renewal. Knockout of LAMP2A can test the role of chaperone-mediated autophagy in virus-induced beta-oxidation.
Point Mutation
Point-mutation knock-in models allow precise dissection of catalytic or regulatory residues. A catalytically dead SMYD3 point mutant can distinguish methyltransferase activity from scaffolding functions in beta-oxidation activation. Phospho-deficient or phospho-mimetic STAT4 mutants can test the role of pSTAT4 in OX40 signaling downstream of beta-oxidation. Homocysteinylation-site mutants of syntaxin 17 can probe NASH-related mechanisms.
Knock-in
Knock-in of reporter tags or epitope tags into endogenous loci enables tracking of protein expression, localization, and interactions. Tagged PPARalpha or PGC-1alpha knock-in cells can be used for chromatin immunoprecipitation or imaging studies to map beta-oxidation gene regulation. Tagged STAT4 knock-in can facilitate analysis of pSTAT4 dynamics in T cells.
Overexpression
Overexpression of PPARalpha, PGC-1alpha, or SMYD3 can test sufficiency for activating fatty acid beta-oxidation. PGC-1alpha overexpression in hepatocytes is expected to increase beta-oxidation gene expression and reduce lipid accumulation. SMYD3 overexpression in leukemia cells may enhance self-renewal through increased beta-oxidation. Overexpression models complement knockout studies by providing gain-of-function evidence.
How EDITGENE Supports positive regulation of fatty acid beta-oxidation Research
Researchers studying positive regulation of fatty acid beta-oxidation-related genes often need to determine whether a candidate gene is causally involved in activating the pathway, and CRISPR-based models provide the most direct way to establish such causality. By combining knockout, point-mutation, knock-in, and overexpression strategies, investigators can move from correlation to mechanism in metabolic disease, cancer, and immunology contexts.
Contact EDITGENE today to design your custom CRISPR model for positive regulation of fatty acid beta-oxidation research.
Frequently Asked Questions About positive regulation of fatty acid beta-oxidation
What is GO:0032000 positive regulation of fatty acid beta-oxidation?
GO:0032000 is a Gene Ontology biological_process term defined as any process that activates or increases the frequency, rate or extent of fatty acid beta-oxidation, the catabolic pathway that breaks down fatty acids into acetyl-CoA.
What genes are involved in positive regulation of fatty acid beta-oxidation?
Key genes include PPARalpha, PGC-1alpha, SIRT1, SMYD3, STAT4, OX40, syntaxin 17, CPT1A, ACOX1, and HADHA, based on studies in NASH, leukemia, and immune cells.
How is fatty acid beta-oxidation positively regulated?
It is positively regulated by nuclear receptor activation (PPARalpha), transcriptional coactivators (PGC-1alpha), deacetylases (SIRT1), methyltransferases (SMYD3), and signaling pathways such as pSTAT4-OX40.
Why is positive regulation of fatty acid beta-oxidation important in disease?
It can protect against NASH and obesity-related liver fat accumulation, but it can also support leukemia stem cell self-renewal and viral replication, making it context-dependent.
What diseases are linked to GO:0032000?
Non-alcoholic steatohepatitis, obesity, leukemia, and viral infections such as African swine fever are linked to positive regulation of fatty acid beta-oxidation.
How do researchers study positive regulation of fatty acid beta-oxidation?
They use RNA-seq, metabolomics, Seahorse flux analysis, Western blotting, and CRISPR knockout, point-mutation, knock-in, and overexpression models.
What is the role of PPARalpha in fatty acid beta-oxidation?
PPARalpha is a nuclear receptor that, upon activation by fatty acids, transcriptionally upregulates peroxisomal and mitochondrial beta-oxidation genes.
Can CRISPR be used to study GO:0032000?
Yes, CRISPR knockout, point-mutation, knock-in, and overexpression models are widely used to test causality of genes in positive regulation of fatty acid beta-oxidation.
What is the SIRT1/PGC-1alpha/PPARalpha pathway?
It is a signaling axis in which SIRT1 activates PGC-1alpha, which coactivates PPARalpha to drive fatty acid beta-oxidation gene expression; formononetin acts through this pathway in NASH.
How does SMYD3 relate to fatty acid beta-oxidation?
SMYD3 activates fatty acid beta-oxidation to promote self-renewal of leukemia stem cells, linking epigenetic regulation to cancer metabolism.
Conclusion
GO:0032000, positive regulation of fatty acid beta-oxidation, is a biologically_process term that captures the upstream signals and molecular events that increase flux through fatty acid catabolism. Its importance spans metabolic liver disease, obesity, leukemia, immune regulation, and host-pathogen interactions, with key regulators including PPARalpha, PGC-1alpha, SIRT1, SMYD3, and pSTAT4-OX40 signaling. Because the consequences of activating this pathway are highly context-dependent, rigorous causal studies using CRISPR knockout, point-mutation, knock-in, and overexpression models are essential. EDITGENE provides end-to-end support for such studies, from model generation to multiomics analysis, enabling researchers to dissect positive regulation of fatty acid beta-oxidation with precision.
References
- 1. Liao J et al.. 2024. Formononetin promotes fatty acid β-oxidation to treat non-alcoholic steatohepatitis through SIRT1/PGC-1α/PPARα pathway.. Phytomedicine 124:155285 PMID: 38185065
- 2. Zhou M et al.. 2025. SMYD3 Activates Fatty Acid β-Oxidation to Promote Self-Renewal of Leukemia Stem Cells.. Cancer Res 85(11):2027-2045 PMID: 40080525
- 3. Zhang WT et al.. 2025. Rumen microbiota-host interactions regulate intramuscular fat deposition in cattle via the alpha-linolenic acid-fatty acid β-oxidation/L-carnitine-MPO axis.. Microbiome 14(1):49 PMID: 41372768
- 4. Dreyer C et al.. 1993. Positive regulation of the peroxisomal beta-oxidation pathway by fatty acids through activation of peroxisome proliferator-activated receptors (PPAR).. Biol Cell 77(1):67-76 PMID: 8390886
- 5. Wang Z et al.. 2025. Fatty acid β-oxidation enhances immune regulatory function of double-negative T cells through pSTAT4-OX40 signaling pathway.. Hepatol Commun 9(9) PMID: 40879484
- 6. Yang X et al.. 2026. African swine fever virus hijacks lipolysis induced by chaperone-mediated autophagy to upregulate fatty acid β-oxidation and promote viral replication.. mBio 17(4):e0336825 PMID: 41801037
- 7. Ou X et al.. 2024. Multiomics reveals the ameliorating effect and underlying mechanism of aqueous extracts of polygonatum sibiricum rhizome on obesity and liver fat accumulation in high-fat diet-fed mice.. Phytomedicine 132:155843 PMID: 38971026
- 8. Tripathi M et al.. 2022. Vitamin B(12) and folate decrease inflammation and fibrosis in NASH by preventing syntaxin 17 homocysteinylation.. J Hepatol 77(5):1246-1255 PMID: 35820507
