GO:0051552 flavone metabolic process: Biosynthesis, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0051552 (flavone metabolic process) describes the chemical reactions and pathways involving flavones, pigmented plant compounds built on a 2-phenyl-4H-1-benzopyran-4-one (2-phenylchromone) backbone.
• Flavone metabolism determines the bioavailability and biological activity of dietary flavones such as tangeretin and nobiletin, which are polymethoxylated flavones found in citrus.
• Flavone C-glycosides from plants such as Dianthus superbus L. attenuate metabolic dysfunction-associated steatotic liver disease (MASLD) through multi-pathway regulation.
• Tangeretin protects against sepsis-induced myocardial dysfunction by inhibiting the PTEN/AKT/mTOR axis and against hepatic ischemia-reperfusion injury via Nrf2-activated mitophagy and ferroptosis suppression.
• Nobiletin, a citrus flavone, shows potential benefits against Alzheimer's and Parkinson's diseases, while tangeretin has documented neuroprotective roles.
• Studying flavone metabolic process genes requires knockout, point-mutation, knock-in, and overexpression cell models combined with CRISPR library screening and bioinformatics to establish causal gene function.
Description
GO:0051552, flavone metabolic process, is a biological process ontology term that covers the chemical reactions and pathways involving flavones, a class of pigmented plant compounds based on 2-phenyl-4H-1-benzopyran-4-one (2-phenylchromone). Flavones are polyphenolic secondary metabolites widely distributed in plants, and their metabolic processing influences both their accumulation in plant tissues and their bioavailability when consumed by humans. Because flavones such as tangeretin and nobiletin exhibit cardioprotective, neuroprotective, anti-inflammatory, and metabolic effects, understanding the enzymes and pathways that constitute flavone metabolism is directly relevant to nutrition, pharmacology, and drug discovery. Research on flavone metabolic process spans plant biochemistry, food science, and human disease biology. Polyphenol bioavailability studies show that the metabolic fate of flavones, including conjugation and glycosylation, strongly determines their systemic exposure and biological activity. Plant-derived flavone C-glycosides have been shown to attenuate metabolic dysfunction-associated steatotic liver disease through multi-pathway regulation, illustrating how flavone metabolism intersects with metabolic disease. In parallel, individual flavones such as tangeretin and nobiletin have been studied in experimental models of sepsis, Alzheimer's disease, Parkinson's disease, adipocyte differentiation, and hepatic ischemia-reperfusion injury. For researchers, GO:0051552 provides a standardized framework for annotating genes and pathways involved in flavone biosynthesis, modification, and turnover. This article summarizes the definition, biological significance, key genes, regulatory context, disease links, and experimental methods, including CRISPR-based models, that are used to study flavone metabolic process.
flavone metabolic process At A Glance
| GO ID | GO:0051552 |
|---|---|
| GO term | flavone metabolic process |
| Ontology | biological_process |
| Synonym | 2-phenyl-4H-1-benzopyran-4-one metabolic process; 2-phenyl-4H-1-benzopyran-4-one metabolism; 2-phenylchromone metabolic process; 2-phenylchromone metabolism; flavone metabolism |
| Major function | Enzymatic biosynthesis, modification, conjugation, and turnover of flavones, a class of pigmented plant compounds based on 2-phenyl-4H-1-benzopyran-4-one (2-phenylchromone) |
| Representative flavones | Tangeretin, nobiletin, and related polymethoxylated and glycosylated flavones studied in citrus and medicinal plants |
| Associated disease areas | Sepsis-induced myocardial dysfunction, Alzheimer's disease, Parkinson's disease, hepatic ischemia-reperfusion injury, metabolic dysfunction-associated steatotic liver disease |
| Research relevance | Flavone metabolism determines bioavailability and bioactivity of dietary flavones, making it a target for nutrition, pharmacology, and gene-function studies |
What Is GO:0051552?
Flavone metabolic process (GO:0051552) is defined as the chemical reactions and pathways involving flavones, a class of pigmented plant compounds based on 2-phenyl-4H-1-benzopyran-4-one (2-phenylchromone). In practical terms, it encompasses the enzymatic steps that build, modify, conjugate, transport, and degrade flavone molecules, as well as the metabolic interconversions that determine flavone bioavailability and biological activity.
Why Is flavone metabolic process Important in Cell Biology?
Flavone metabolic process is important because the metabolic handling of flavones dictates whether these compounds reach target tissues in active forms and at effective concentrations. Flavones such as tangeretin and nobiletin have demonstrated cardioprotective, neuroprotective, anti-inflammatory, and metabolic effects in experimental models, and these effects depend on the pathways that produce, modify, and clear flavones. In plants, flavone metabolism contributes to pigmentation and defense, while in human nutrition and pharmacology it shapes the bioavailability of polyphenols. Plant flavone C-glycosides have been linked to attenuation of MASLD through multi-pathway regulation, showing that flavone metabolic pathways can be harnessed for metabolic disease research. Consequently, GO:0051552 provides a critical annotation framework for gene-function studies, CRISPR screening, and translational research on flavone-based interventions.
• Defines the enzymatic and pathway framework for flavone biosynthesis, modification, and turnover in plants.
• Determines the bioavailability and systemic exposure of dietary flavones such as tangeretin and nobiletin.
• Underpins the cardioprotective effect of tangeretin via inhibition of the PTEN/AKT/mTOR axis in sepsis-induced myocardial dysfunction.
• Connects to neuroprotection, as nobiletin shows potential benefits against Alzheimer's and Parkinson's diseases and tangeretin has documented neuroprotective roles.
• Links to hepatic protection, where tangeretin's protection against hepatic ischemia-reperfusion injury is mediated by Nrf2-activated mitophagy and ferroptosis suppression.
• Relevant to metabolic disease, since flavone C-glycosides attenuate MASLD through multi-pathway regulation.
• Provides a target for anti-adipogenic research, as nobiletin suppresses adipocyte differentiation of 3T3-L1 cells.
• Supports anti-inflammatory and anti-tumor research, as icariin and its derivative ICT modulate myeloid derived suppressive cells.
• Enables CRISPR-based causal gene studies through knockout, point-mutation, knock-in, and overexpression models.
• Facilitates bioinformatics-driven pathway annotation and CRISPR library screening for flavone-related gene discovery.
What Happens During flavone metabolic process?
Flavone biosynthesis and scaffold formation
In simple terms: Plants build the basic flavone skeleton from simpler building blocks.
Flavone metabolic process begins with the formation of the 2-phenyl-4H-1-benzopyran-4-one (2-phenylchromone) core, the defining chemical structure of flavones. This scaffold is the basis for the pigmented plant compounds classified as flavones, and its formation is the entry point for the metabolic pathways annotated under GO:0051552. The resulting flavone aglycones can then undergo further metabolic modification, which determines their chemical diversity and biological properties.
Glycosylation and conjugation of flavones
In simple terms: Sugar and other groups are attached to flavones, changing how they behave in the body.
Flavones are frequently modified by glycosylation and other conjugation reactions, producing derivatives such as flavone C-glycosides. These modifications are part of flavone metabolic process and influence the physicochemical properties, stability, and bioavailability of the parent flavone. Flavone C-glycosides from Dianthus superbus L. have been shown to attenuate metabolic dysfunction-associated steatotic liver disease via multi-pathway regulations, demonstrating that glycosylated flavone metabolites retain biological activity relevant to human disease.
Bioavailability and metabolic fate of dietary flavones
In simple terms: Once eaten, flavones are processed by the body in ways that affect how much actually reaches tissues.
Polyphenol bioavailability studies indicate that the metabolic fate of flavones, including conjugation and other transformations, is a major determinant of their systemic exposure and bioactivity. This means that flavone metabolic process is not only a plant pathway but also a determinant of the pharmacological potential of dietary flavones such as tangeretin and nobiletin. Understanding these metabolic steps is therefore essential for interpreting experimental results on flavone bioactivity.
Biological actions of flavone metabolites
In simple terms: The flavones and their metabolic products can trigger protective effects in cells and tissues.
Flavone metabolites and parent flavones exert biological effects through defined molecular pathways. Tangeretin protects against sepsis-induced myocardial dysfunction by inhibiting the PTEN/AKT/mTOR axis, and it protects against hepatic ischemia-reperfusion injury through Nrf2-activated mitophagy and ferroptosis suppression. Nobiletin suppresses adipocyte differentiation of 3T3-L1 cells and shows potential benefits against Alzheimer's and Parkinson's diseases. Tangeretin has also been reviewed for its neuroprotective role, and icariin and its derivative ICT exert anti-inflammatory and anti-tumor effects while modulating myeloid derived suppressive cells. These findings illustrate how flavone metabolic process products can influence diverse disease-relevant pathways.
Pathway integration and multi-pathway regulation
In simple terms: Flavone metabolism is connected to many other cellular pathways rather than acting alone.
Flavone metabolic process intersects with multiple signaling and metabolic pathways. Flavone C-glycosides from Dianthus superbus L. attenuate MASLD via multi-pathway regulations, indicating that flavone metabolites can simultaneously affect several disease-related processes. Similarly, tangeretin's cardioprotective and hepatoprotective effects involve distinct axes such as PTEN/AKT/mTOR and Nrf2-mediated mitophagy. This multi-pathway integration makes GO:0051552 a useful annotation hub for systems-level studies of flavone biology.
Key Genes Involved in GO:0051552 flavone metabolic process
The following genes and proteins are representative of flavone metabolic process research, based on the verified literature covering flavone biosynthesis, bioavailability, and biological activity.
| Gene | Major Role | Research Relevance |
|---|---|---|
| PTEN | Negative regulator of the PI3K/AKT pathway; tangeretin inhibits the PTEN/AKT/mTOR axis in sepsis-induced myocardial dysfunction | Target for cardioprotection studies using tangeretin in experimental sepsis models |
| AKT | Serine/threonine kinase in the PTEN/AKT/mTOR axis modulated by tangeretin | Readout of flavone-mediated cardioprotection and signaling studies |
| mTOR | Kinase in the PTEN/AKT/mTOR axis inhibited by tangeretin in myocardial dysfunction | Target for mechanistic studies of flavone cardioprotection |
| Nrf2 | Transcription factor mediating antioxidant responses; tangeretin activates Nrf2-linked mitophagy in hepatic ischemia-reperfusion injury | Target for hepatoprotection and ferroptosis suppression studies |
| NF-kB (NFKB1) | Inflammatory transcription factor modulated by icariin and its derivative ICT | Target for anti-inflammatory and anti-tumor flavone research |
| MDSC-associated markers | Myeloid derived suppressive cell functions modulated by icariin and ICT | Readouts for immunomodulatory effects of flavone-related compounds |
| Adipocyte differentiation regulators | Nobiletin suppresses adipocyte differentiation of 3T3-L1 cells | Model for anti-adipogenic and metabolic studies of flavones |
| Amyloid-beta pathway components | Nobiletin shows potential benefits against Alzheimer's disease | Target for neuroprotective flavone research |
| Alpha-synuclein pathway components | Nobiletin shows potential benefits against Parkinson's disease | Target for neuroprotective flavone research |
| Flavone C-glycoside biosynthetic enzymes | Produce flavone C-glycosides from Dianthus superbus L. that attenuate MASLD | Target for plant flavone metabolism and metabolic disease studies |
| Polyphenol conjugation enzymes | Determine bioavailability of dietary polyphenols including flavones | Target for bioavailability and pharmacokinetic studies |
| Tangeretin-responsive signaling nodes | Mediate cardioprotective and neuroprotective effects of tangeretin | Target for multi-organ protection studies |
| Nobiletin-responsive signaling nodes | Mediate neuroprotective and anti-adipogenic effects of nobiletin | Target for neurodegeneration and metabolic studies |
| Icariin/ICT-responsive immune nodes | Mediate anti-inflammatory and anti-tumor effects and MDSC modulation | Target for immunology and oncology flavone research |
| MASLD-associated metabolic regulators | Modulated by flavone C-glycosides in MASLD models | Target for steatotic liver disease research |
| Ferroptosis regulators | Suppressed by tangeretin in hepatic ischemia-reperfusion injury | Target for cell death pathway studies |
| Mitophagy regulators | Activated by Nrf2 in tangeretin-mediated hepatoprotection | Target for organelle quality control studies |
| Bioavailability-related transporters and enzymes | Influence systemic exposure to flavones | Target for nutrition and pharmacology research |
How Is flavone metabolic process Regulated?
Flavone metabolic process is regulated at multiple levels. In experimental models, tangeretin inhibits the PTEN/AKT/mTOR axis, indicating that flavone-related compounds can modulate a central growth and survival signaling pathway. Tangeretin also activates Nrf2-dependent mitophagy and suppresses ferroptosis, linking flavone metabolism to redox and organelle quality-control regulation. Nobiletin regulates adipocyte differentiation in 3T3-L1 cells, showing that flavones can influence differentiation programs. Icariin and its derivative ICT modulate inflammatory signaling and myeloid derived suppressive cell functions, indicating immune-related regulatory effects. At the organismal level, polyphenol bioavailability studies show that conjugation and metabolic transformation regulate the effective concentration of flavones reaching target tissues. Plant flavone C-glycosides regulate multiple pathways simultaneously in MASLD models, further supporting the view that flavone metabolic process is embedded in a broader regulatory network.
flavone metabolic process and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| PTEN/AKT/mTOR axis | Sepsis-induced myocardial dysfunction | Knockout or point-mutation models of PTEN/AKT/mTOR components in cardiomyocytes treated with tangeretin |
| Nrf2 | Hepatic ischemia-reperfusion injury | Nrf2 knockout or knock-in reporter models in hepatocytes with tangeretin treatment |
| Amyloid-beta and alpha-synuclein pathways | Alzheimer's disease and Parkinson's disease | Overexpression or knockout neuronal models treated with nobiletin |
| MASLD-associated metabolic regulators | Metabolic dysfunction-associated steatotic liver disease | Knockout or overexpression hepatocyte models treated with flavone C-glycosides |
| NF-kB and MDSC-related genes | Inflammation and cancer | Knockout or knock-in immune cell models treated with icariin or ICT |
Flavone metabolic process and cardiovascular disease
Tangeretin, a flavone, exerts a cardioprotective effect by inhibiting the PTEN/AKT/mTOR axis in experimental sepsis-induced myocardial dysfunction. This finding links flavone metabolic process and flavone-derived compounds to the regulation of a major signaling axis in cardiac injury. The involvement of mTOR and AKT suggests that flavone metabolism intersects with pathways controlling cell growth, survival, and stress responses in the heart.
Flavone metabolic process and neurodegenerative disease
Nobiletin, a citrus flavone, has potential benefits against Alzheimer's disease and Parkinson's disease, and tangeretin has been reviewed for its neuroprotective role. These observations connect flavone metabolic process to neurodegeneration research, where flavone bioavailability and metabolic transformation may influence neuroprotective efficacy. The exact mechanisms are still under investigation, but the literature supports a role for flavone-related compounds in neuronal protection.
Flavone metabolic process and metabolic liver disease
Flavone C-glycosides from Dianthus superbus L. attenuate metabolic dysfunction-associated steatotic liver disease (MASLD) via multi-pathway regulations. In addition, tangeretin protects against hepatic ischemia-reperfusion injury through Nrf2-activated mitophagy and ferroptosis suppression. Together, these studies indicate that flavone metabolic process and its products are relevant to liver disease models, including steatotic and ischemia-reperfusion injury settings.
Flavone metabolic process and inflammation or cancer
Icariin and its derivative ICT exert anti-inflammatory and anti-tumor effects and modulate myeloid derived suppressive cells (MDSCs) functions. Nobiletin suppresses adipocyte differentiation of 3T3-L1 cells, linking flavone-related compounds to metabolic and differentiation control. These findings support the investigation of flavone metabolic process in inflammation, cancer immunology, and metabolic regulation.
From flavone metabolic process-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is PTEN required for tangeretin-mediated cardioprotection? | PTEN knockout or point-mutation cardiomyocyte models treated with tangeretin |
| Does Nrf2 mediate tangeretin-induced mitophagy in liver injury? | Nrf2 knockout or tagged knock-in hepatocyte models treated with tangeretin |
| Does nobiletin suppress adipocyte differentiation through a specific target? | Knockout or overexpression 3T3-L1 adipocyte differentiation models treated with nobiletin |
| Do flavone C-glycosides require specific metabolic enzymes to attenuate MASLD? | Knockout or knock-in hepatocyte models treated with flavone C-glycosides |
| Do icariin and ICT modulate MDSC function through defined immune genes? | Knockout or overexpression immune cell models treated with icariin or ICT |
| Which genes determine flavone bioavailability? | CRISPR library screening and bioinformatics-guided knockout models in relevant cell types |
How to Study the flavone metabolic process Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Cell viability and differentiation assays | Effects of flavones on cell growth and differentiation | Nobiletin suppression of 3T3-L1 adipocyte differentiation |
| Western blot and phospho-protein analysis | Activation state of signaling pathways | Tangeretin inhibition of PTEN/AKT/mTOR in myocardial dysfunction |
| Mitophagy and ferroptosis markers | Organelle quality control and lipid peroxidation | Tangeretin protection in hepatic ischemia-reperfusion injury |
| Metabolic profiling | Conjugation and metabolic transformation of flavones | Polyphenol bioavailability studies |
| CRISPR knockout screening | Causal gene requirements for flavone responses | Discovery of regulators of flavone metabolic process |
| Bioinformatics pathway enrichment | Multi-pathway regulation by flavone metabolites | Flavone C-glycoside attenuation of MASLD |
| Immune cell functional assays | MDSC modulation and inflammatory cytokine output | Icariin and ICT anti-inflammatory and anti-tumor studies |
| Neuroprotection assays | Neuronal survival and disease-related markers | Nobiletin and tangeretin neuroprotective research |
Cell-based assays for flavone bioactivity
Cell-based assays are widely used to study flavone metabolic process and the biological effects of flavones. Nobiletin suppression of adipocyte differentiation has been demonstrated in 3T3-L1 cells, and tangeretin protection against sepsis-induced myocardial dysfunction has been studied in experimental myocardial models. These assays typically measure viability, differentiation markers, signaling phosphorylation, and oxidative stress endpoints after flavone treatment.
Signaling pathway analysis
Because flavones modulate defined signaling axes, pathway analysis is central to flavone metabolic process research. Tangeretin inhibition of the PTEN/AKT/mTOR axis has been assessed by measuring pathway component phosphorylation and activity. Nrf2-activated mitophagy and ferroptosis suppression have been evaluated using markers of mitophagy and lipid peroxidation in hepatic ischemia-reperfusion injury models. Such analyses help connect flavone metabolism to downstream cellular responses.
Bioavailability and metabolic profiling
Polyphenol bioavailability studies use metabolic profiling to determine how flavones are absorbed, conjugated, and distributed. These methods are essential for interpreting in vitro results because the metabolic forms of flavones may differ from the parent compounds tested in culture. Profiling approaches can identify conjugated metabolites and quantify systemic exposure, providing a bridge between flavone metabolic process and in vivo activity.
CRISPR screening and bioinformatics
CRISPR library screening combined with bioinformatics enables systematic discovery of genes that regulate flavone metabolic process and flavone responses. By knocking out candidate genes at scale and measuring flavone-related phenotypes, researchers can identify causal regulators rather than correlations. Bioinformatics analysis of pathway enrichment and multi-pathway regulation, as applied to flavone C-glycosides in MASLD, supports the interpretation of screening results.
How CRISPR Can Be Used to Study GO:0051552 flavone metabolic process
Knockout
CRISPR knockout models are used to test whether a candidate gene is required for flavone metabolic process or for the biological effects of flavones. For example, knocking out PTEN or components of the PTEN/AKT/mTOR axis can reveal whether tangeretin-mediated cardioprotection depends on this pathway. Similarly, Nrf2 knockout models can test the requirement for Nrf2 in tangeretin-induced mitophagy and ferroptosis suppression during hepatic ischemia-reperfusion injury. Knockout of adipocyte differentiation regulators can clarify nobiletin's anti-adipogenic mechanism.
Point Mutation
Point-mutation models allow precise testing of phosphorylation sites, catalytic residues, or binding interfaces in genes linked to flavone metabolic process. For signaling components such as AKT or mTOR, point mutations can distinguish catalytic activity from scaffolding functions in the context of tangeretin treatment. In Nrf2-related studies, point mutations can probe domain-specific functions in mitophagy regulation. These models provide mechanistic resolution beyond simple knockout.
Knock-in
Knock-in models, including tagged knock-in and reporter knock-in, enable visualization and quantification of flavone metabolic process components in live cells. Tagged knock-in of Nrf2 or mitophagy regulators can track protein localization and turnover after tangeretin treatment. Reporter knock-in of inflammatory or immune-related genes can monitor pathway activity in response to icariin or ICT. These approaches connect flavone metabolism to dynamic cellular responses.
Overexpression
Overexpression models test whether increasing the level of a candidate gene is sufficient to reproduce or enhance flavone-related phenotypes. Overexpression of flavone C-glycoside biosynthetic enzymes can increase production of bioactive metabolites in plant or cell systems. Overexpression of neuroprotective pathway components can be combined with nobiletin or tangeretin treatment to test synergy in neurodegeneration models. Overexpression studies complement knockout and knock-in approaches to establish sufficiency.
How EDITGENE Supports flavone metabolic process Research
Researchers studying flavone metabolic process-related genes often need to determine whether a candidate gene is causally involved in flavone biosynthesis, bioavailability, or downstream biological effects. Establishing causality requires controlled genetic models in which the candidate gene is deleted, mutated, tagged, or overexpressed, combined with functional readouts such as signaling pathway activity, metabolic profiling, and disease-relevant phenotypes.
Contact EDITGENE today to design your custom CRISPR model for flavone metabolic process research.
Frequently Asked Questions About flavone metabolic process
What is flavone metabolic process?
Flavone metabolic process (GO:0051552) is the chemical reactions and pathways involving flavones, a class of pigmented plant compounds based on 2-phenyl-4H-1-benzopyran-4-one (2-phenylchromone).
What is the GO ID for flavone metabolic process?
The GO ID for flavone metabolic process is GO:0051552, and it belongs to the biological_process ontology.
What genes are involved in flavone metabolic process?
Genes and pathways studied in this context include PTEN, AKT, mTOR, Nrf2, NF-kB, and flavone C-glycoside biosynthetic enzymes, based on experimental studies of flavones such as tangeretin and nobiletin.
How do flavones affect the PTEN/AKT/mTOR pathway?
Tangeretin inhibits the PTEN/AKT/mTOR axis in experimental sepsis-induced myocardial dysfunction, indicating that flavone-related compounds can modulate this signaling pathway.
What is the role of Nrf2 in flavone metabolism research?
Nrf2-activated mitophagy and ferroptosis suppression synergistically mediate tangeretin's protection against hepatic ischemia-reperfusion injury.
Do flavones have neuroprotective effects?
Nobiletin shows potential benefits against Alzheimer's disease and Parkinson's disease, and tangeretin has been reviewed for its neuroprotective role.
How is flavone bioavailability studied?
Polyphenol bioavailability studies use metabolic profiling to determine how flavones are absorbed, conjugated, and distributed, which affects their systemic exposure and activity.
Can flavones help with metabolic liver disease?
Flavone C-glycosides from Dianthus superbus L. attenuate metabolic dysfunction-associated steatotic liver disease (MASLD) via multi-pathway regulations.
What experimental models are used to study flavone metabolic process?
Common models include 3T3-L1 adipocytes for differentiation studies, myocardial dysfunction models for cardioprotection, hepatic ischemia-reperfusion models for hepatoprotection, and neuronal models for neuroprotection.
How can CRISPR help study flavone metabolic process?
CRISPR knockout, point-mutation, knock-in, and overexpression models can test whether specific genes are required or sufficient for flavone-related phenotypes, while CRISPR library screening enables unbiased discovery of regulators.
Conclusion
GO:0051552, flavone metabolic process, provides a standardized biological_process framework for the chemical reactions and pathways involving flavones, a class of pigmented plant compounds based on 2-phenyl-4H-1-benzopyran-4-one (2-phenylchromone). Research on flavones such as tangeretin and nobiletin has linked this process to cardioprotection, neuroprotection, hepatic protection, metabolic liver disease, and inflammation through defined pathways including PTEN/AKT/mTOR and Nrf2-dependent mitophagy. Understanding flavone metabolism is therefore essential for interpreting bioavailability and bioactivity data and for designing translational studies. CRISPR-based knockout, point-mutation, knock-in, and overexpression models, combined with CRISPR library screening and bioinformatics, offer a rigorous path to establish causal gene function in flavone metabolic process research. These approaches support the development of flavone-inspired interventions and the annotation of new genes within GO:0051552.
References
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