GO:0002538 arachidonate metabolite production involved in inflammatory response: Lipid Mediator Pathway, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0002538 describes the synthesis or release of arachidonic acid metabolites following a stimulus as part of an inflammatory response, increasing their intracellular or extracellular levels.
• Arachidonic acid is liberated from membrane phospholipids and converted by cyclooxygenases, lipoxygenases, and cytochrome P450 enzymes into prostaglandins, leukotrienes, hydroxyeicosatetraenoic acids, and epoxyeicosatrienoic acids.
• These lipid mediators are central to acute and chronic inflammation, and their dysregulation is implicated in sepsis, periodontitis, asthma, neurologic disorders, and type 1 diabetes.
• Key enzymes include ALOX5, ALOX12, ALOX15, PTGS1, PTGS2, CYP2C, CYP2J, and PLA2 family phospholipases, which are attractive targets for anti-inflammatory drug discovery.
• CRISPR knockout, point-mutation, knock-in, and overexpression cell models enable causal interrogation of arachidonate metabolite production in inflammatory pathways.
• Understanding GO:0002538 supports the development of pro-resolving and anti-inflammatory therapeutics that modulate lipid mediator profiles.
Description
Arachidonate metabolite production involved in inflammatory response (GO:0002538) is a biological process that encompasses the synthesis or release of products derived from arachidonic acid metabolism following a stimulus, leading to increased intracellular or extracellular levels of these mediators. Arachidonic acid, a polyunsaturated fatty acid, is released from membrane phospholipids by phospholipases and subsequently oxygenated by cyclooxygenases, lipoxygenases, and cytochrome P450 enzymes to generate a diverse family of bioactive lipids, including prostaglandins, leukotrienes, hydroxyeicosatetraenoic acids (HETEs), and epoxyeicosatrienoic acids (EETs). These metabolites act as local hormones and signaling molecules that orchestrate vascular permeability, leukocyte recruitment, pain, and fever during inflammation. The process is not merely a downstream consequence of inflammation but a critical amplifier and regulator of innate and adaptive immune responses. Dysregulated arachidonate metabolite production is a hallmark of many human diseases, ranging from acute conditions such as sepsis to chronic disorders including periodontitis, bronchial asthma, and neurologic diseases. For researchers, GO:0002538 provides a structured framework to study the enzymatic machinery, regulatory checkpoints, and therapeutic potential of lipid mediator pathways. This article synthesizes authoritative QuickGO annotation and verified PubMed literature to deliver a research-grade overview of GO:0002538, covering its definition, molecular players, disease relevance, and state-of-the-art CRISPR-based methods for functional dissection.
arachidonate metabolite production involved in inflammatory response At A Glance
| GO ID | GO:0002538 |
|---|---|
| GO term | arachidonate metabolite production involved in inflammatory response |
| Ontology | biological_process |
| Synonym | arachidonic acid metabolite production involved in acute inflammatory response; arachidonic acid metabolite production involved in inflammatory response; production of arachidonic acid metabolites involved in acute inflammatory response; production of arachidonic acid metabolites involved in inflammatory response |
| Major function | Synthesis or release of arachidonic acid-derived lipid mediators (prostaglandins, leukotrienes, HETEs, EETs) during inflammation |
| Definition | The synthesis or release of products of arachidonic acid metabolism following a stimulus as part of an inflammatory response, resulting in an increase in their intracellular or extracellular levels. |
| Related enzymes | Phospholipases A2, cyclooxygenases (PTGS1/PTGS2), lipoxygenases (ALOX5, ALOX12, ALOX15), cytochrome P450 epoxygenases (CYP2C, CYP2J) |
| Cellular location | Cytosol, endoplasmic reticulum, nuclear envelope, and extracellular space (for released mediators) |
| Key mediators | Prostaglandins, thromboxanes, leukotrienes, lipoxins, HETEs, EETs, and other oxylipins |
What Is GO:0002538?
GO:0002538, arachidonate metabolite production involved in inflammatory response, is defined as the synthesis or release of products of arachidonic acid metabolism following a stimulus as part of an inflammatory response, resulting in an increase in their intracellular or extracellular levels. In simpler terms, it is the cellular process that generates lipid messengers from arachidonic acid to drive or sustain inflammation.
Why Is arachidonate metabolite production involved in inflammatory response Important in Cell Biology?
GO:0002538 is critically important because arachidonic acid metabolites are central to the initiation, amplification, and resolution of inflammation. These lipid mediators regulate vascular tone, platelet aggregation, leukocyte chemotaxis, and cytokine production, and their imbalance contributes to a wide spectrum of inflammatory and immune-mediated diseases. Understanding this process at the molecular level is essential for identifying therapeutic targets and developing interventions that either suppress pathological inflammation or promote its resolution.
• Arachidonic acid metabolites such as prostaglandins and leukotrienes are key drivers of acute inflammatory responses, including fever, pain, and edema.
• The 12/15-lipoxygenase (ALOX15) pathway produces HETEs and lipoxins that modulate both pro-inflammatory and pro-resolving signals in human pathologies.
• Dysregulated arachidonate metabolism is implicated in chronic inflammatory diseases such as periodontitis, where mediators like prostaglandin E2 and leukotriene B4 contribute to tissue destruction.
• In bronchial asthma, hydroxyeicosatetraenoic acids (HETEs) regulate airway inflammation and bronchoconstriction, making them potential biomarkers and drug targets.
• Neurologic disorders including Alzheimer's disease and multiple sclerosis show altered arachidonic acid metabolite profiles, linking this process to neuroinflammation.
• Sepsis and severe systemic inflammation involve excessive production of arachidonic acid-derived mediators, and pro-resolving molecules derived from the same pathway are being explored as therapies.
• Type 1 diabetes pathogenesis involves fatty acid-mediated signaling, and modulating arachidonic acid metabolism is a candidate therapeutic strategy.
• Polyunsaturated fatty acids, including arachidonic acid, influence immune cell function and inflammatory gene expression, highlighting dietary and pharmacological modulation opportunities.
• Enzymes in this pathway (e.g., PTGS2, ALOX5) are validated drug targets, and CRISPR-based models can accelerate target validation.
• GO:0002538 provides a standardized framework for annotating and comparing lipid mediator production across experimental systems and disease models.
What Happens During arachidonate metabolite production involved in inflammatory response?
Release of Arachidonic Acid from Membrane Phospholipids
In simple terms: The first step is freeing arachidonic acid from the cell membrane so it can be converted into inflammatory messengers.
Upon an inflammatory stimulus, cytosolic phospholipase A2 (cPLA2) and other phospholipases are activated and hydrolyze membrane phospholipids at the sn-2 position to release arachidonic acid. This release is the rate-limiting step for the entire pathway and is tightly regulated by calcium and phosphorylation signals. The liberated arachidonic acid can then be oxygenated by three major enzyme families: cyclooxygenases, lipoxygenases, and cytochrome P450 enzymes.
Cyclooxygenase Pathway: Prostaglandins and Thromboxanes
In simple terms: Cyclooxygenases convert arachidonic acid into prostaglandins and thromboxanes, which cause pain, fever, and blood vessel changes.
Cyclooxygenase-1 (PTGS1) and cyclooxygenase-2 (PTGS2) catalyze the conversion of arachidonic acid to prostaglandin H2 (PGH2), which is further metabolized by specific synthases to prostaglandin E2 (PGE2), PGD2, PGF2alpha, prostacyclin (PGI2), and thromboxane A2 (TXA2). These mediators act through G-protein-coupled receptors to induce vasodilation, vascular permeability, pain sensitization, and fever during inflammation. PTGS2 is rapidly induced by inflammatory stimuli and is a major target of nonsteroidal anti-inflammatory drugs.
Lipoxygenase Pathway: Leukotrienes, HETEs, and Lipoxins
In simple terms: Lipoxygenases produce leukotrienes and related molecules that attract immune cells and can either promote or resolve inflammation.
5-lipoxygenase (ALOX5) converts arachidonic acid to 5-HPETE and then leukotriene A4 (LTA4), which is further processed to leukotriene B4 (LTB4), a potent neutrophil chemoattractant, or cysteinyl leukotrienes (LTC4, LTD4, LTE4) that cause bronchoconstriction and vascular permeability. 12/15-lipoxygenase (ALOX15) generates 12-HETE and 15-HETE, which have context-dependent pro- and anti-inflammatory roles, and also contributes to lipoxin biosynthesis, which promotes resolution of inflammation. These HETEs are implicated in asthma, atherosclerosis, and neurologic disorders.
Cytochrome P450 Pathway: EETs and HETEs
In simple terms: Cytochrome P450 enzymes produce epoxyeicosatrienoic acids and HETEs that regulate blood flow and inflammation.
Cytochrome P450 epoxygenases (e.g., CYP2C8, CYP2C9, CYP2J2) convert arachidonic acid to epoxyeicosatrienoic acids (EETs), which have vasodilatory and anti-inflammatory properties, while CYP4A and CYP4F omega-hydroxylases produce 20-HETE, which can be pro-inflammatory and vasoconstrictive. The balance between EETs and 20-HETE influences vascular tone, endothelial function, and inflammatory cell recruitment. These metabolites are also being investigated in metabolic and cardiovascular diseases.
Resolution of Inflammation and Pro-Resolving Mediators
In simple terms: The same pathway can switch to producing molecules that help stop inflammation and promote tissue repair.
Lipoxins, resolvins, and protectins are specialized pro-resolving mediators derived from arachidonic acid and other polyunsaturated fatty acids that actively terminate inflammation and promote tissue repair. Lipoxin A4, generated via 15-lipoxygenase and 5-lipoxygenase pathways, inhibits neutrophil recruitment and stimulates macrophage clearance of apoptotic cells. Dysregulation of this resolution phase contributes to chronic inflammatory diseases such as sepsis and periodontitis.
Key Genes Involved in GO:0002538 arachidonate metabolite production involved in inflammatory response
The following genes encode key enzymes and regulatory proteins that mediate arachidonate metabolite production involved in inflammatory response (GO:0002538).
| Gene | Major Role | Research Relevance |
|---|---|---|
| PLA2G4A | Cytosolic phospholipase A2; releases arachidonic acid from membrane phospholipids | Rate-limiting enzyme; target for anti-inflammatory drugs; KO models reduce eicosanoid production |
| PTGS1 | Cyclooxygenase-1; constitutive production of prostaglandins | Housekeeping eicosanoid synthesis; KO models show gastric and platelet effects |
| PTGS2 | Cyclooxygenase-2; inducible prostaglandin synthesis during inflammation | Major drug target (NSAIDs); overexpression models mimic inflammatory states |
| ALOX5 | 5-lipoxygenase; produces leukotrienes from arachidonic acid | Asthma and allergy target; KO models show reduced leukotriene synthesis |
| ALOX5AP | 5-lipoxygenase activating protein; required for ALOX5 activity | Genetic variants linked to asthma and cardiovascular disease; target for inhibitor drugs |
| LTA4H | Leukotriene A4 hydrolase; converts LTA4 to LTB4 | Pro-inflammatory LTB4 production; KO models impair neutrophil recruitment |
| LTC4S | Leukotriene C4 synthase; produces cysteinyl leukotrienes | Asthma and anaphylaxis; KO models reduce bronchoconstriction |
| ALOX12 | 12-lipoxygenase; produces 12-HETE | Implicated in cancer, thrombosis, and inflammation; KO models show altered platelet function |
| ALOX15 | 12/15-lipoxygenase; produces 12-HETE, 15-HETE, and lipoxins | Roles in atherosclerosis, asthma, and neurodegeneration; KO models show pro-resolving effects |
| CYP2C8 | Cytochrome P450 epoxygenase; produces EETs | Vascular and anti-inflammatory effects; KO models show altered blood pressure regulation |
| CYP2C9 | Cytochrome P450 epoxygenase; produces EETs | Drug metabolism and inflammation; KO models show altered eicosanoid profiles |
| CYP2J2 | Cytochrome P450 epoxygenase; produces EETs | Cardiovascular protection; overexpression models show anti-inflammatory effects |
| CYP4A11 | Cytochrome P450 omega-hydroxylase; produces 20-HETE | Pro-inflammatory and vasoconstrictive; KO models show altered vascular tone |
| CYP4F2 | Cytochrome P450 omega-hydroxylase; produces 20-HETE | Involved in hypertension and inflammation; KO models show altered eicosanoid balance |
| PTGES | Prostaglandin E synthase; converts PGH2 to PGE2 | Pain and fever mediator; KO models show reduced inflammatory pain |
| PTGIS | Prostacyclin synthase; produces PGI2 | Vasodilation and anti-thrombotic; KO models show cardiovascular phenotypes |
| TBXAS1 | Thromboxane A synthase; produces TXA2 | Platelet aggregation and vasoconstriction; KO models show bleeding tendency |
| ALOX12B | 12R-lipoxygenase; produces 12R-HETE | Skin barrier and inflammation; KO models show epidermal defects |
How Is arachidonate metabolite production involved in inflammatory response Regulated?
The production of arachidonate metabolites during inflammation is regulated at multiple levels. Phospholipase A2 activity is controlled by calcium influx and phosphorylation via MAPK and PKC pathways. Cyclooxygenase-2 (PTGS2) is transcriptionally induced by NF-kB, AP-1, and C/EBP in response to inflammatory stimuli such as LPS and cytokines. Lipoxygenase activity is regulated by calcium, ATP, and interacting proteins such as ALOX5AP. Cytochrome P450 epoxygenase expression is modulated by nuclear receptors and dietary factors. Additionally, the resolution phase is actively regulated by pro-resolving mediators that shift the balance from pro-inflammatory to anti-inflammatory lipid profiles. Post-translational modifications, including phosphorylation and ubiquitination, also influence enzyme stability and subcellular localization.
arachidonate metabolite production involved in inflammatory response and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| ALOX5 | Asthma, allergic inflammation | Knockout cell line (e.g., HEK293 or primary airway epithelial cells) to assess leukotriene production |
| PTGS2 | Sepsis, periodontitis, cancer | Overexpression in macrophages or epithelial cells to model chronic inflammation |
| ALOX15 | Atherosclerosis, neurodegeneration | Knock-in of human ALOX15 variants in mouse or cell lines to study HETE profiles |
| CYP2J2 | Cardiovascular disease, inflammation | Overexpression in endothelial cells to measure EET-mediated anti-inflammatory effects |
| PLA2G4A | Sepsis, asthma | Knockout in immune cells to determine arachidonic acid release capacity |
Sepsis and Systemic Inflammatory Response
Severe sepsis is characterized by an uncontrolled systemic inflammatory response in which arachidonic acid metabolites such as thromboxane A2, prostacyclin, and leukotrienes contribute to vasodilation, hypotension, and organ dysfunction. Excessive production of these mediators is associated with poor outcomes, and pro-resolving molecules derived from the same pathway are being investigated as therapeutic agents to restore homeostasis. Targeting arachidonate metabolite production is therefore a rational strategy for sepsis management.
Periodontitis
Periodontitis is a chronic inflammatory disease of the tooth-supporting tissues in which arachidonic acid metabolites, particularly prostaglandin E2 and leukotriene B4, drive tissue destruction and bone resorption. Inflammatory mediators in the gingival crevicular fluid correlate with disease severity, and modulation of the arachidonic acid pathway is a potential adjunctive therapy. The process defined by GO:0002538 is directly relevant to the pathogenesis of periodontitis.
Bronchial Asthma
In bronchial asthma, hydroxyeicosatetraenoic acids (HETEs) and cysteinyl leukotrienes produced via the arachidonic acid pathway contribute to airway inflammation, bronchoconstriction, and mucus hypersecretion. 5-lipoxygenase (ALOX5) and its activating protein (ALOX5AP) are genetically linked to asthma susceptibility, and leukotriene receptor antagonists are established therapies. Understanding the regulation of arachidonate metabolite production is essential for developing new asthma treatments.
Neurologic Disorders and Type 1 Diabetes
Arachidonic acid metabolites are implicated in neurologic disorders such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis, where they modulate neuroinflammation and neuronal survival. In type 1 diabetes, fatty acid-mediated signaling, including arachidonic acid metabolism, contributes to beta-cell dysfunction and autoimmune destruction. These findings highlight GO:0002538 as a cross-disease process with therapeutic potential.
From arachidonate metabolite production involved in inflammatory response-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of ALOX5 reduce leukotriene production during inflammation? | CRISPR knockout of ALOX5 in macrophage cell lines (e.g., THP-1) |
| Does a specific PTGS2 polymorphism alter prostaglandin synthesis? | Point mutation knock-in of PTGS2 variant in HEK293 cells |
| Can overexpression of CYP2J2 increase anti-inflammatory EETs? | Overexpression of CYP2J2 in endothelial cells |
| What is the role of ALOX15 in lipoxin-mediated resolution? | Knock-in of tagged ALOX15 for live-cell imaging |
| Does ALOX5AP deficiency affect leukotriene biosynthesis? | Knockout of ALOX5AP in primary neutrophils |
| Can CRISPR activation of PTGIS enhance prostacyclin production? | CRISPR activation (dCas9-VP64) of PTGIS in vascular smooth muscle cells |
How to Study the arachidonate metabolite production involved in inflammatory response Process
| Method | What It Measures | Typical Application |
|---|---|---|
| LC-MS/MS lipidomics | Quantification of arachidonic acid metabolites (prostaglandins, leukotrienes, HETEs, EETs) | Profiling inflammatory mediator production in CRISPR-edited cells |
| RNA-seq | Transcript levels of arachidonate metabolism genes | Assessing transcriptional regulation after inflammatory stimulus |
| Proteomics | Protein expression and post-translational modifications of pathway enzymes | Validating knockout or overexpression effects |
| Enzyme activity assay | Catalytic activity of COX, LOX, and CYP enzymes | Functional characterization of point mutations |
| ELISA | Concentration of specific eicosanoids (e.g., PGE2, LTB4) | High-throughput screening of inflammatory mediator release |
| Fluorescent biosensors | Real-time intracellular lipid mediator dynamics | Live-cell imaging of arachidonic acid release |
| CRISPR screen | Identification of genes regulating arachidonate metabolite production | Unbiased discovery of novel pathway components |
| Bioinformatics pathway analysis | Enrichment of GO:0002538 and related terms in omics data | Interpreting transcriptomic or proteomic datasets |
Lipidomics and Mass Spectrometry
Liquid chromatography-tandem mass spectrometry (LC-MS/MS) is the gold standard for quantifying arachidonic acid metabolites such as prostaglandins, leukotrienes, HETEs, and EETs in cell culture supernatants and tissues. Targeted lipidomics enables profiling of multiple mediators simultaneously, providing a comprehensive readout of GO:0002538 activity. This method is essential for validating CRISPR knockout or overexpression models.
Transcriptional and Proteomic Profiling
RNA-seq and quantitative proteomics can measure the expression of enzymes involved in arachidonate metabolism (e.g., PTGS2, ALOX5, CYP2J2) following inflammatory stimulation. These approaches reveal regulatory mechanisms and identify compensatory changes in CRISPR-edited cells. Phosphoproteomics can further uncover signaling events that control enzyme activity.
Enzyme Activity Assays
Specific enzyme activity assays using radiolabeled or fluorescent substrates measure the catalytic capacity of cyclooxygenases, lipoxygenases, and cytochrome P450 enzymes in cell lysates or intact cells. These assays are useful for determining the functional impact of point mutations introduced by CRISPR.
Imaging and Reporter Systems
Fluorescent reporters and biosensors can monitor arachidonic acid release and metabolite production in live cells. For example, genetically encoded sensors for prostaglandins or leukotrienes enable real-time visualization of inflammatory lipid signaling. These tools complement CRISPR-based models by providing spatial and temporal resolution.
How CRISPR Can Be Used to Study GO:0002538 arachidonate metabolite production involved in inflammatory response
Knockout
CRISPR knockout of genes encoding arachidonic acid pathway enzymes (e.g., ALOX5, PTGS2, PLA2G4A) provides definitive loss-of-function models to test their contribution to inflammatory mediator production. Knockout cell lines can be stimulated with LPS or cytokines and analyzed by lipidomics to quantify changes in prostaglandin, leukotriene, and HETE levels. These models are essential for target validation in drug discovery.
Point Mutation
CRISPR point mutation (base editing or homology-directed repair) allows introduction of disease-associated or catalytically dead mutations in arachidonate metabolism genes. For example, mutating the catalytic serine of ALOX15 or the active-site tyrosine of PTGS2 can reveal enzyme-specific contributions to inflammatory lipid profiles. Such models are valuable for understanding genetic variants linked to asthma or cardiovascular disease.
Knock-in
Knock-in of tagged versions of pathway enzymes (e.g., GFP-ALOX5, HA-PTGS2) enables live-cell imaging and immunoprecipitation studies to determine subcellular localization and interacting partners during inflammation. Knock-in of human orthologs into mouse models can humanize the pathway for drug testing. These models help dissect spatial and temporal regulation of arachidonate metabolite production.
Overexpression
CRISPR activation (dCas9-VP64) or lentiviral overexpression of rate-limiting enzymes such as PTGS2, ALOX5, or CYP2J2 can amplify specific branches of arachidonic acid metabolism. Overexpression models are useful for studying the consequences of excessive mediator production in diseases like sepsis and asthma. They also enable screening of inhibitors that target the overactive pathway.
How EDITGENE Supports arachidonate metabolite production involved in inflammatory response Research
Researchers studying arachidonate metabolite production involved in inflammatory response-related genes often need to determine whether a candidate gene is causally involved in lipid mediator synthesis, how specific mutations alter enzyme activity, and whether therapeutic modulation can shift the balance toward resolution. EDITGENE provides end-to-end CRISPR services to answer these questions with rigor and reproducibility.
Contact EDITGENE today to design your custom CRISPR model for arachidonate metabolite production involved in inflammatory response research.
Frequently Asked Questions About arachidonate metabolite production involved in inflammatory response
What is GO:0002538?
GO:0002538 is a Gene Ontology biological process term defined as the synthesis or release of products of arachidonic acid metabolism following a stimulus as part of an inflammatory response, resulting in an increase in their intracellular or extracellular levels.
What genes are involved in arachidonate metabolite production involved in inflammatory response?
Key genes include PLA2G4A, PTGS1, PTGS2, ALOX5, ALOX5AP, LTA4H, LTC4S, ALOX12, ALOX15, CYP2C8, CYP2C9, CYP2J2, CYP4A11, CYP4F2, PTGES, PTGIS, and TBXAS1, which encode enzymes that synthesize prostaglandins, leukotrienes, HETEs, and EETs.
What are the main products of arachidonic acid metabolism during inflammation?
The main products include prostaglandins (e.g., PGE2, PGI2), thromboxanes (TXA2), leukotrienes (LTB4, LTC4), hydroxyeicosatetraenoic acids (HETEs), and epoxyeicosatrienoic acids (EETs).
How is arachidonic acid released from cell membranes?
Arachidonic acid is released from membrane phospholipids by phospholipase A2 enzymes, particularly cytosolic phospholipase A2 (PLA2G4A), in response to inflammatory stimuli and calcium signals.
What diseases are associated with dysregulated arachidonate metabolite production?
Dysregulated production is associated with sepsis, periodontitis, bronchial asthma, neurologic disorders such as Alzheimer's disease, and type 1 diabetes.
How can CRISPR be used to study arachidonate metabolite production?
CRISPR knockout, point mutation, knock-in, and overexpression models allow researchers to test the causal role of specific genes in lipid mediator synthesis and to validate drug targets.
What methods are used to measure arachidonic acid metabolites?
Liquid chromatography-tandem mass spectrometry (LC-MS/MS) is the gold standard, complemented by ELISA, enzyme activity assays, and fluorescent biosensors.
What is the role of ALOX15 in inflammation?
ALOX15 (12/15-lipoxygenase) produces 12-HETE and 15-HETE and contributes to lipoxin biosynthesis, with context-dependent pro-inflammatory and pro-resolving roles in human pathologies.
How is GO:0002538 regulated?
The process is regulated at multiple levels, including calcium-dependent phospholipase A2 activation, transcriptional induction of PTGS2 by NF-kB, and post-translational modifications of lipoxygenases and cytochrome P450 enzymes.
Why is arachidonate metabolite production important for drug discovery?
Enzymes in this pathway, such as PTGS2 and ALOX5, are validated drug targets, and modulating metabolite profiles offers therapeutic opportunities for inflammatory diseases, asthma, and sepsis.
Conclusion
GO:0002538, arachidonate metabolite production involved in inflammatory response, represents a central biological process that converts arachidonic acid into a diverse array of lipid mediators controlling inflammation. Its dysregulation is implicated in sepsis, periodontitis, asthma, neurologic disorders, and type 1 diabetes, making it a high-value area for therapeutic intervention. Advances in CRISPR-based genome editing, combined with lipidomics and bioinformatics, now enable precise dissection of the enzymatic machinery and regulatory networks underlying this process. EDITGENE provides comprehensive CRISPR services, including knockout, point mutation, knock-in, overexpression, library screening, and bioinformatics, to support researchers in uncovering causal mechanisms and developing novel anti-inflammatory strategies targeting arachidonate metabolite production.
References
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