GO:0035336 long-chain fatty-acyl-CoA metabolic process: Fatty Acid Activation and Trafficking, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0035336 describes the chemical reactions and pathways involving long-chain fatty-acyl-CoAs, which are coenzyme A derivatives with a thioester-linked aliphatic tail of 13 to 22 carbons.
• Long-chain fatty-acyl-CoAs are central intermediates in mitochondrial beta-oxidation, membrane lipid synthesis, protein acylation, and metabolic signaling [1, 7].
• The pathway is initiated by long-chain fatty acyl-CoA synthetases (ACSL family) and is coupled to carnitine shuttle transport for mitochondrial import [1, 5].
• Long-chain fatty-acyl-CoA levels are sensed by AMPK and influence insulin sensitivity, hepatic fatty acid oxidation, and macrophage polarization [4, 6, 8, 3].
• Dysregulation of long-chain fatty-acyl-CoA metabolism is linked to nonalcoholic fatty liver disease, insulin resistance, and metabolic reprogramming in immune cells [6, 8, 3].
• CRISPR knockout, point mutation, knock-in, and overexpression models enable causal dissection of ACSL, CPT, and ACAD family genes in this pathway [1, 5, 6].
Description
Long-chain fatty-acyl-CoA metabolic process (GO:0035336) encompasses the chemical reactions and pathways involving long-chain fatty-acyl-CoAs, which are derivatives of coenzyme A in which the sulfhydryl group is in a thioester linkage with a long-chain fatty-acyl group containing 13 to 22 carbons. These molecules are not merely metabolic intermediates; they serve as substrates for beta-oxidation, building blocks for complex lipids, and signaling molecules that report fatty acid availability to cellular sensors [1, 4, 7]. The pathway is essential for energy homeostasis, membrane biogenesis, and protein acylation, and its dysfunction is increasingly recognized in metabolic and inflammatory diseases [1, 6, 8]. For researchers, GO:0035336 provides a structured framework to study fatty acid activation, intracellular trafficking, and oxidation. The process begins with the ATP-dependent ligation of a long-chain fatty acid to coenzyme A, catalyzed by acyl-CoA synthetases such as ACSL family enzymes. The resulting long-chain fatty acyl-CoAs can be directed toward mitochondrial beta-oxidation via the carnitine shuttle, incorporated into glycerolipids and phospholipids, or used for protein S-acylation by zDHHC acyltransferases [1, 7]. Because these acyl-CoAs are both metabolites and signals, their levels are tightly regulated and can be monitored using biochemical and genetic approaches [4, 5]. Understanding GO:0035336 is critical for dissecting metabolic diseases, cancer, and immune cell function. For example, ACSL5-mediated deacetylation by SIRT6 promotes hepatic fatty acid oxidation and protects against nonalcoholic fatty liver disease. Etomoxir, an inhibitor of carnitine palmitoyltransferase 1, disrupts CoA homeostasis and macrophage polarization, highlighting the importance of long-chain fatty-acyl-CoA metabolism in immunometabolism. AMPK senses long-chain fatty acyl-CoA esters to adjust energy balance, linking this pathway to insulin resistance and exercise physiology [4, 8]. This article integrates authoritative GO annotation with verified literature to provide a research-grade overview of GO:0035336.
long-chain fatty-acyl-CoA metabolic process At A Glance
| GO ID | GO:0035336 |
|---|---|
| GO term | long-chain fatty-acyl-CoA metabolic process |
| Ontology | biological_process |
| Synonym | long-chain fatty acyl CoA metabolic process; long-chain fatty acyl-CoA metabolism |
| Major function | Metabolism of coenzyme A thioesters of fatty acids with 13-22 carbon aliphatic tails, central to beta-oxidation, lipid synthesis, and acyl-CoA signaling [1, 7] |
| Key substrates | Long-chain fatty acids (C13-C22), coenzyme A, ATP [1, 5] |
| Key products | Long-chain fatty acyl-CoA thioesters, acyl-carnitines, acetyl-CoA, membrane lipids [1, 7] |
| Cellular locations | Cytosol, mitochondria, peroxisomes, endoplasmic reticulum [1, 7] |
| Related enzymes | ACSL family, CPT1/CPT2, ACAD family, zDHHC acyltransferases [1, 5, 7] |
What Is GO:0035336?
GO:0035336, long-chain fatty-acyl-CoA metabolic process, is defined as the chemical reactions and pathways involving long-chain fatty-acyl-CoAs, any derivative of coenzyme A in which the sulfhydryl group is in a thioester linkage with a long-chain fatty-acyl group. A long-chain fatty acid has an aliphatic tail containing 13 to 22 carbons. In practice, this term covers the synthesis, interconversion, transport, and utilization of these acyl-CoA thioesters, including their oxidation, incorporation into lipids, and participation in signaling and protein modification [1, 7].
Why Is long-chain fatty-acyl-CoA metabolic process Important in Cell Biology?
GO:0035336 is important because long-chain fatty-acyl-CoAs sit at the intersection of energy production, membrane biogenesis, and cellular signaling. They are the obligatory substrates for mitochondrial beta-oxidation, the primary pathway for ATP generation from fatty acids during fasting and exercise. They also serve as precursors for phospholipids, triacylglycerols, and sphingolipids, and as donors for protein S-acylation, which influences protein localization and function. Moreover, long-chain fatty acyl-CoA levels are sensed by AMPK and contribute to insulin resistance in skeletal muscle, making this pathway a therapeutic target for metabolic syndrome and type 2 diabetes [4, 8]. In immune cells, disruption of long-chain fatty-acyl-CoA metabolism by etomoxir alters macrophage polarization, underscoring its role in inflammation and immunometabolism. In the liver, SIRT6-mediated deacetylation of ACSL5 enhances fatty acid oxidation and protects against nonalcoholic fatty liver disease. Thus, GO:0035336 is a nexus for metabolic, cardiovascular, hepatic, and immune research.
• Provides the essential acyl-CoA substrates for mitochondrial beta-oxidation and ATP production during fasting.
• Supplies long-chain fatty acyl-CoAs for membrane phospholipid and glycerolipid synthesis [1, 7].
• Enables protein S-acylation by zDHHC acyltransferases, affecting protein trafficking and signaling.
• Links fatty acid availability to AMPK signaling and insulin sensitivity in skeletal muscle [4, 8].
• Plays a role in macrophage polarization and inflammatory responses, as shown by etomoxir studies.
• Is implicated in nonalcoholic fatty liver disease through ACSL5 regulation by SIRT6.
• Serves as a target for metabolic disease therapies aimed at modulating fatty acid oxidation [1, 8].
• Can be studied using enzyme activity assays, acyl-CoA quantification, and genetic models [4, 5].
• Involves multiple organelles (mitochondria, peroxisomes, ER), making it relevant to organelle biology [1, 7].
• Dysregulation contributes to lipotoxicity and metabolic reprogramming in cancer and immune cells [3, 6].
What Happens During long-chain fatty-acyl-CoA metabolic process?
Fatty acid activation to long-chain fatty acyl-CoA
In simple terms: A fatty acid is joined to coenzyme A to make it reactive and ready for further metabolism.
The first step in GO:0035336 is the ATP-dependent ligation of a long-chain fatty acid (C13-C22) to coenzyme A, forming a long-chain fatty acyl-CoA thioester. This reaction is catalyzed by long-chain fatty acyl-CoA synthetases, including the ACSL family, and requires ATP and Mg2+ [1, 5]. The resulting acyl-CoA is a high-energy thioester that can be directed toward oxidation, lipid synthesis, or protein modification [1, 7]. Measurement of ACSL activity is a standard approach to study this step.
Mitochondrial import via the carnitine shuttle
In simple terms: The activated fatty acid is carried into mitochondria by a shuttle system so it can be burned for energy.
Long-chain fatty acyl-CoAs cannot cross the inner mitochondrial membrane directly. They are converted to acyl-carnitines by carnitine palmitoyltransferase 1 (CPT1) on the outer membrane, translocated by the carnitine-acylcarnitine translocase, and reconverted to acyl-CoAs by CPT2 on the inner membrane. This carnitine shuttle is rate-limiting for mitochondrial beta-oxidation and is a target of pharmacological inhibitors such as etomoxir, which disrupts CoA homeostasis and affects macrophage polarization.
Beta-oxidation and acetyl-CoA generation
In simple terms: The fatty acid chain is chopped into two-carbon units to produce energy.
Inside the mitochondrial matrix, long-chain fatty acyl-CoAs undergo beta-oxidation, a cycle of dehydrogenation, hydration, thiolysis, and dehydrogenation that removes two carbons per cycle as acetyl-CoA. The acyl-CoA dehydrogenase (ACAD) family, including very-long-chain, long-chain, and medium-chain acyl-CoA dehydrogenases, catalyzes the initial step. Acetyl-CoA then enters the TCA cycle to generate NADH and FADH2 for oxidative phosphorylation. Short- and medium-chain fatty acids can also contribute to energy metabolism through related pathways.
Acyl-CoA sensing and signaling
In simple terms: The cell monitors how much activated fatty acid is present and adjusts its metabolism accordingly.
Long-chain fatty acyl-CoAs are not only substrates but also signaling molecules. AMPK senses long-chain fatty acyl-CoA esters to modulate energy balance, and this sensing is relevant to insulin resistance and exercise adaptation. Malonyl-CoA, a precursor for fatty acid synthesis, inhibits CPT1 and thereby regulates long-chain fatty acyl-CoA entry into mitochondria, linking lipogenesis to oxidation. In skeletal muscle, elevated long-chain fatty acyl-CoA levels are associated with insulin resistance, suggesting a role in metabolic dysfunction.
Utilization for lipid synthesis and protein acylation
In simple terms: Activated fatty acids are also used to build membranes and modify proteins.
Beyond oxidation, long-chain fatty acyl-CoAs serve as substrates for glycerolipid and phospholipid synthesis in the endoplasmic reticulum and for protein S-acylation by zDHHC protein acyltransferases. This acylation modifies protein localization and function, influencing signaling pathways. The balance between oxidation and lipid synthesis is critical for cellular homeostasis, and its disruption can lead to steatosis and lipotoxicity [6, 7].
Key Genes Involved in GO:0035336 long-chain fatty-acyl-CoA metabolic process
The following genes and proteins are central to long-chain fatty-acyl-CoA metabolism, based on their established roles in fatty acid activation, transport, oxidation, and signaling.
| Gene | Major Role | Research Relevance |
|---|---|---|
| ACSL1 | Long-chain fatty acyl-CoA synthetase; activates fatty acids for oxidation and lipid synthesis | Key enzyme for acyl-CoA production; knockout models show impaired fatty acid oxidation [1, 5] |
| ACSL5 | Long-chain fatty acyl-CoA synthetase; hepatic isoform regulated by SIRT6 | Deacetylation by SIRT6 promotes fatty acid oxidation and protects against NAFLD |
| CPT1A | Carnitine palmitoyltransferase 1A; rate-limiting for mitochondrial long-chain fatty acyl-CoA import | Target of etomoxir; regulates beta-oxidation and macrophage polarization [1, 3] |
| CPT2 | Carnitine palmitoyltransferase 2; reconverts acyl-carnitines to acyl-CoAs inside mitochondria | Defects cause CPT2 deficiency and impaired fatty acid oxidation |
| ACADVL | Very-long-chain acyl-CoA dehydrogenase; first step of beta-oxidation for long-chain acyl-CoAs | Mutations cause VLCAD deficiency; model for fatty acid oxidation disorders |
| ACADL | Long-chain acyl-CoA dehydrogenase; catalyzes beta-oxidation of long-chain acyl-CoAs | Studied in mitochondrial fatty acid oxidation and energy metabolism |
| ACADM | Medium-chain acyl-CoA dehydrogenase; oxidizes medium-chain acyl-CoAs | Deficiency causes MCAD deficiency; relevant to energy metabolism [1, 2] |
| SIRT6 | NAD+-dependent deacetylase; deacetylates ACSL5 | Regulates hepatic fatty acid oxidation and NAFLD progression |
| PRKAA1/PRKAA2 | AMPK catalytic subunits; sense long-chain fatty acyl-CoA esters | Mediate metabolic adaptation to fatty acid availability |
| zDHHC family | Protein acyltransferases that use long-chain fatty acyl-CoA for S-acylation | Regulate protein trafficking and signaling via acylation |
| ACOX1 | Peroxisomal acyl-CoA oxidase; oxidizes long-chain acyl-CoAs in peroxisomes | Important for peroxisomal beta-oxidation of very-long-chain fatty acids |
| HADHA | Mitochondrial trifunctional protein subunit; catalyzes beta-oxidation steps | Defects cause fatty acid oxidation disorders |
| HADHB | Mitochondrial trifunctional protein subunit; catalyzes beta-oxidation steps | Defects cause fatty acid oxidation disorders |
| SLC25A20 | Carnitine-acylcarnitine translocase; transports acyl-carnitines across inner mitochondrial membrane | Defects cause carnitine-acylcarnitine translocase deficiency |
| MLYCD | Malonyl-CoA decarboxylase; regulates malonyl-CoA levels | Modulates CPT1 activity and fatty acid oxidation |
| ACACA | Acetyl-CoA carboxylase alpha; produces malonyl-CoA | Malonyl-CoA inhibits CPT1, linking lipogenesis to oxidation |
| PPARA | Peroxisome proliferator-activated receptor alpha; transcription factor regulating fatty acid oxidation genes | Controls expression of ACSL, CPT1, and ACAD genes |
| PPARGC1A | PGC-1alpha; coactivator of mitochondrial biogenesis and fatty acid oxidation | Regulates oxidative capacity and acyl-CoA metabolism |
How Is long-chain fatty-acyl-CoA metabolic process Regulated?
Long-chain fatty-acyl-CoA metabolic process is regulated at multiple levels. Transcriptionally, PPAR alpha and PGC-1 alpha promote the expression of genes involved in fatty acid uptake, activation, and beta-oxidation. Post-translationally, ACSL5 is deacetylated by SIRT6, which enhances its activity and facilitates hepatic fatty acid oxidation, protecting against nonalcoholic fatty liver disease. AMPK senses long-chain fatty acyl-CoA esters and phosphorylates downstream targets to adjust energy balance, linking acyl-CoA levels to insulin sensitivity. Malonyl-CoA, produced by acetyl-CoA carboxylase, inhibits CPT1 and thereby reduces long-chain fatty acyl-CoA entry into mitochondria, providing feedback regulation between fatty acid synthesis and oxidation. Additionally, the availability of coenzyme A and carnitine influences flux through the pathway, and etomoxir disrupts CoA homeostasis, affecting macrophage polarization.
long-chain fatty-acyl-CoA metabolic process and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| ACSL5 | Nonalcoholic fatty liver disease; hepatic fatty acid oxidation | Liver-specific knockout or SIRT6 deacetylation-mimic knock-in in mice |
| CPT1A | Insulin resistance; fatty acid oxidation disorders | Point mutation (e.g., P479L) knock-in or knockout in cell lines [1, 3] |
| ACADVL | VLCAD deficiency; cardiomyopathy | Knockout or patient-derived point mutations in iPSC-derived cardiomyocytes |
| SIRT6 | NAFLD; metabolic regulation | Knockout and overexpression in hepatocytes |
| PRKAA1/PRKAA2 | Insulin resistance; energy sensing | AMPK knockout or point mutation to disrupt acyl-CoA sensing |
Nonalcoholic fatty liver disease (NAFLD)
Hepatic long-chain fatty-acyl-CoA metabolism is critical for lipid homeostasis. SIRT6-mediated deacetylation of ACSL5 promotes fatty acid oxidation and impedes NAFLD progression in mouse models. Dysregulation of this pathway leads to triglyceride accumulation and lipotoxicity, contributing to steatohepatitis and insulin resistance [6, 8].
Insulin resistance and type 2 diabetes
Elevated long-chain fatty acyl-CoA levels in skeletal muscle are associated with insulin resistance, and malonyl-CoA-mediated inhibition of CPT1 links lipid availability to glucose metabolism. AMPK sensing of long-chain fatty acyl-CoA esters is a key mechanism for maintaining energy balance, and its dysfunction contributes to metabolic disease.
Inherited fatty acid oxidation disorders
Mutations in genes encoding carnitine shuttle components (CPT1A, CPT2, SLC25A20) and beta-oxidation enzymes (ACADVL, ACADL, ACADM, HADHA, HADHB) cause inherited disorders characterized by impaired long-chain fatty-acyl-CoA oxidation, hypoglycemia, cardiomyopathy, and rhabdomyolysis. These conditions highlight the essential role of GO:0035336 in energy metabolism.
Immunometabolism and inflammation
Etomoxir, an inhibitor of CPT1, disrupts CoA homeostasis and inhibits macrophage polarization, demonstrating that long-chain fatty-acyl-CoA metabolism is required for inflammatory responses. This has implications for diseases involving macrophage activation, such as atherosclerosis and obesity-related inflammation.
From long-chain fatty-acyl-CoA metabolic process-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of ACSL5 impair hepatic fatty acid oxidation? | ACSL5 knockout hepatocytes or liver-specific knockout mice |
| Does a specific point mutation in CPT1A alter acyl-CoA transport? | CRISPR point mutation knock-in in cell lines, followed by acyl-carnitine profiling |
| Does SIRT6-mediated deacetylation of ACSL5 regulate its activity? | ACSL5 acetylation-site mutant knock-in (K-to-Q or K-to-R) |
| How does AMPK sense long-chain fatty acyl-CoA esters? | AMPK point mutations or knockout cells treated with acyl-CoA analogs |
| What is the role of zDHHC acyltransferases in protein S-acylation? | zDHHC knockout or tagged knock-in for localization studies |
| Can overexpression of ACSL1 enhance fatty acid oxidation? | ACSL1 overexpression in cell lines or mice [1, 5] |
How to Study the long-chain fatty-acyl-CoA metabolic process Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Acyl-CoA synthetase activity assay | Enzymatic conversion of fatty acids to acyl-CoAs | Assessing ACSL function in knockout or mutant cells |
| LC-MS/MS acyl-CoA profiling | Levels of individual long-chain fatty acyl-CoA species | Metabolic flux studies and drug effects [3, 4] |
| Seahorse extracellular flux analysis | Mitochondrial oxidation and fatty acid dependence | Evaluating beta-oxidation capacity |
| CRISPR knockout screens | Genes required for growth under fatty acid stress | Identifying novel regulators of GO:0035336 |
| Click chemistry for S-acylation | Protein S-acylation levels | Studying zDHHC substrate specificity |
| Immunoblotting for beta-oxidation enzymes | Protein expression of ACAD, CPT, HADH | Validating genetic models |
| RNA-seq | Transcriptional changes in fatty acid metabolism genes | Profiling PPAR alpha and PGC-1 alpha targets |
| Isotope tracing | Flux of 13C-labeled fatty acids into metabolites | Quantifying beta-oxidation and TCA cycle activity |
Measuring long-chain fatty acyl-CoA synthetase activity
Long-chain fatty acyl-CoA synthetase activity can be measured using radiolabeled fatty acids or coupled enzyme assays that detect acyl-CoA formation. These methods are essential for quantifying the first step of GO:0035336 and for assessing the impact of genetic perturbations.
Quantifying long-chain fatty acyl-CoA levels
Liquid chromatography-tandem mass spectrometry (LC-MS/MS) allows sensitive quantification of individual long-chain fatty acyl-CoA species in cells and tissues. This approach is used to study metabolic flux and the effects of AMPK activation or etomoxir treatment [3, 4].
Genetic screens and CRISPR knockout
CRISPR-Cas9 knockout screens can identify genes required for long-chain fatty-acyl-CoA metabolism, such as ACSL, CPT, and ACAD family members. Pooled screens coupled with acyl-CoA profiling or cell viability under fatty acid stress reveal novel regulators [1, 6].
Protein acylation analysis
Protein S-acylation by zDHHC acyltransferases can be studied using click chemistry with azide-modified fatty acids, followed by mass spectrometry or immunoblotting. These methods link long-chain fatty-acyl-CoA metabolism to protein function.
How CRISPR Can Be Used to Study GO:0035336 long-chain fatty-acyl-CoA metabolic process
Knockout
CRISPR knockout of genes such as ACSL5, CPT1A, or ACADVL in cell lines or primary cells can abolish long-chain fatty-acyl-CoA metabolism, leading to impaired fatty acid oxidation and altered lipid homeostasis. These models are used to study the consequences of pathway loss in hepatocytes, macrophages, and cardiomyocytes [1, 3, 6].
Point Mutation
Point mutations in CPT1A, CPT2, or ACADVL that mimic human disease variants can be introduced using CRISPR base editing or homology-directed repair. These models help dissect the impact of specific residues on enzyme activity and acyl-CoA handling.
Knock-in
Knock-in of tags (e.g., FLAG, GFP) into endogenous ACSL or zDHHC genes allows visualization and immunoprecipitation of these enzymes in their native context. Knock-in of acetylation-site mutants in ACSL5 can test the role of SIRT6-mediated deacetylation [6, 7].
Overexpression
Overexpression of ACSL1 or ACSL5 via CRISPR activation or lentiviral delivery can enhance long-chain fatty-acyl-CoA synthesis and oxidation. These models are useful for studying the effects of increased flux on cellular metabolism and disease phenotypes [1, 5].
How EDITGENE Supports long-chain fatty-acyl-CoA metabolic process Research
Researchers studying long-chain fatty-acyl-CoA metabolic process-related genes often need to determine whether a candidate gene is causally involved in fatty acid activation, transport, or oxidation. EDITGENE provides a comprehensive suite of CRISPR services to generate precisely engineered cell models, enabling rigorous functional validation of genes within GO:0035336.
Contact EDITGENE today to design your custom CRISPR model for long-chain fatty-acyl-CoA metabolic process research.
Frequently Asked Questions About long-chain fatty-acyl-CoA metabolic process
What is long-chain fatty-acyl-CoA metabolic process?
It is the set of chemical reactions and pathways involving coenzyme A derivatives of fatty acids with 13 to 22 carbon chains, central to fatty acid oxidation and lipid synthesis.
What genes are involved in long-chain fatty-acyl-CoA metabolic process?
Key genes include ACSL1, ACSL5, CPT1A, CPT2, ACADVL, ACADL, ACADM, HADHA, HADHB, SLC25A20, SIRT6, and zDHHC family members [1, 5, 6, 7].
What is the GO ID for long-chain fatty-acyl-CoA metabolic process?
The Gene Ontology ID is GO:0035336.
How is long-chain fatty-acyl-CoA metabolism regulated?
It is regulated by transcription factors such as PPAR alpha, by AMPK sensing of acyl-CoA levels, by SIRT6-mediated deacetylation of ACSL5, and by malonyl-CoA inhibition of CPT1 [1, 4, 6, 8].
What diseases are associated with long-chain fatty-acyl-CoA metabolism?
Diseases include nonalcoholic fatty liver disease, insulin resistance, type 2 diabetes, inherited fatty acid oxidation disorders, and inflammatory conditions involving macrophage polarization [1, 3, 6, 8].
How can I study long-chain fatty-acyl-CoA metabolism in the lab?
Common methods include acyl-CoA synthetase activity assays, LC-MS/MS acyl-CoA profiling, Seahorse flux analysis, and CRISPR knockout screens [1, 3, 4, 5].
What is the role of ACSL5 in fatty liver disease?
ACSL5 is deacetylated by SIRT6, which enhances hepatic fatty acid oxidation and impedes nonalcoholic fatty liver disease progression.
How does etomoxir affect long-chain fatty-acyl-CoA metabolism?
Etomoxir inhibits CPT1 and disrupts CoA homeostasis, thereby blocking mitochondrial long-chain fatty acyl-CoA import and affecting macrophage polarization.
What is the carnitine shuttle?
The carnitine shuttle transports long-chain fatty acyl-CoAs into mitochondria via CPT1, carnitine-acylcarnitine translocase, and CPT2.
Can CRISPR be used to model long-chain fatty-acyl-CoA metabolic disorders?
Yes, CRISPR knockout, point mutation, knock-in, and overexpression models can replicate disease-associated variants and dissect gene function in this pathway [1, 6].
Conclusion
GO:0035336, long-chain fatty-acyl-CoA metabolic process, is a fundamental biological process that governs fatty acid activation, mitochondrial import, beta-oxidation, lipid synthesis, and protein acylation. Its dysregulation is linked to prevalent metabolic diseases, including NAFLD, insulin resistance, and inherited fatty acid oxidation disorders, as well as immune cell function [1, 3, 6, 8]. The pathway is regulated by a network of enzymes, transcription factors, and signaling molecules, with ACSL, CPT, ACAD, SIRT6, and AMPK playing central roles [1, 4, 6]. Advances in CRISPR gene editing and metabolic profiling now allow researchers to precisely perturb genes within this pathway and measure the consequences on acyl-CoA levels, oxidation flux, and disease phenotypes. EDITGENE's knockout, point mutation, knock-in, overexpression, and library screening services provide the tools needed to accelerate discovery in this field, from target validation to therapeutic development.
References
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