GO:0009922 fatty acid elongase activity: Mechanism, Genes and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0009922 (fatty acid elongase activity) catalyzes the first condensation step of the four-step fatty acid elongation cycle in the endoplasmic reticulum, extending C16 or longer acyl-CoAs by two carbons using malonyl-CoA.
• The reaction consumes a very-long-chain acyl-CoA, H+, and malonyl-CoA to produce a very-long-chain 3-oxoacyl-CoA, CO2, and CoA, and is synonymous with ELOVL and very-long-chain 3-ketoacyl-CoA synthase activity.
• ELOVL family enzymes (ELOVL1-7) determine acyl-chain length of ceramides, phospholipids, and sphingolipids, with ELOVL6 controlling hepatic ceramide length and insulin sensitivity in mice.
• Fatty acid elongase activity is required for synthesis of very-long-chain fatty acids and downstream lipids that influence membrane organization, vision, skin immunity, and bone mineral accrual.
• Dysregulated elongation contributes to neurotoxic astrocyte-mediated cell death, diabetic nephropathy, and retinal aging phenotypes, making elongases candidate therapeutic nodes.
• CRISPR knockout, point-mutation, knock-in, and overexpression models plus CRISPR library screening enable causal dissection of ELOVL and associated elongase genes in disease-relevant cells.
Description
Fatty acid elongase activity (GO:0009922) is a molecular function that catalyzes the first, rate-limiting condensation reaction of the four-step fatty acid elongation cycle in the endoplasmic reticulum, converting a very-long-chain acyl-CoA plus malonyl-CoA into a very-long-chain 3-oxoacyl-CoA, CO2, and CoA. This activity extends fatty acids of C16 or longer by an additional two-carbon unit and is therefore central to the biosynthesis of very-long-chain fatty acids (VLCFAs) and their derivatives, including ceramides, sphingolipids, and membrane phospholipids. Because the acyl-chain length of these lipids determines their biophysical behavior and signaling properties, fatty acid elongase activity sits at the interface of lipid metabolism, membrane biology, and metabolic disease. Researchers study GO:0009922 to understand how cells tune lipid composition in response to nutritional, hormonal, and inflammatory cues. Genetic and biochemical work in plants has shown that fatty acid elongase complexes exhibit functional redundancy, requiring combinatorial perturbation to reveal subunit-specific roles. In mammals, ELOVL6 determines hepatic ceramide acyl-chain length and systemic insulin sensitivity, directly linking this enzymatic activity to glucose homeostasis. Additional studies connect elongation-dependent lipid species to retinal aging, skin immune homeostasis, and bone mineral accrual, underscoring the broad physiological reach of this single catalytic step. From a methods perspective, GO:0009922 is tractable with modern CRISPR and lipidomics workflows. Knockout of ELOVL genes, point mutations in catalytic residues, and knock-in reporters allow precise interrogation of substrate specificity and downstream lipid remodeling. Because elongation products feed into pathways that can trigger ferroptosis and neurotoxic lipid stress, the term is also relevant to cell-death biology and inflammation. This article integrates the QuickGO definition with verified PubMed literature to provide a research-grade overview of fatty acid elongase activity, its genes, regulation, disease links, and experimental models.
fatty acid elongase activity At A Glance
| GO ID | GO:0009922 |
|---|---|
| GO term | fatty acid elongase activity |
| Ontology | molecular_function |
| Synonym | condensing enzyme; elongation of very long chain fatty acids activity; ELOVL; very-long-chain 3-ketoacyl-CoA synthase; very-long-chain 3-oxoacyl-CoA synthase; very-long-chain beta-ketoacyl-CoA synthase |
| Major function | Catalyzes the first condensation step of the four-step fatty acid elongation cycle in the endoplasmic reticulum, extending C16 or longer acyl-CoAs by two carbons using malonyl-CoA |
| Reaction | a very-long-chain acyl-CoA + H+ + malonyl-CoA = a very-long-chain 3-oxoacyl-CoA + CO2 + CoA |
| Pathway context | Endoplasmic reticulum fatty acid elongation cycle; upstream of 3-ketoacyl-CoA reduction, dehydration, and enoyl-CoA reduction |
| Representative enzymes | ELOVL family elongases including ELOVL6 and related condensing enzymes |
| Disease relevance | Hepatic insulin sensitivity, retinal aging, neurotoxic astrocyte-mediated cell death, diabetic nephropathy, skin immune homeostasis, bone mineral accrual |
What Is GO:0009922?
GO:0009922 describes the catalytic activity that performs the condensation step of fatty acid elongation: a very-long-chain acyl-CoA + H+ + malonyl-CoA = a very-long-chain 3-oxoacyl-CoA + CO2 + CoA. This is the first of four reactions in the endoplasmic reticulum elongation cycle that adds a two-carbon unit to fatty acids of C16 or longer. The term is synonymous with condensing enzyme, elongation of very long chain fatty acids activity, ELOVL, very-long-chain 3-ketoacyl-CoA synthase, very-long-chain 3-oxoacyl-CoA synthase, and very-long-chain beta-ketoacyl-CoA synthase.
Why Is fatty acid elongase activity Important in Cell Biology?
Fatty acid elongase activity is important because it sets the acyl-chain length of very-long-chain fatty acids and their lipid derivatives, which in turn control membrane fluidity, lipid raft organization, ceramide signaling, and inflammatory lipid mediator production. Perturbing this single catalytic step changes the balance between saturated and unsaturated VLCFAs, alters ceramide and sphingolipid profiles, and can reprogram cellular stress responses such as ferroptosis. Consequently, GO:0009922 is a focal point for research on metabolic disease, neurodegeneration, retinal degeneration, skin immunity, and bone development, and it is a tractable target for CRISPR-based functional genomics.
• Determines acyl-chain length of ceramides and sphingolipids, with ELOVL6 controlling hepatic ceramide length and insulin sensitivity in mice.
• Supports biosynthesis of very-long-chain fatty acids required for retinal function and reversal of aging-related vision decline in mice.
• Contributes to neurotoxic reactive astrocyte-mediated cell death via saturated lipids, linking elongation to neurodegeneration.
• Is implicated in diabetic nephropathy through lactylation-dependent regulation of lipid metabolism and ferroptosis.
• Influences skin immune homeostasis by tuning lipid metabolism and neutrophil chemotaxis.
• Associates with plasma fatty acid composition that predicts bone mineral accrual from childhood to adolescence.
• Exhibits functional redundancy in plant elongase complexes, informing combinatorial genetic strategies.
• Provides a mechanistic entry point for CRISPR knockout, point-mutation, and knock-in studies of lipid metabolism.
• Links nutritional and hormonal signals to membrane lipid remodeling and metabolic disease risk.
• Enables lipidomics-guided discovery of biomarkers and therapeutic targets across multiple organ systems.
What Happens During fatty acid elongase activity?
Condensation of acyl-CoA with malonyl-CoA
In simple terms: The enzyme joins a long fatty acid chain to a two-carbon building block, starting the elongation process.
The defining catalytic event of GO:0009922 is the condensation of a very-long-chain acyl-CoA with malonyl-CoA, releasing CO2 and CoA and forming a very-long-chain 3-oxoacyl-CoA. This reaction is the first and rate-limiting step of the four-step elongation cycle in the endoplasmic reticulum and determines whether a given acyl chain will be extended by two carbons. ELOVL family enzymes such as ELOVL6 catalyze this step with acyl-chain-length specificity, thereby setting the substrate pool for downstream reductions and dehydrations.
Four-step elongation cycle in the endoplasmic reticulum
In simple terms: After the first joining step, three more reactions complete the addition of two carbons to the fatty acid.
Following condensation, the elongation cycle proceeds through 3-ketoacyl-CoA reduction, dehydration, and enoyl-CoA reduction to yield a fatty acyl-CoA extended by two carbons. The cycle can repeat, producing very-long-chain fatty acids of increasing length that are incorporated into ceramides, sphingolipids, and phospholipids. Functional redundancy among elongase subunits, as demonstrated in Arabidopsis, means that disrupting one component may be compensated by others, requiring combinatorial perturbation to reveal phenotypes.
Acyl-chain-length determination and lipid remodeling
In simple terms: The enzyme decides how long the final fatty acid will be, which changes the properties of lipids in membranes.
The specificity of the condensing enzyme dictates the acyl-chain length of downstream lipids. Hepatocyte ELOVL6 determines ceramide acyl-chain length and hepatic insulin sensitivity in mice, showing that this catalytic step directly influences systemic metabolism. Lipid-induced stress can regulate elongase components such as HACD3 through TCF7l2, linking transcriptional stress responses to elongation capacity. These findings position GO:0009922 as a control point for membrane lipid remodeling under metabolic load.
Physiological outputs: vision, skin, and bone
In simple terms: The products of elongation affect organs as different as the eye, skin, and bone.
Retinal polyunsaturated fatty acid supplementation reverses aging-related vision decline in mice, implicating elongation-dependent lipid composition in visual function. N6-methyladenosine modification-tuned lipid metabolism controls skin immune homeostasis via neutrophil chemotaxis, connecting elongation-related pathways to cutaneous immunity. Plasma fatty acid composition predicts bone mineral accrual from childhood to adolescence, suggesting that elongation products serve as systemic biomarkers of skeletal development.
Stress and cell-death signaling
In simple terms: When elongation goes wrong, lipids can become toxic and trigger cell death.
Neurotoxic reactive astrocytes induce cell death via saturated lipids, a process dependent on lipid elongation and saturation status. AARS1-mediated lactylation of H3K18 and STAT1 promotes ferroptosis in diabetic nephropathy, linking epigenetic regulation of lipid metabolism to iron-dependent cell death. Together, these studies show that GO:0009922 products can act as either structural components or stress signals depending on context.
Key Genes Involved in GO:0009922 fatty acid elongase activity
The following genes and proteins are directly or functionally associated with fatty acid elongase activity (GO:0009922) in the verified literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| ELOVL6 | Elongase catalyzing condensation of C16 acyl-CoAs; determines ceramide acyl-chain length | Hepatic insulin sensitivity and ceramide biology in mice |
| ELOVL family (ELOVL1-7) | Very-long-chain fatty acid elongases with distinct substrate specificities | Core enzymes defining GO:0009922 activity |
| HACD3 | 3-hydroxyacyl-CoA dehydratase component of elongation | Regulated by TCF7l2 during lipid-induced stress |
| TCF7l2 | Transcription factor regulating HACD3 and lipid metabolism | Links transcriptional stress to elongase function |
| AARS1 | Aminoacyl-tRNA synthetase mediating lactylation | Promotes ferroptosis in diabetic nephropathy via lipid metabolism |
| STAT1 | Transcription factor lactylated by AARS1 | Epigenetic regulation of ferroptosis and lipid stress |
| H3K18 | Histone mark subject to lactylation | Chromatin-level control of lipid and stress genes |
| ELOVL2 | Elongase for polyunsaturated fatty acids | Retinal lipid composition and vision decline |
| ELOVL4 | Elongase for very-long-chain polyunsaturated fatty acids | Retinal and skin lipid biology |
| ELOVL5 | Elongase for polyunsaturated fatty acids | Lipid metabolism and immune regulation |
| ELOVL1 | Elongase for saturated and monounsaturated VLCFAs | Sphingolipid and membrane biology |
| ELOVL3 | Elongase in skin and sebaceous glands | Skin immune homeostasis |
| ELOVL7 | Elongase for saturated VLCFAs | Metabolic and lipid stress studies |
| KCS (plant) | Very-long-chain 3-ketoacyl-CoA synthase | Functional redundancy in plant elongase complexes |
| CER (plant) | Condensing enzyme in plant wax biosynthesis | Model for elongase complex assembly |
| FAE1 (plant) | Fatty acid elongase 1 condensing enzyme | Seed oil and wax lipid engineering |
| HACD1-4 | Dehydratase components of the elongation cycle | Downstream steps of GO:0009922 pathway |
| KAR | 3-ketoacyl-CoA reductase | Elongation cycle enzyme |
How Is fatty acid elongase activity Regulated?
Fatty acid elongase activity is regulated at multiple levels. Transcriptionally, TCF7l2 regulates the fatty acid chain elongase HACD3 during lipid-induced stress, linking nutrient and stress signaling to elongation capacity. Epigenetically, AARS1-mediated lactylation of H3K18 and STAT1 promotes ferroptosis in diabetic nephropathy, indicating that chromatin modifications can tune lipid metabolic programs that depend on elongation. Nutritionally, plasma fatty acid composition reflects elongation activity and predicts bone mineral accrual from childhood to adolescence. In plants, functional redundancy within elongase complexes means that regulation is distributed across multiple subunits, and single-gene perturbation may not fully abolish activity. Together, these mechanisms allow cells to adjust very-long-chain fatty acid production in response to metabolic, inflammatory, and developmental cues.
fatty acid elongase activity and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| ELOVL6 | Hepatic insulin sensitivity and ceramide acyl-chain length | Hepatocyte-specific knockout mice and lipidomics |
| HACD3 / TCF7l2 | Lipid-induced stress and metabolic dysfunction | CRISPR knockout or knockdown in hepatocyte cell lines |
| AARS1 / STAT1 | Diabetic nephropathy and ferroptosis | Knockout or point-mutation models in kidney cells |
| ELOVL2 / ELOVL4 | Retinal aging and vision decline | Retinal organoids and mouse supplementation models |
| ELOVL3 / ELOVL5 | Skin immune homeostasis and neutrophil chemotaxis | Skin cell knockout and immune co-culture |
Metabolic disease and insulin resistance
Hepatocyte ELOVL6 determines ceramide acyl-chain length and hepatic insulin sensitivity in mice, directly connecting fatty acid elongase activity to glucose homeostasis and metabolic disease. Lipid-induced stress regulates HACD3 through TCF7l2, suggesting that elongation is part of a transcriptional stress response that can worsen metabolic dysfunction. These findings position GO:0009922 as a candidate target for modulating ceramide profiles and insulin sensitivity.
Neurodegeneration and retinal aging
Neurotoxic reactive astrocytes induce cell death via saturated lipids, a process that depends on lipid elongation and saturation. Retinal polyunsaturated fatty acid supplementation reverses aging-related vision decline in mice, implicating elongation-dependent lipid composition in visual function. Together, these studies link GO:0009922 to neurodegeneration and age-related retinal degeneration.
Diabetic nephropathy and ferroptosis
AARS1-mediated lactylation of H3K18 and STAT1 promotes ferroptosis in diabetic nephropathy, connecting epigenetic regulation of lipid metabolism to iron-dependent cell death in kidney disease. Because elongation products influence membrane lipid peroxidation susceptibility, fatty acid elongase activity may modulate ferroptosis sensitivity in diabetic kidney injury.
Skin immunity and bone development
N6-methyladenosine modification-tuned lipid metabolism controls skin immune homeostasis via regulating neutrophil chemotaxis, linking elongation-related pathways to cutaneous immunity. Plasma fatty acid composition predicts bone mineral accrual from childhood to adolescence, suggesting that elongation products serve as systemic biomarkers of skeletal development.
From fatty acid elongase activity-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of ELOVL6 alter ceramide length and insulin sensitivity? | Hepatocyte-specific knockout mouse |
| Which catalytic residues are required for condensation? | Point-mutation knock-in of ELOVL catalytic residues |
| How does TCF7l2 regulate HACD3 under lipid stress? | CRISPR knockout or knockdown in hepatocyte lines |
| Can elongation products modulate ferroptosis? | Knockout and overexpression in kidney cells |
| What is the role of elongases in retinal lipid composition? | Retinal organoids and mouse supplementation models |
| How do elongase complexes assemble in plants? | Combinatorial knockout in Arabidopsis |
How to Study the fatty acid elongase activity Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Lipidomics (LC-MS) | Acyl-chain-length profiles of ceramides and phospholipids | ELOVL6 and elongase substrate specificity |
| CRISPR knockout | Loss-of-function phenotypes for elongase genes | Causal testing of ELOVL and HACD3 |
| Point-mutation knock-in | Catalytic residue requirements | Mechanistic dissection of condensation step |
| RNA-seq | Transcriptional changes in lipid metabolic genes | TCF7l2-HACD3 regulation |
| Epitranscriptomics (m6A) | RNA modification landscape | Skin immune lipid metabolism |
| Imaging | Lipid droplet and membrane organization | Retinal and astrocyte lipid phenotypes |
| Ferroptosis assays | Iron-dependent cell death sensitivity | Diabetic nephropathy models |
| Neutrophil chemotaxis assays | Immune cell migration | Skin immune homeostasis |
Lipidomics and mass spectrometry
Lipidomics by mass spectrometry measures acyl-chain-length distributions of ceramides, sphingolipids, and phospholipids, directly reporting the output of fatty acid elongase activity. This approach is essential for linking ELOVL6 and related enzymes to hepatic insulin sensitivity and retinal lipid composition.
CRISPR knockout and point-mutation screens
CRISPR knockout and point-mutation strategies enable causal testing of elongase genes and catalytic residues. Combinatorial knockout in Arabidopsis revealed functional redundancy of fatty acid elongase complexes, demonstrating the value of multiplexed perturbation. In mammalian cells, knockout of ELOVL6 and related genes can be paired with lipidomics to define substrate specificity.
Transcriptomics and epitranscriptomics
RNA-seq and epitranscriptomic profiling reveal how TCF7l2 and m6A modifications regulate elongase components such as HACD3 and lipid metabolic programs. These methods connect transcriptional and RNA modification layers to fatty acid elongase activity.
Imaging and functional assays
Imaging of lipid droplets, membranes, and retinal tissue, combined with functional assays such as neutrophil chemotaxis and ferroptosis measurements, links GO:0009922 to cellular phenotypes. Neurotoxic astrocyte co-culture assays further demonstrate how saturated lipids induce cell death.
How CRISPR Can Be Used to Study GO:0009922 fatty acid elongase activity
Knockout
CRISPR knockout of ELOVL6 and related elongase genes enables loss-of-function studies of fatty acid elongase activity, revealing effects on ceramide acyl-chain length, insulin sensitivity, and lipid remodeling. Combinatorial knockout in plants demonstrated functional redundancy, showing that single-gene knockouts may be compensated by paralogs.
Point Mutation
Point-mutation knock-in of catalytic residues in ELOVL enzymes allows precise testing of the condensation mechanism and substrate specificity without confounding effects of protein loss. Such models are valuable for distinguishing catalytic activity from scaffolding functions.
Knock-in
Knock-in of epitope tags or fluorescent reporters at endogenous ELOVL loci enables localization and interaction studies of the elongase complex in the endoplasmic reticulum. Tagged knock-in models also facilitate proteomic identification of elongase complex components.
Overexpression
Overexpression of ELOVL genes or elongase subunits can amplify very-long-chain fatty acid production and reveal gain-of-function phenotypes in lipid metabolism, ferroptosis, and immune regulation. Overexpression models complement knockout studies by testing sufficiency of the catalytic activity.
How EDITGENE Supports fatty acid elongase activity Research
Researchers studying fatty acid elongase activity-related genes often need to determine whether a candidate gene is causally involved in lipid remodeling, metabolic disease, or cell-death phenotypes. EDITGENE provides end-to-end CRISPR services that convert hypotheses about GO:0009922 into validated cell models, from knockout and point-mutation lines to knock-in reporters, overexpression systems, and CRISPR library screening with bioinformatics support.
Contact EDITGENE today to design your custom CRISPR model for fatty acid elongase activity research.
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| ELOVL5 Knockout HEK293 Cell Line | EDJ-KQ3092 | Human | 60481 | Details Get a Quote |
| ELOVL4 Knockout HEK293 Cell Line | EDJ-KQ3151 | Human | 6785 | Details Get a Quote |
| ELOVL3 Knockout HEK293 Cell Line | EDJ-KQ9839 | Human | 83401 | Details Get a Quote |
| ELOVL2 Knockout HEK293 Cell Line | EDJ-KQ11923 | Human | 54898 | Details Get a Quote |
| ELOVL1 Knockout HEK293 Cell Line | EDJ-KQ13277 | Human | 64834 | Details Get a Quote |
| ELOVL6 Knockout HEK293 Cell Line | EDJ-KQ13278 | Human | 79071 | Details Get a Quote |
| ELOVL7 Knockout HEK293 Cell Line | EDJ-KQ13280 | Human | 79993 | Details Get a Quote |
| ELOVL4 Knockout HeLa Cell Line | EDJ-KQ23165 | Human | 6785 | Details Get a Quote |
| ELOVL7 Knockout A-549 Cell Line | EDJ-KQ41475 | Human | 79993 | Details Get a Quote |
| ELOVL5 Knockout A-549 Cell Line | EDJ-KQ24403 | Human | 60481 | Details Get a Quote |
| ELOVL5 Knockout HCT 116 Cell Line | EDJ-KQ24404 | Human | 60481 | Details Get a Quote |
| ELOVL5 Knockout HeLa Cell Line | EDJ-KQ24405 | Human | 60481 | Details Get a Quote |
| ELOVL4 Knockout A-549 Cell Line | EDJ-KQ24550 | Human | 6785 | Details Get a Quote |
| ELOVL3 Knockout A-549 Cell Line | EDJ-KQ36686 | Human | 83401 | Details Get a Quote |
| ELOVL3 Knockout HCT 116 Cell Line | EDJ-KQ36687 | Human | 83401 | Details Get a Quote |
Displaying Records 1 To 15 Of 28 Records
Frequently Asked Questions About fatty acid elongase activity
What is fatty acid elongase activity (GO:0009922)?
It is the molecular function that catalyzes the first condensation step of the four-step fatty acid elongation cycle in the endoplasmic reticulum, extending C16 or longer acyl-CoAs by two carbons using malonyl-CoA.
What reaction does GO:0009922 catalyze?
A very-long-chain acyl-CoA + H+ + malonyl-CoA = a very-long-chain 3-oxoacyl-CoA + CO2 + CoA.
What genes are involved in fatty acid elongase activity?
ELOVL family genes such as ELOVL6, along with HACD3, TCF7l2, and plant condensing enzymes like KCS and FAE1, are involved.
What are the synonyms of GO:0009922?
Synonyms include condensing enzyme, elongation of very long chain fatty acids activity, ELOVL, very-long-chain 3-ketoacyl-CoA synthase, very-long-chain 3-oxoacyl-CoA synthase, and very-long-chain beta-ketoacyl-CoA synthase.
How is fatty acid elongase activity linked to insulin sensitivity?
Hepatocyte ELOVL6 determines ceramide acyl-chain length and hepatic insulin sensitivity in mice, directly linking this activity to glucose homeostasis.
Does fatty acid elongase activity play a role in vision?
Retinal polyunsaturated fatty acid supplementation reverses aging-related vision decline in mice, implicating elongation-dependent lipid composition in visual function.
How is fatty acid elongase activity regulated?
It is regulated transcriptionally by TCF7l2 via HACD3, epigenetically through AARS1-mediated lactylation, and nutritionally as reflected by plasma fatty acid composition.
What diseases are associated with fatty acid elongase activity?
It is associated with metabolic disease and insulin resistance, neurodegeneration, retinal aging, diabetic nephropathy, skin immune dysregulation, and bone development.
What methods are used to study GO:0009922?
Lipidomics, CRISPR knockout, point-mutation knock-in, RNA-seq, epitranscriptomics, imaging, ferroptosis assays, and neutrophil chemotaxis assays are commonly used.
How can CRISPR models help study fatty acid elongase activity?
CRISPR knockout, point-mutation, knock-in, and overexpression models enable causal testing of elongase genes and catalytic residues in lipid metabolism and disease phenotypes.
Conclusion
Fatty acid elongase activity (GO:0009922) is a central molecular function that determines the acyl-chain length of very-long-chain fatty acids and their lipid derivatives, with far-reaching consequences for membrane biology, ceramide signaling, and metabolic disease. Verified literature links this activity to hepatic insulin sensitivity, retinal aging, neurotoxic astrocyte-mediated cell death, diabetic nephropathy, skin immunity, and bone mineral accrual. CRISPR-based knockout, point-mutation, knock-in, and overexpression models, combined with lipidomics and transcriptomics, provide a robust toolkit for dissecting GO:0009922 in health and disease. EDITGENE supports these efforts with custom cell model generation, library screening, and bioinformatics services tailored to fatty acid elongase research.
References
- 1. Matsuzaka T et al.. 2020. Hepatocyte ELOVL Fatty Acid Elongase 6 Determines Ceramide Acyl-Chain Length and Hepatic Insulin Sensitivity in Mice.. Hepatology 71(5):1609-1625 PMID: 31529722
- 2. Gao F et al.. 2025. Retinal polyunsaturated fatty acid supplementation reverses aging-related vision decline in mice.. Sci Transl Med 17(817):eads5769 PMID: 40991728
- 3. Mondal A et al.. 2025. TCF7l2 Regulates Fatty Acid Chain Elongase HACD3 during Lipid-Induced Stress.. Biochemistry 64(8):1828-1840 PMID: 40172138
- 4. Guttenplan KA et al.. 2021. Neurotoxic reactive astrocytes induce cell death via saturated lipids.. Nature 599(7883):102-107 PMID: 34616039
- 5. Hong J et al.. 2026. AARS1-mediated lactylation of H3K18 and STAT1 promotes ferroptosis in diabetic nephropathy.. Cell Death Differ 33(3):589-604 PMID: 40987895
- 6. Batsale M et al.. 2023. Tackling functional redundancy of Arabidopsis fatty acid elongase complexes.. Front Plant Sci 14:1107333 PMID: 36798704
- 7. Cui L et al.. 2024. N(6)-methyladenosine modification-tuned lipid metabolism controls skin immune homeostasis via regulating neutrophil chemotaxis.. Sci Adv 10(40):eadp5332 PMID: 39356764
- 8. Lakka TA et al.. 2025. Plasma fatty acid composition predicts bone mineral accrual from childhood to adolescence: the Physical Activity and Nutrition in Children study.. J Bone Miner Res 40(11):1265-1277 PMID: 40747984
