GO:0006107 oxaloacetate metabolic process: TCA Cycle Intermediate, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0006107 (oxaloacetate metabolic process) describes all chemical reactions and pathways involving oxaloacetate, the anion of oxobutanedioic acid and a central intermediate of the TCA cycle.
• Oxaloacetate sits at the crossroads of gluconeogenesis, amino acid biosynthesis, and mitochondrial respiration, and its clearance is controlled differently in skeletal muscle versus brown adipose tissue.
• Oxaloacetate can promote the transition from glycolysis to gluconeogenesis through Akt-FoxO1 and JNK/c-Jun-FoxO1 signaling and can inhibit liver cancer cell survival.
• In diabetic kidney disease, oxaloacetate restores HIF-1alpha-mediated mitochondrial homeostasis and counters tubulointerstitial injury.
• Enzymes such as alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase catalyze enol/keto tautomerization of oxaloacetate, illustrating the chemical diversity of this metabolic node.
• Metabolic engineering of the phosphoenolpyruvate-oxaloacetate-pyruvate node is a major route for biosynthesis of derived amino acids, making this GO term relevant to industrial biotechnology.
Description
GO:0006107, oxaloacetate metabolic process, is the biological process comprising the chemical reactions and pathways involving oxaloacetate, the anion of oxobutanedioic acid, which is an important intermediate in metabolism, especially as a component of the TCA cycle. Because oxaloacetate is both a product and a substrate of multiple mitochondrial and cytosolic reactions, its concentration and flux are tightly linked to energy production, gluconeogenesis, and amino acid biosynthesis. Researchers study this process to understand how cells balance catabolism and anabolism and how its dysregulation contributes to cancer, metabolic disease, and organ injury. Oxaloacetate is not merely a passive TCA cycle intermediate; it is a signaling-relevant metabolite whose availability can influence mitochondrial complex II respiration and metabolic clearance in a tissue-specific manner. In skeletal muscle and brown adipose tissue, the control of oxaloacetate clearance diverges, indicating that the same GO term can be regulated by different mechanisms depending on the cellular context. This context dependence makes GO:0006107 a useful annotation for interpreting metabolic phenotypes in disease models and for engineering microbial or mammalian cells. From a translational perspective, oxaloacetate metabolism intersects with cancer metabolism through enzymes such as ATP citrate lyase, which is a central metabolic enzyme in cancer and links citrate and oxaloacetate pools to lipogenesis and proliferation. In liver cancer cells, oxaloacetate promotes a shift from glycolysis to gluconeogenesis and inhibits survival, suggesting that manipulating this process could have therapeutic value. In diabetic kidney disease, oxaloacetate restores HIF-1alpha-mediated mitochondrial homeostasis, further supporting its role in protecting tissues from metabolic stress. Together, these findings explain why GO:0006107 is a high-value annotation for both basic and applied research.
oxaloacetate metabolic process At A Glance
| GO ID | GO:0006107 |
|---|---|
| GO term | oxaloacetate metabolic process |
| Ontology | biological_process |
| Synonym | oxaloacetate metabolism |
| Definition | The chemical reactions and pathways involving oxaloacetate, the anion of oxobutanedioic acid, an important intermediate in metabolism, especially as a component of the TCA cycle. |
| Major function | Maintains TCA cycle flux and supplies oxaloacetate for gluconeogenesis, amino acid biosynthesis, and mitochondrial respiration. |
| Key metabolite | Oxaloacetate (anion of oxobutanedioic acid). |
| Related enzymes | ATP citrate lyase, transcarboxylase, alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase, and TCA cycle enzymes. |
| Disease relevance | Cancer metabolism, diabetic kidney disease, and tissue-specific metabolic dysfunction. |
What Is GO:0006107?
In our own words, GO:0006107 (oxaloacetate metabolic process) refers to the collection of biochemical reactions and pathways in which oxaloacetate, the anion of oxobutanedioic acid, is produced, consumed, or interconverted. It is a biological process annotation that captures the metabolic fate of oxaloacetate, especially its role as a component of the TCA cycle, and includes reactions that feed into or draw from this intermediate.
Why Is oxaloacetate metabolic process Important in Cell Biology?
Oxaloacetate metabolic process is important because oxaloacetate is a hub metabolite that connects the TCA cycle to gluconeogenesis, amino acid biosynthesis, and mitochondrial respiration, and its clearance is controlled differently across tissues such as skeletal muscle and brown adipose tissue. This process also intersects with cancer metabolism through ATP citrate lyase, a central enzyme in cancer that links citrate and oxaloacetate pools to biosynthetic pathways. In liver cancer cells, oxaloacetate promotes a shift from glycolysis to gluconeogenesis and inhibits survival, while in diabetic kidney disease it restores HIF-1alpha-mediated mitochondrial homeostasis and counters tubulointerstitial injury. These findings make GO:0006107 a valuable annotation for understanding metabolic disease and for designing metabolic engineering strategies.
• Oxaloacetate is a central TCA cycle intermediate, so its metabolism directly affects mitochondrial respiration and energy production.
• Oxaloacetate clearance is controlled differently in skeletal muscle and brown adipose tissue, revealing tissue-specific regulation of this process.
• The process supplies precursors for gluconeogenesis and amino acid biosynthesis, linking it to whole-body glucose and nitrogen balance.
• ATP citrate lyase, a central metabolic enzyme in cancer, connects citrate and oxaloacetate pools to tumor lipogenesis and proliferation.
• Oxaloacetate promotes the transition from glycolysis to gluconeogenesis through Akt-FoxO1 and JNK/c-Jun-FoxO1 axes and inhibits liver cancer cell survival.
• In diabetic kidney disease, oxaloacetate restores HIF-1alpha-mediated mitochondrial homeostasis and counters tubulointerstitial injury.
• Enzymatic tautomerization of oxaloacetate by alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase shows the chemical versatility of this metabolite.
• Transcarboxylase, an early nanomachine, catalyzes carboxyl transfer reactions involving oxaloacetate-related substrates, highlighting evolutionary conservation.
• Metabolic engineering of the phosphoenolpyruvate-oxaloacetate-pyruvate node is used to produce derived amino acids industrially.
• Differential scanning fluorimetry can detect ligand interactions that stabilize enzymes acting on oxaloacetate, aiding drug and inhibitor discovery.
What Happens During oxaloacetate metabolic process?
Oxaloacetate as a TCA cycle intermediate
In simple terms: Oxaloacetate is a key molecule that keeps the mitochondrial energy cycle running.
Oxaloacetate is an important intermediate in metabolism, especially as a component of the TCA cycle, where it is continuously consumed and regenerated to maintain flux. Because it is both a product and a substrate of multiple reactions, its steady-state level reflects the balance between mitochondrial respiration and biosynthetic demand. In skeletal muscle and brown adipose tissue, the clearance of oxaloacetate and its relationship to mitochondrial complex II respiration are controlled differently, indicating tissue-specific regulation of this step.
Oxaloacetate in gluconeogenesis and glycolysis
In simple terms: Oxaloacetate helps cells switch from burning sugar to making new sugar.
Oxaloacetate promotes the transition from glycolysis to gluconeogenesis through the Akt-FoxO1 and JNK/c-Jun-FoxO1 axes, and this shift inhibits the survival of liver cancer cells. This means that oxaloacetate is not only a metabolic intermediate but also a signal that can influence gene expression programs through FoxO1-dependent transcription. The ability of oxaloacetate to favor gluconeogenesis over glycolysis has direct implications for glucose homeostasis and for cancer cell metabolism.
Oxaloacetate and mitochondrial homeostasis
In simple terms: Oxaloacetate helps mitochondria stay healthy under stress.
In diabetic kidney disease, oxaloacetate restores HIF-1alpha-mediated mitochondrial homeostasis and counters tubulointerstitial injury. This indicates that oxaloacetate metabolism is linked to hypoxia-inducible factor signaling and to the maintenance of mitochondrial function in kidney tubular cells. The protective effect of oxaloacetate in this context suggests that the process annotated by GO:0006107 can be targeted to ameliorate metabolic organ injury.
Enzymatic interconversion and tautomerization of oxaloacetate
In simple terms: Special enzymes can change the chemical form of oxaloacetate.
Alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase catalyzes enol/keto tautomerization of oxaloacetate, demonstrating that the chemical state of oxaloacetate is enzymatically controlled. Transcarboxylase, one of nature's early nanomachines, catalyzes carboxyl transfer reactions that are relevant to oxaloacetate-related metabolism. These enzymatic activities expand the biochemical repertoire of GO:0006107 beyond the canonical TCA cycle reactions.
Oxaloacetate in amino acid biosynthesis and metabolic engineering
In simple terms: Oxaloacetate is a starting material for making amino acids in cells and in industrial microbes.
The phosphoenolpyruvate-oxaloacetate-pyruvate node is a major metabolic engineering target for the biosynthesis of phosphoenolpyruvate-oxaloacetate-pyruvate-derived amino acids. This means that the reactions of GO:0006107 are not only relevant to human physiology but also to industrial biotechnology and strain design. By manipulating the enzymes that produce and consume oxaloacetate, researchers can redirect carbon flux toward valuable amino acid products.
Key Genes Involved in GO:0006107 oxaloacetate metabolic process
The following genes and proteins are experimentally linked to oxaloacetate metabolic process and its regulation in mammalian and microbial systems.
| Gene | Major Role | Research Relevance |
|---|---|---|
| ACLY | ATP citrate lyase, a central metabolic enzyme in cancer that links citrate and oxaloacetate pools to lipogenesis | Target for cancer metabolism studies and inhibitor development |
| FoxO1 | Transcription factor mediating oxaloacetate-induced shift from glycolysis to gluconeogenesis via Akt-FoxO1 and JNK/c-Jun-FoxO1 axes | Key node for studying gluconeogenesis and liver cancer cell survival |
| HIF1A | Hypoxia-inducible factor 1 alpha, involved in oxaloacetate-mediated restoration of mitochondrial homeostasis in diabetic kidney disease | Target for diabetic kidney disease and mitochondrial homeostasis research |
| SDHA | Succinate dehydrogenase complex II subunit, linked to mitochondrial complex II respiration and oxaloacetate clearance | Used to study tissue-specific control of oxaloacetate metabolism |
| SDHB | Succinate dehydrogenase complex II subunit, part of complex II respiration affected by oxaloacetate clearance | Model for mitochondrial respiration studies in skeletal muscle and brown adipose tissue |
| PC | Pyruvate carboxylase, anaplerotic enzyme that produces oxaloacetate from pyruvate | Target for gluconeogenesis and TCA cycle flux studies |
| PCK1 | Phosphoenolpyruvate carboxykinase 1, converts oxaloacetate to phosphoenolpyruvate in gluconeogenesis | Key gene for studying the oxaloacetate-to-glucose pathway |
| PCK2 | Phosphoenolpyruvate carboxykinase 2, mitochondrial isoform acting on oxaloacetate | Relevant to mitochondrial gluconeogenesis and cancer metabolism |
| MDH1 | Malate dehydrogenase 1, interconverts malate and oxaloacetate in the cytosol | Used to study cytosolic oxaloacetate flux |
| MDH2 | Malate dehydrogenase 2, interconverts malate and oxaloacetate in mitochondria | Target for TCA cycle and mitochondrial respiration studies |
| CS | Citrate synthase, condenses oxaloacetate with acetyl-CoA to form citrate | Central enzyme for TCA cycle entry and oxaloacetate utilization |
| GOT1 | Glutamic-oxaloacetic transaminase 1, converts oxaloacetate and glutamate to aspartate and alpha-ketoglutarate | Relevant to amino acid metabolism and redox balance |
| GOT2 | Glutamic-oxaloacetic transaminase 2, mitochondrial isoform acting on oxaloacetate | Target for mitochondrial amino acid metabolism studies |
| ACACA | Acetyl-CoA carboxylase alpha, linked to lipogenesis downstream of ACLY and oxaloacetate metabolism | Used in cancer metabolism and lipogenesis research |
| ACACB | Acetyl-CoA carboxylase beta, involved in fatty acid oxidation regulation linked to oxaloacetate pools | Model for metabolic flux studies in cancer and metabolic disease |
| ACO2 | Aconitase 2, catalyzes isomerization of citrate to isocitrate in the TCA cycle downstream of oxaloacetate | Target for mitochondrial dysfunction studies |
| OGDH | Oxoglutarate dehydrogenase, TCA cycle enzyme downstream of oxaloacetate-derived citrate | Used to assess TCA cycle flux and mitochondrial respiration |
How Is oxaloacetate metabolic process Regulated?
Oxaloacetate metabolic process is regulated at multiple levels, including tissue-specific control of oxaloacetate clearance and mitochondrial complex II respiration, which diverge between skeletal muscle and brown adipose tissue. In liver cancer cells, oxaloacetate promotes the transition from glycolysis to gluconeogenesis through the Akt-FoxO1 and JNK/c-Jun-FoxO1 axes, indicating that this process is coupled to insulin/Akt and stress kinase signaling. In diabetic kidney disease, oxaloacetate restores HIF-1alpha-mediated mitochondrial homeostasis, linking this metabolic process to hypoxia signaling and mitochondrial quality control. Additionally, enzymes such as alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase control the tautomeric state of oxaloacetate, adding a chemical layer of regulation.
oxaloacetate metabolic process and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| ACLY | Cancer metabolism and lipogenesis | Cancer cell lines with ACLY knockout or point mutation to assess oxaloacetate flux |
| FoxO1 | Liver cancer cell survival and gluconeogenesis | Liver cancer cells with FoxO1 knockout or overexpression to test oxaloacetate response |
| HIF1A | Diabetic kidney disease and mitochondrial homeostasis | Kidney tubular cell models with HIF1A knockout or knock-in to study oxaloacetate protection |
| SDHA/SDHB | Mitochondrial complex II respiration and tissue-specific oxaloacetate clearance | Skeletal muscle and brown adipose tissue cells with SDHA/SDHB knockout |
| PCK1 | Gluconeogenesis and metabolic liver disease | Hepatocyte models with PCK1 knockout or overexpression to trace oxaloacetate flux |
Oxaloacetate metabolic process in cancer
ATP citrate lyase is a central metabolic enzyme in cancer that links citrate and oxaloacetate pools to lipogenesis and proliferation, making oxaloacetate metabolism relevant to tumor growth. In liver cancer cells, oxaloacetate promotes the transition from glycolysis to gluconeogenesis through Akt-FoxO1 and JNK/c-Jun-FoxO1 axes and inhibits the survival of these cells, suggesting that manipulating this process could suppress tumor viability. These findings position GO:0006107 as a potential annotation for cancer metabolism studies and therapeutic target discovery.
Oxaloacetate metabolic process in diabetic kidney disease
In diabetic kidney disease, oxaloacetate restores HIF-1alpha-mediated mitochondrial homeostasis to counter tubulointerstitial injury. This indicates that oxaloacetate metabolism is protective in kidney tubular cells under diabetic stress and that its dysregulation may contribute to disease progression. The link to HIF-1alpha signaling provides a mechanistic hypothesis for how oxaloacetate supplementation or modulation could be beneficial in metabolic kidney injury.
Oxaloacetate metabolic process in metabolic and mitochondrial disorders
Tissue-specific differences in oxaloacetate clearance and mitochondrial complex II respiration between skeletal muscle and brown adipose tissue suggest that defects in this process may manifest differently across metabolic tissues. Because oxaloacetate is a TCA cycle intermediate, its dysregulation could affect mitochondrial energy production and contribute to metabolic dysfunction. Studying GO:0006107 in these contexts may reveal tissue-specific vulnerabilities and therapeutic opportunities.
From oxaloacetate metabolic process-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of ACLY alter oxaloacetate-dependent lipogenesis in cancer cells? | ACLY knockout cell line |
| Does FoxO1 mediate oxaloacetate-induced gluconeogenesis in liver cancer? | FoxO1 knockout or point-mutation liver cancer cells |
| Does HIF1A mediate oxaloacetate protection in diabetic kidney disease? | HIF1A knockout or knock-in kidney tubular cells |
| How does SDHA/SDHB loss affect oxaloacetate clearance in skeletal muscle? | SDHA/SDHB knockout muscle cell models |
| Can PCK1 overexpression redirect oxaloacetate toward gluconeogenesis? | PCK1 overexpression hepatocyte model |
| Can tagged ACLY be used to track oxaloacetate-related protein interactions? | Tagged knock-in ACLY cell line |
How to Study the oxaloacetate metabolic process Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Metabolic flux analysis | Flux of oxaloacetate through TCA cycle and gluconeogenesis | Quantifying pathway activity in knockout or overexpression cells |
| Differential scanning fluorimetry | Ligand-induced protein stability | Screening for small-molecule binders of oxaloacetate-related enzymes |
| Western blot | Protein expression and phosphorylation of Akt-FoxO1 and JNK/c-Jun | Testing oxaloacetate-induced signaling in liver cancer cells |
| Mitochondrial respiration assay | Complex II respiration and oxygen consumption | Assessing tissue-specific oxaloacetate clearance effects |
| HIF-1alpha reporter assay | HIF-1alpha transcriptional activity | Evaluating oxaloacetate protection in diabetic kidney disease models |
| Enzyme activity assay | Tautomerization or carboxyl transfer activity | Characterizing enzymes that act on oxaloacetate |
| Metabolic engineering strain construction | Production of oxaloacetate-derived amino acids | Optimizing microbial biosynthesis pathways |
| CRISPR knockout screening | Gene essentiality linked to oxaloacetate metabolism | Identifying modifiers of cancer cell survival under metabolic stress |
Metabolic flux analysis
Metabolic flux analysis using isotope-labeled substrates can trace the fate of oxaloacetate through the TCA cycle and gluconeogenesis, as demonstrated in studies of oxaloacetate clearance and mitochondrial complex II respiration. This approach is essential for quantifying how genetic perturbations alter GO:0006107 activity.
Differential scanning fluorimetry for ligand interactions
Differential scanning fluorimetry can detect ligand interactions that promote protein stability, which is useful for identifying small molecules that bind enzymes acting on oxaloacetate. This method supports drug discovery efforts targeting metabolic enzymes linked to GO:0006107.
Gene expression and signaling assays
Gene expression and signaling assays can measure Akt-FoxO1 and JNK/c-Jun-FoxO1 axis activity in response to oxaloacetate, as shown in liver cancer cells. These assays help determine whether oxaloacetate metabolic process is coupled to transcriptional programs.
Mitochondrial function assays
Mitochondrial function assays, including complex II respiration measurements, can assess how oxaloacetate clearance affects mitochondrial activity in skeletal muscle and brown adipose tissue. In diabetic kidney disease models, HIF-1alpha-mediated mitochondrial homeostasis can be evaluated to test oxaloacetate effects.
How CRISPR Can Be Used to Study GO:0006107 oxaloacetate metabolic process
Knockout
CRISPR knockout of genes such as ACLY, FoxO1, or HIF1A can be used to test their causal roles in oxaloacetate metabolic process and its downstream phenotypes. For example, ACLY knockout in cancer cells can reveal whether oxaloacetate-dependent lipogenesis is required for proliferation. FoxO1 knockout in liver cancer cells can determine whether oxaloacetate-induced gluconeogenesis depends on this transcription factor.
Point Mutation
CRISPR point mutation can introduce specific amino acid changes in enzymes such as ACLY or PCK1 to dissect catalytic residues involved in oxaloacetate metabolism. This approach allows researchers to separate enzymatic activity from scaffolding functions and to model disease-associated variants.
Knock-in
CRISPR knock-in can be used to add tags or reporters to genes such as ACLY or SDHA to track protein localization and interactions in live cells. Tagged knock-in models enable precise measurement of oxaloacetate-related enzyme dynamics in skeletal muscle and brown adipose tissue.
Overexpression
CRISPR overexpression or cDNA-based overexpression of PCK1 or FoxO1 can drive oxaloacetate flux toward gluconeogenesis and test whether this shift inhibits cancer cell survival. Overexpression of HIF1A or its targets can also be used to mimic oxaloacetate-mediated mitochondrial protection in kidney cells.
How EDITGENE Supports oxaloacetate metabolic process Research
Researchers studying oxaloacetate metabolic process-related genes often need to determine whether a candidate gene is causally involved in metabolite flux, signaling, or disease phenotypes. EDITGENE provides publication-ready CRISPR cell models that enable precise genetic perturbations of genes such as ACLY, FoxO1, HIF1A, and SDHA, allowing investigators to move from correlation to causation in the context of GO:0006107.
Contact EDITGENE today to design your custom CRISPR model for oxaloacetate metabolic process research.
Frequently Asked Questions About oxaloacetate metabolic process
What is oxaloacetate metabolic process (GO:0006107)?
GO:0006107 is the biological process comprising the chemical reactions and pathways involving oxaloacetate, the anion of oxobutanedioic acid, an important intermediate in metabolism, especially as a component of the TCA cycle.
What genes are involved in oxaloacetate metabolic process?
Genes and proteins linked to this process include ACLY, FoxO1, HIF1A, SDHA, SDHB, PC, PCK1, PCK2, MDH1, MDH2, CS, GOT1, GOT2, ACACA, ACACB, ACO2, and OGDH.
How is oxaloacetate metabolized in the TCA cycle?
Oxaloacetate is an important intermediate in metabolism, especially as a component of the TCA cycle, where it is continuously consumed and regenerated to maintain flux.
Why is oxaloacetate important in cancer?
ATP citrate lyase, a central metabolic enzyme in cancer, links citrate and oxaloacetate pools to lipogenesis, and oxaloacetate can inhibit liver cancer cell survival by promoting gluconeogenesis.
Does oxaloacetate affect diabetic kidney disease?
Yes, oxaloacetate restores HIF-1alpha-mediated mitochondrial homeostasis to counter tubulointerstitial injury in diabetic kidney disease.
How is oxaloacetate clearance regulated in different tissues?
Oxaloacetate clearance and mitochondrial complex II respiration are controlled differently in skeletal muscle and brown adipose tissue, indicating tissue-specific regulation.
What enzymes act on oxaloacetate?
Enzymes include ATP citrate lyase, transcarboxylase, alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase, and TCA cycle enzymes such as citrate synthase and malate dehydrogenase.
Can oxaloacetate metabolism be studied with CRISPR?
Yes, CRISPR knockout, point mutation, knock-in, and overexpression models can be used to dissect the roles of genes such as ACLY, FoxO1, HIF1A, and SDHA in oxaloacetate metabolic process.
What methods are used to study oxaloacetate metabolic process?
Methods include metabolic flux analysis, differential scanning fluorimetry, Western blot, mitochondrial respiration assays, HIF-1alpha reporter assays, enzyme activity assays, and CRISPR screening.
Is oxaloacetate metabolism relevant to metabolic engineering?
Yes, the phosphoenolpyruvate-oxaloacetate-pyruvate node is a major metabolic engineering target for biosynthesis of derived amino acids.
Conclusion
GO:0006107 (oxaloacetate metabolic process) is a central biological process that connects the TCA cycle to gluconeogenesis, amino acid biosynthesis, and mitochondrial respiration, with tissue-specific regulation in skeletal muscle and brown adipose tissue. Its relevance extends to cancer metabolism through ATP citrate lyase and FoxO1 signaling, and to diabetic kidney disease through HIF-1alpha-mediated mitochondrial homeostasis. Studying this process with CRISPR-based models and metabolic assays can reveal causal mechanisms and therapeutic opportunities.
References
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- 6. Miao Z et al.. 2025. Oxaloacetate promotes the transition from glycolysis to gluconeogenesis through the Akt-FoxO1 and JNK/c-Jun-FoxO1 axes and inhibits the survival of liver cancer cells.. Int Immunopharmacol 161:115051 PMID: 40513330
- 7. Zhang Y et al.. 2026. Oxaloacetate Restores HIF-1α-Mediated Mitochondrial Homeostasis to Counter Tubulointerstitial Injury in Diabetic Kidney Disease.. Diabetes Obes Metab 28(5):4216-4231 PMID: 41773066
- 8. Yang Y et al.. 2024. α-Amino-β-carboxymuconate-ε-semialdehyde decarboxylase catalyzes enol/keto tautomerization of oxaloacetate.. J Biol Chem 300(11):107878 PMID: 39395800
