GO:0006104 succinyl-CoA metabolic process: Mitochondrial Energy and Chromatin Regulation, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0006104 succinyl-CoA metabolic process describes all chemical reactions and pathways involving succinyl-CoA, a central acyl-CoA intermediate in the mitochondrial matrix.
• Succinyl-CoA is produced mainly by the TCA cycle enzyme alpha-ketoglutarate dehydrogenase (alpha-KGDH) and is consumed by succinyl-CoA synthetase (SUCL) to generate succinate and ATP/GTP.
• Beyond energy metabolism, succinyl-CoA serves as a substrate for histone succinylation by KAT2A, directly linking mitochondrial metabolism to chromatin regulation.
• Dysregulation of succinyl-CoA metabolism is implicated in chronic heart failure, multiple cancers, and mitochondrial disease.
• Key genes include SUCLG1, SUCLG2, SUCLA2, OXCT1, and KAT2A, which are actively studied as therapeutic targets and biomarkers.
• CRISPR knockout, point-mutation, knock-in, and overexpression models are essential tools for dissecting the causal roles of these genes in succinyl-CoA metabolism.
Description
Succinyl-CoA metabolic process (GO:0006104) encompasses the chemical reactions and pathways involving succinyl-CoA, a thioester of coenzyme A and succinic acid that sits at the crossroads of the tricarboxylic acid (TCA) cycle, ketone body catabolism, and heme biosynthesis. This intermediate is not merely a metabolic fuel; it acts as a substrate for post-translational modifications, including histone succinylation, thereby connecting mitochondrial flux to nuclear gene expression. Researchers study GO:0006104 because its dysregulation is increasingly linked to human disease, from chronic heart failure to aggressive cancers. The compartmentalized nature of acyl-CoA metabolism further complicates its regulation, as succinyl-CoA pools in mitochondria, cytosol, and nucleus serve distinct functions. Understanding the enzymes that produce and consume succinyl-CoA, such as alpha-ketoglutarate dehydrogenase and succinyl-CoA synthetase, is therefore critical for both basic biology and therapeutic development. This article synthesizes authoritative QuickGO annotations and verified PubMed literature to provide a research-grade overview of succinyl-CoA metabolic process, its key genes, disease relevance, and modern CRISPR-based methods for its study.
succinyl-CoA metabolic process At A Glance
| GO ID | GO:0006104 |
|---|---|
| GO term | succinyl-CoA metabolic process |
| Ontology | biological_process |
| Synonym | succinyl-CoA metabolism |
| Major function | Production and utilization of succinyl-CoA in the TCA cycle, ketone body catabolism, and as a substrate for post-translational modifications such as histone succinylation. |
| Key enzymes | Alpha-ketoglutarate dehydrogenase (alpha-KGDH), succinyl-CoA synthetase (SUCL), and 3-oxoacid CoA-transferase 1 (OXCT1). |
| Subcellular locations | Mitochondrial matrix, with emerging roles in the nucleus and cytosol. |
| Related diseases | Chronic heart failure, leukemia, gliomagenesis, and metastatic cancer. |
What Is GO:0006104?
According to the Gene Ontology, succinyl-CoA metabolic process (GO:0006104) is defined as the chemical reactions and pathways involving succinyl-CoA, a compound composed of the monovalent acyl group 3-carboxypropanoyl, derived from succinic acid by loss of one OH group, linked to coenzyme A. In simpler terms, it covers all the ways cells make, use, and break down succinyl-CoA, a key metabolic intermediate that carries both energy and acyl groups for diverse cellular functions.
Why Is succinyl-CoA metabolic process Important in Cell Biology?
Succinyl-CoA metabolic process is fundamentally important because it integrates carbon flux from the TCA cycle with energy production, ketone body utilization, and epigenetic regulation. The succinyl-CoA pool directly influences mitochondrial ATP/GTP generation through succinyl-CoA synthetase and serves as a substrate for KAT2A-mediated histone succinylation, thereby linking metabolic state to gene expression. Dysregulation of this process has been observed in chronic heart failure, where succinyl-CoA-based energy metabolism is impaired, and in multiple cancers where altered succinyl-CoA metabolism supports tumor growth and metastasis. Moreover, nuclear GTPSCS can function as a lactyl-CoA synthetase to promote histone lactylation and gliomagenesis, revealing unexpected moonlighting roles for succinyl-CoA-related enzymes. Thus, understanding GO:0006104 is essential for deciphering how cells balance energy production, redox homeostasis, and chromatin regulation in health and disease.
• Central hub of the TCA cycle: succinyl-CoA is an obligatory intermediate in oxidative metabolism.
• Energy production: succinyl-CoA synthetase converts succinyl-CoA to succinate, generating ATP or GTP.
• Ketone body catabolism: OXCT1 uses succinyl-CoA as a CoA acceptor to activate ketone bodies for energy.
• Epigenetic regulation: succinyl-CoA serves as a substrate for histone succinyltransferases such as KAT2A.
• Mitochondrial biogenesis: SUCLG1 restricts POLRMT succinylation to enhance mitochondrial biogenesis.
• Cancer progression: altered succinyl-CoA metabolism drives leukemia, glioma, and metastatic cancers.
• Heart failure: succinyl-CoA-based energy metabolism dysfunction is observed in chronic heart failure.
• Stress granule assembly: SUCLG2 promotes stress granule assembly to regulate redox and metastasis.
• Therapeutic target: enzymes of succinyl-CoA metabolism are being explored as drug targets.
• CRISPR modeling: knockout and knock-in models are essential to establish causality in disease.
What Happens During succinyl-CoA metabolic process?
Synthesis of succinyl-CoA from alpha-ketoglutarate
In simple terms: The cell makes succinyl-CoA by chopping off a carbon from alpha-ketoglutarate.
The primary route for succinyl-CoA production is the oxidative decarboxylation of alpha-ketoglutarate by the alpha-ketoglutarate dehydrogenase (alpha-KGDH) complex within the TCA cycle. This multi-enzyme complex couples the release of CO2 to the reduction of NAD+ and the attachment of coenzyme A, forming succinyl-CoA. The alpha-KGDH complex is also found in the nucleus, where it associates with KAT2A to locally generate succinyl-CoA for histone succinylation. This dual localization highlights the compartmentalized nature of succinyl-CoA metabolism and its role in chromatin regulation.
Utilization of succinyl-CoA by succinyl-CoA synthetase
In simple terms: Succinyl-CoA is broken down to succinate, releasing energy that is captured as ATP or GTP.
Succinyl-CoA synthetase (SUCL) catalyzes the reversible conversion of succinyl-CoA to succinate, coupled to the phosphorylation of ADP to ATP (SUCLA2/SUCLG2) or GDP to GTP (SUCLG1/SUCLG2). This reaction is a key step in the TCA cycle and represents a major source of substrate-level phosphorylation. Structural studies have shown that tartryl-CoA, a succinyl-CoA analog, inhibits succinyl-CoA synthetase, providing insights into its catalytic mechanism. The enzyme is a heterodimer composed of an alpha subunit (SUCLG1) and a beta subunit (SUCLA2 or SUCLG2), and its activity is critical for maintaining mitochondrial energy homeostasis.
Succinyl-CoA in ketone body catabolism
In simple terms: Succinyl-CoA helps the cell burn ketone bodies for energy by donating its CoA group.
During ketone body catabolism, 3-oxoacid CoA-transferase 1 (OXCT1) transfers CoA from succinyl-CoA to acetoacetate, yielding acetoacetyl-CoA and succinate. This reaction is essential for utilizing ketone bodies as an alternative fuel source, particularly in the heart and brain during fasting or starvation. Recent work has shown that OXCT1 is regulated by succinylation and activation by SUCLA2, linking succinyl-CoA metabolism directly to ketolysis and liver tumor growth. Thus, succinyl-CoA serves as both a product and a regulator of ketone body metabolism.
Succinyl-CoA as a substrate for post-translational modifications
In simple terms: Succinyl-CoA can tag proteins, including histones, with a succinyl chemical mark that changes gene activity.
Beyond its role in energy metabolism, succinyl-CoA is a substrate for lysine succinylation, a post-translational modification that can alter protein function and chromatin state. KAT2A, in complex with the alpha-KGDH complex, acts as a histone H3 succinyltransferase, using succinyl-CoA to succinylate histone H3 at lysine 79. This modification is associated with active transcription and links mitochondrial metabolic flux to epigenetic regulation. Additionally, nuclear GTPSCS can function as a lactyl-CoA synthetase to promote histone lactylation and gliomagenesis, revealing further moonlighting roles for succinyl-CoA-related enzymes in the nucleus.
Compartmentalization and regulation of succinyl-CoA pools
In simple terms: Succinyl-CoA levels are kept separate in different parts of the cell, each with its own job.
Succinyl-CoA metabolism is compartmentalized, with distinct pools in the mitochondrial matrix, cytosol, and nucleus. Mitochondrial succinyl-CoA is primarily used for energy production and ketolysis, while nuclear succinyl-CoA supports histone succinylation and gene regulation. The transport and exchange of acyl-CoAs between compartments are tightly regulated, and dysregulation can lead to metabolic and epigenetic reprogramming in disease. For example, SUCLG1 restricts POLRMT succinylation to enhance mitochondrial biogenesis, demonstrating how succinyl-CoA metabolism can influence mitochondrial function beyond the TCA cycle.
Key Genes Involved in GO:0006104 succinyl-CoA metabolic process
The following genes encode enzymes and regulatory proteins that directly participate in or regulate succinyl-CoA metabolic process (GO:0006104).
| Gene | Major Role | Research Relevance |
|---|---|---|
| SUCLG1 | Alpha subunit of succinyl-CoA synthetase; catalyzes succinyl-CoA to succinate conversion | Restricts POLRMT succinylation to enhance mitochondrial biogenesis; implicated in leukemia progression |
| SUCLA2 | Beta subunit of succinyl-CoA synthetase (ATP-forming); activates OXCT1 via succinylation | Promotes ketolysis and liver tumor growth; target for cancer metabolism studies |
| SUCLG2 | Beta subunit of succinyl-CoA synthetase (GTP-forming); promotes stress granule assembly | Regulates redox homeostasis and drives cancer metastasis |
| OXCT1 | 3-oxoacid CoA-transferase 1; transfers CoA from succinyl-CoA to acetoacetate | Essential for ketone body catabolism; succinylated and activated by SUCLA2 in liver cancer |
| KAT2A | Histone H3 succinyltransferase; couples with alpha-KGDH complex | Uses succinyl-CoA to succinylate histone H3, linking metabolism to chromatin |
| GTPSCS | Nuclear GTP-dependent succinyl-CoA synthetase; can act as lactyl-CoA synthetase | Promotes histone lactylation and gliomagenesis |
| Alpha-KGDH complex | Produces succinyl-CoA from alpha-ketoglutarate | Nuclear pool supports histone succinylation; target for metabolic studies |
| POLRMT | Mitochondrial RNA polymerase; regulated by succinylation | Succinylation by succinyl-CoA affects mitochondrial biogenesis |
| ACAT1 | Acetyl-CoA acetyltransferase; can interconvert acyl-CoAs | Potential regulator of succinyl-CoA pools; not directly cited in this list |
| HAT1 | Histone acetyltransferase; may interact with succinyl-CoA metabolism | Potential crosstalk with succinylation; not directly cited in this list |
| SIRT5 | NAD+-dependent desuccinylase | Removes succinyl marks from proteins; potential regulator of succinyl-CoA metabolism |
| SIRT3 | Mitochondrial deacetylase and desuccinylase | Regulates mitochondrial protein succinylation; potential link to succinyl-CoA |
| GLS | Glutaminase; feeds alpha-ketoglutarate into TCA cycle | Indirectly affects succinyl-CoA production; not directly cited in this list |
| IDH2 | Isocitrate dehydrogenase 2; produces alpha-ketoglutarate | Indirectly affects succinyl-CoA levels; not directly cited in this list |
| SDHA | Succinate dehydrogenase subunit A; oxidizes succinate | Downstream of succinyl-CoA; not directly cited in this list |
| FH | Fumarate hydratase; converts fumarate to malate | Downstream of succinyl-CoA; not directly cited in this list |
| MDH2 | Malate dehydrogenase 2; converts malate to oxaloacetate | Downstream of succinyl-CoA; not directly cited in this list |
| DLST | Dihydrolipoamide succinyltransferase; component of alpha-KGDH complex | Directly produces succinyl-CoA; not directly cited in this list |
How Is succinyl-CoA metabolic process Regulated?
Succinyl-CoA metabolic process is regulated at multiple levels, including enzyme expression, post-translational modification, and substrate availability. The alpha-KGDH complex, which produces succinyl-CoA, is inhibited by its products, NADH and succinyl-CoA, providing feedback control. Succinyl-CoA synthetase activity can be modulated by succinylation; for example, OXCT1 is succinylated and activated by SUCLA2, linking succinyl-CoA levels to ketolysis. Additionally, SUCLG1 restricts POLRMT succinylation to enhance mitochondrial biogenesis, indicating that succinyl-CoA metabolism influences mitochondrial gene expression. Compartmentalization further regulates succinyl-CoA pools, as nuclear alpha-KGDH and KAT2A generate and utilize succinyl-CoA for histone succinylation, coupling metabolic state to chromatin. Sirtuins such as SIRT3 and SIRT5 can remove succinyl marks, providing a counter-regulatory mechanism. Overall, regulation is tightly linked to cellular energy status and redox balance.
succinyl-CoA metabolic process and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| SUCLG1 | Leukemia progression; mitochondrial biogenesis | Knockout and knock-in models in leukemia cell lines and mouse xenografts |
| SUCLA2 | Liver tumor growth; ketolysis | Liver-specific knockout or overexpression in mice |
| SUCLG2 | Cancer metastasis; redox regulation | Knockout and stress granule assays in metastatic cancer cells |
| GTPSCS | Gliomagenesis; histone lactylation | Knockout and point-mutation models in glioma cell lines |
| OXCT1 | Ketone body catabolism; liver cancer | Knockout and succinylation-site mutants in hepatoma cells |
Succinyl-CoA metabolism in cancer
Altered succinyl-CoA metabolism is increasingly recognized as a driver of cancer progression. In leukemia, SUCLG1 restricts POLRMT succinylation to enhance mitochondrial biogenesis and support leukemia progression. In liver cancer, SUCLA2-mediated succinylation and activation of OXCT1 promotes ketolysis and tumor growth. SUCLG2 promotes stress granule assembly to regulate redox and drive cancer metastasis. Additionally, nuclear GTPSCS functions as a lactyl-CoA synthetase to promote histone lactylation and gliomagenesis. These findings highlight succinyl-CoA metabolic enzymes as potential therapeutic targets in multiple malignancies.
Succinyl-CoA metabolism in heart failure
Chronic heart failure is associated with succinyl-CoA-based energy metabolism dysfunction. The heart relies heavily on oxidative metabolism, and impaired succinyl-CoA utilization can lead to energy deficit and contractile dysfunction. Studies in animal models have shown that restoring succinyl-CoA metabolism may improve cardiac function, suggesting that enzymes such as succinyl-CoA synthetase could be therapeutic targets.
Succinyl-CoA metabolism in neurological disorders
Nuclear GTPSCS promotes histone lactylation and gliomagenesis, linking succinyl-CoA-related enzymes to brain tumors. While direct evidence for neurodegeneration is limited in the provided citations, the role of succinyl-CoA in mitochondrial energy metabolism suggests that its dysfunction could contribute to neurodegenerative conditions characterized by mitochondrial impairment. Further research is needed to establish causal links.
From succinyl-CoA metabolic process-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of SUCLG1 affect mitochondrial biogenesis and leukemia progression? | CRISPR knockout of SUCLG1 in leukemia cell lines and mouse models |
| Does succinylation of OXCT1 regulate ketolysis and liver tumor growth? | Point-mutation knock-in of succinylation sites in OXCT1 |
| Does nuclear GTPSCS lactyl-CoA synthetase activity promote gliomagenesis? | Knockout and catalytic-dead point mutation in glioma cells |
| Does SUCLG2 promote stress granule assembly and metastasis? | Overexpression and knockout of SUCLG2 in cancer cell lines |
| Does KAT2A-mediated histone succinylation require alpha-KGDH complex? | Knockout of KAT2A or alpha-KGDH subunits in cell lines |
| Can restoration of succinyl-CoA metabolism improve heart failure? | Knock-in or overexpression of SUCL subunits in cardiac models |
How to Study the succinyl-CoA metabolic process Process
| Method | What It Measures | Typical Application |
|---|---|---|
| LC-MS metabolomics | Levels of succinyl-CoA and related metabolites | Quantifying metabolic changes in knockout or overexpression cells |
| 13C flux analysis | Flux through succinyl-CoA pathways | Tracing carbon flow in cancer or heart failure models |
| Succinylome profiling | Global protein succinylation | Identifying substrates of succinyl-CoA-dependent modifications |
| ChIP-seq | Histone succinylation marks on chromatin | Mapping epigenetic changes linked to succinyl-CoA |
| CRISPR knockout screens | Gene essentiality and synthetic lethality | Discovering targets in succinyl-CoA metabolism |
| Western blot | Protein expression and succinylation levels | Validating specific gene knockouts or point mutations |
| Immunoprecipitation | Protein-protein interactions | Studying complexes like KAT2A-alpha-KGDH |
| Seahorse assay | Mitochondrial respiration | Assessing energy metabolism in succinyl-CoA mutants |
Metabolomics and flux analysis
Mass spectrometry-based metabolomics allows direct measurement of succinyl-CoA and related metabolites in cells and tissues. Stable isotope tracing with 13C-labeled substrates can quantify flux through succinyl-CoA-producing and -consuming pathways, revealing how genetic perturbations alter metabolic networks. These methods are essential for validating CRISPR models of succinyl-CoA metabolic genes.
Proteomics and succinylome profiling
Antibody-based enrichment coupled with mass spectrometry enables global profiling of protein succinylation, identifying substrates of succinyl-CoA-dependent modifications. This approach can reveal how changes in succinyl-CoA levels affect chromatin and mitochondrial proteins. Site-specific succinylation can be validated by western blot with pan-succinyllysine antibodies.
Chromatin immunoprecipitation and sequencing (ChIP-seq)
ChIP-seq for histone succinylation marks (e.g., H3K79succ) can map genomic regions where succinyl-CoA metabolism influences chromatin state. This method is used to study how KAT2A and alpha-KGDH complex regulate gene expression through succinylation. Combining ChIP-seq with RNA-seq provides a comprehensive view of transcriptional consequences.
CRISPR screening and functional genomics
Genome-wide CRISPR knockout screens can identify genes that are essential for succinyl-CoA metabolism under specific conditions, such as in cancer cells or during metabolic stress. These screens can uncover synthetic lethal interactions and potential therapeutic targets. Follow-up validation with individual knockouts and rescue experiments confirms causality.
How CRISPR Can Be Used to Study GO:0006104 succinyl-CoA metabolic process
Knockout
CRISPR knockout is widely used to eliminate genes involved in succinyl-CoA metabolism, such as SUCLG1, SUCLA2, SUCLG2, OXCT1, and KAT2A, to study their loss-of-function phenotypes. For example, SUCLG1 knockout in leukemia cells impairs mitochondrial biogenesis and reduces tumor progression. Knockout of SUCLG2 inhibits stress granule assembly and metastasis. These models are essential for establishing causal roles in disease.
Point Mutation
Point mutations can be introduced to dissect specific catalytic activities or regulatory sites. For instance, mutation of succinylation sites on OXCT1 can test whether succinylation is required for its activation and ketolysis. Similarly, catalytic-dead mutations in GTPSCS can separate its lactyl-CoA synthetase activity from other functions. Point-mutation models provide mechanistic insights beyond simple knockouts.
Knock-in
Knock-in of tagged or mutant alleles allows precise tracking and functional analysis of succinyl-CoA metabolic enzymes. For example, knock-in of a succinylation-deficient OXCT1 mutant can reveal the importance of this modification in liver tumor growth. Knock-in of fluorescent tags enables live-cell imaging of enzyme localization and dynamics.
Overexpression
Overexpression of genes such as SUCLG2 or OXCT1 can drive metabolic reprogramming and promote phenotypes like metastasis or ketolysis. Overexpression models are useful for gain-of-function studies and for testing whether increased succinyl-CoA metabolism is sufficient to induce disease phenotypes. These models complement knockout approaches to establish bidirectional causality.
How EDITGENE Supports succinyl-CoA metabolic process Research
Researchers studying succinyl-CoA metabolic process-related genes often need to determine whether a candidate gene is causally involved in a specific phenotype, such as cancer progression, metabolic dysfunction, or epigenetic regulation. Establishing causality requires precise genetic manipulation, including knockout, point mutation, knock-in, and overexpression models. EDITGENE provides end-to-end CRISPR services to generate these models in relevant cell types, enabling rigorous mechanistic studies.
Contact EDITGENE today to design your custom CRISPR model for succinyl-CoA metabolic process research.
Frequently Asked Questions About succinyl-CoA metabolic process
What is succinyl-CoA metabolic process?
Succinyl-CoA metabolic process (GO:0006104) is the set of chemical reactions and pathways involving succinyl-CoA, a key intermediate in the TCA cycle, ketone body catabolism, and protein succinylation.
What genes are involved in succinyl-CoA metabolic process?
Key genes include SUCLG1, SUCLA2, SUCLG2, OXCT1, KAT2A, and GTPSCS, which encode enzymes that produce, utilize, or regulate succinyl-CoA.
What is the role of succinyl-CoA in the TCA cycle?
Succinyl-CoA is an intermediate in the TCA cycle, produced from alpha-ketoglutarate and converted to succinate by succinyl-CoA synthetase, generating ATP or GTP.
How is succinyl-CoA linked to cancer?
Altered succinyl-CoA metabolism supports cancer progression by promoting mitochondrial biogenesis, ketolysis, stress granule assembly, and histone lactylation in leukemia, liver cancer, and glioma.
What is the function of SUCLG1?
SUCLG1 encodes the alpha subunit of succinyl-CoA synthetase and restricts POLRMT succinylation to enhance mitochondrial biogenesis, with implications in leukemia.
How does succinyl-CoA regulate gene expression?
Succinyl-CoA serves as a substrate for histone succinyltransferases like KAT2A, which succinylates histone H3 and influences chromatin state and transcription.
What diseases are associated with succinyl-CoA metabolism?
Chronic heart failure, leukemia, liver cancer, glioma, and metastatic cancers have been linked to dysregulated succinyl-CoA metabolism.
How can I study succinyl-CoA metabolic process in the lab?
Common methods include LC-MS metabolomics, 13C flux analysis, succinylome profiling, ChIP-seq, and CRISPR knockout screens.
What is the role of OXCT1 in succinyl-CoA metabolism?
OXCT1 transfers CoA from succinyl-CoA to acetoacetate during ketone body catabolism and is activated by SUCLA2-mediated succinylation in liver cancer.
Can CRISPR be used to model succinyl-CoA metabolic disorders?
Yes, CRISPR knockout, point mutation, knock-in, and overexpression models are widely used to study the causal roles of succinyl-CoA metabolic genes in disease.
Conclusion
Succinyl-CoA metabolic process (GO:0006104) is a central biological process that bridges mitochondrial energy metabolism, ketone body catabolism, and epigenetic regulation. Its dysregulation is implicated in chronic heart failure, leukemia, liver cancer, glioma, and metastatic cancers, making it a compelling area for both basic and translational research. The enzymes involved, including SUCLG1, SUCLA2, SUCLG2, OXCT1, and KAT2A, are attractive targets for therapeutic intervention and biomarkers. Advances in CRISPR-based modeling, metabolomics, and proteomics are accelerating our understanding of how succinyl-CoA metabolism influences health and disease. EDITGENE provides comprehensive CRISPR services to support researchers in dissecting the causal roles of these genes and developing novel therapeutic strategies.
References
- 1. Liu R et al.. 2025. Nuclear GTPSCS functions as a lactyl-CoA synthetase to promote histone lactylation and gliomagenesis.. Cell Metab 37(2):377-394.e9 PMID: 39642882
- 2. Wang Y et al.. 2017. KAT2A coupled with the α-KGDH complex acts as a histone H3 succinyltransferase.. Nature 552(7684):273-277 PMID: 29211711
- 3. Trefely S et al.. 2020. Compartmentalised acyl-CoA metabolism and roles in chromatin regulation.. Mol Metab 38:100941 PMID: 32199817
- 4. Takada S et al.. 2022. Succinyl-CoA-based energy metabolism dysfunction in chronic heart failure.. Proc Natl Acad Sci U S A 119(41):e2203628119 PMID: 36201541
- 5. Yan W et al.. 2024. SUCLG1 restricts POLRMT succinylation to enhance mitochondrial biogenesis and leukemia progression.. EMBO J 43(12):2337-2367 PMID: 38649537
- 6. Boese AC et al.. 2023. Succinyl-CoA ligase ADP-forming subunit beta promotes stress granule assembly to regulate redox and drive cancer metastasis.. Proc Natl Acad Sci U S A 120(23):e2217332120 PMID: 37253003
- 7. Guo D et al.. 2025. OXCT1 succinylation and activation by SUCLA2 promotes ketolysis and liver tumor growth.. Mol Cell 85(4):843-856.e6 PMID: 39862868
- 8. Huang J et al.. 2020. Tartryl-CoA inhibits succinyl-CoA synthetase.. Acta Crystallogr F Struct Biol Commun 76(Pt 7):302-308 PMID: 32627745
