GO:0019747 regulation of isoprenoid metabolic process: Metabolic Control, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0019747 describes any process that modulates the frequency, rate or extent of the chemical reactions and pathways involving isoprenoids.
• Isoprenoid metabolism is controlled at multiple levels, including transcriptional regulation of pathway genes, post-translational regulation of rate-limiting enzymes such as HMGCR, and feedback control by sterol and non-sterol intermediates.
• The mevalonate (MVA) and methylerythritol phosphate (MEP) pathways are the two major routes for isoprenoid precursor biosynthesis, and their activities are coordinately regulated in plants, apicomplexan parasites, and bacteria.
• Protein prenylation is a key downstream isoprenoid-dependent process that is regulated by the availability of farnesyl and geranylgeranyl diphosphate and by prenyltransferase activity.
• Dysregulation of isoprenoid metabolism contributes to cancer, cardiovascular disease, infectious disease, and metabolic disorders, making this GO term relevant to diverse biomedical research areas.
• CRISPR-based knockout, point-mutation, knock-in, and overexpression models enable causal testing of genes that regulate isoprenoid metabolic processes.
Description
GO:0019747, regulation of isoprenoid metabolic process, is a Gene Ontology biological process term that encompasses any process that modulates the frequency, rate or extent of the chemical reactions and pathways involving isoprenoids. Isoprenoids, also called terpenoids, are a large and structurally diverse class of natural products derived from the five-carbon precursors isopentenyl diphosphate (IPP) and dimethylallyl diphosphate (DMAPP). These molecules serve essential roles in membrane integrity, electron transport, hormone signaling, protein prenylation, and defense, and their biosynthesis is tightly regulated in all domains of life. Researchers study GO:0019747 because isoprenoid metabolic flux must be precisely controlled to meet cellular demands while avoiding toxic intermediate accumulation. In plants, transcriptional regulation of isoprenoid pathway genes facilitates metabolic engineering of valuable terpenoids. In apicomplexan parasites such as Plasmodium falciparum, isoprenoid biosynthesis is essential and is a validated drug target. In bacteria such as Mycobacterium marinum, the mevalonate pathway supports metabolic flexibility during infection. In humans, dysregulated isoprenoid metabolism, particularly through the mevalonate pathway, is linked to cancer, cardiovascular disease, and developmental disorders. Understanding how isoprenoid metabolic processes are regulated requires integrating transcriptional, post-translational, and metabolic control mechanisms. This article provides a research-grade overview of GO:0019747, covering its definition, biological significance, key genes, disease connections, experimental models, and methods for investigation.
regulation of isoprenoid metabolic process At A Glance
| GO ID | GO:0019747 |
|---|---|
| GO term | regulation of isoprenoid metabolic process |
| Ontology | biological_process |
| Synonym | regulation of isoprenoid metabolism |
| Definition | Any process that modulates the frequency, rate or extent of the chemical reactions and pathways involving isoprenoids. |
| Major function | Controls the flux, timing, and extent of isoprenoid biosynthesis and utilization, including the mevalonate and MEP pathways, protein prenylation, and sterol synthesis. |
| Related pathways | Mevalonate (MVA) pathway, methylerythritol phosphate (MEP) pathway, protein prenylation, sterol biosynthesis, carotenoid biosynthesis. |
| Key regulatory nodes | HMGCR, FPPS, GGPPS, DXS, DXR, prenyltransferases. |
| Disease relevance | Cancer, cardiovascular disease, infectious disease, metabolic disorders, developmental defects. |
What Is GO:0019747?
According to the Gene Ontology, GO:0019747 (regulation of isoprenoid metabolic process) is defined as any process that modulates the frequency, rate or extent of the chemical reactions and pathways involving isoprenoids. This term is a biological process and includes both positive and negative regulation of isoprenoid metabolism. It encompasses regulatory mechanisms that act on the biosynthesis, interconversion, or utilization of isoprenoid compounds, such as transcriptional control of pathway enzymes, post-translational modification of rate-limiting enzymes, and feedback regulation by pathway intermediates or end products.
Why Is regulation of isoprenoid metabolic process Important in Cell Biology?
GO:0019747 is important because isoprenoid metabolism is essential for fundamental cellular processes, including membrane biosynthesis, protein prenylation, electron transport, and hormone production, and its dysregulation is associated with major human diseases. The mevalonate pathway, a central isoprenoid biosynthetic route, is the target of statins and bisphosphonates, and its regulatory mechanisms influence cancer cell survival, immune function, and cardiovascular risk. In infectious disease, isoprenoid biosynthesis is essential for the survival of pathogens such as Plasmodium falciparum and Mycobacterium marinum, making regulatory enzymes attractive drug targets. In biotechnology, understanding the regulation of isoprenoid metabolism enables metabolic engineering of high-value terpenoids in plants and microbes.
• Isoprenoid metabolism provides essential precursors for cholesterol, steroid hormones, vitamin K, ubiquinone, heme A, and prenylated proteins.
• Regulation of HMGCR, the rate-limiting enzyme of the mevalonate pathway, is a paradigm for feedback control of isoprenoid metabolism and is targeted by statins.
• Protein prenylation, a major isoprenoid-dependent modification, regulates Ras, Rho, and Rab GTPases, which are critical in cancer and immune signaling.
• In Plasmodium falciparum, the MEP pathway for isoprenoid biosynthesis is essential and is a validated antimalarial target.
• In Mycobacterium marinum, the mevalonate pathway supports metabolic flexibility and survival during infection.
• Transcriptional regulation of isoprenoid pathway genes enables metabolic engineering of terpenoid accumulation in Arabidopsis and other plants.
• Diatom isoprenoid metabolism is a promising source of bioactive compounds and biofuels, and its regulation is an active research area.
• Dysregulation of isoprenoid metabolism contributes to cancer, cardiovascular disease, and metabolic syndrome, making it a therapeutic target.
• Nutritional interventions can modulate isoprenoid metabolism, as reviewed in the context of nutritargeting.
• Understanding GO:0019747 aids in the development of CRISPR-based models to test causal roles of regulatory genes.
What Happens During regulation of isoprenoid metabolic process?
Transcriptional control of isoprenoid pathway genes
In simple terms: Cells adjust how much of each isoprenoid-making enzyme they produce by turning gene transcription up or down.
Transcriptional regulation is a major mechanism controlling isoprenoid metabolic flux. In plants, comprehensive assessment of transcriptional regulation of isoprenoid pathway genes has facilitated metabolic engineering of isoprenoid accumulation, demonstrating that coordinated expression of multiple biosynthetic genes is required for efficient terpenoid production. In Arabidopsis, transcription factors and developmental signals modulate the expression of genes in the MVA and MEP pathways, thereby influencing the supply of IPP and DMAPP for downstream isoprenoids. Similarly, in diatoms, transcriptional regulation of isoprenoid biosynthesis is being explored for biotechnological applications. These studies highlight that regulation of isoprenoid metabolic process often begins at the level of gene expression.
Post-translational regulation of rate-limiting enzymes
In simple terms: Even after enzymes are made, their activity can be switched on or off by chemical modifications or degradation.
Post-translational regulation of HMG-CoA reductase (HMGCR), the rate-limiting enzyme of the mevalonate pathway, is a well-characterized example of regulation of isoprenoid metabolic process. HMGCR activity is controlled by phosphorylation, ubiquitination, and sterol-induced degradation, allowing rapid adjustments in isoprenoid flux in response to cellular sterol levels. This regulation ensures that cholesterol and non-sterol isoprenoid products are produced in appropriate amounts. In Mycobacterium marinum, the mevalonate pathway supports metabolic flexibility, and its regulation likely involves post-translational mechanisms that respond to host-derived stresses. Thus, post-translational control is a critical layer in the regulation of isoprenoid metabolism.
Feedback regulation by sterol and non-sterol intermediates
In simple terms: The end products of the pathway tell the cell to slow down or speed up production, like a thermostat.
Feedback regulation by sterols and non-sterol isoprenoid intermediates is a conserved mechanism for controlling isoprenoid metabolic process. In mammalian cells, accumulation of cholesterol or oxysterols suppresses HMGCR transcription and promotes HMGCR degradation, while depletion of sterols activates the SREBP pathway to increase expression of mevalonate pathway genes. Non-sterol intermediates such as farnesyl diphosphate and geranylgeranyl diphosphate also participate in feedback regulation, particularly through effects on protein prenylation and cell signaling. In Plasmodium falciparum, the MEP pathway is regulated by feedback from downstream isoprenoid products, although the precise mechanisms are still being elucidated. These feedback loops maintain metabolic homeostasis and prevent toxic accumulation of intermediates.
Regulation of protein prenylation as a downstream isoprenoid-dependent process
In simple terms: Isoprenoids are attached to proteins to help them stick to membranes, and this attachment is carefully controlled.
Protein prenylation is a post-translational modification in which farnesyl or geranylgeranyl groups are covalently attached to cysteine residues of target proteins, such as Ras and Rho GTPases. The regulation of protein prenylation depends on the availability of isoprenoid donors (FPP and GGPP), the activity of prenyltransferases (FTase, GGTase-I, GGTase-II), and the expression of substrate proteins. Because prenylation is essential for the membrane localization and function of many signaling proteins, its regulation is intimately linked to the regulation of isoprenoid metabolic process. Dysregulated prenylation contributes to cancer and other diseases, making this crosstalk a therapeutic target.
Coordination of the MVA and MEP pathways in plants and microbes
In simple terms: Plants and many microbes have two different assembly lines for isoprenoid building blocks, and they coordinate them.
Plants possess both the mevalonate (MVA) pathway in the cytosol and the methylerythritol phosphate (MEP) pathway in plastids, which produce isoprenoid precursors for different downstream products. Network analysis of these pathways has revealed extensive regulation and crosstalk, including exchange of intermediates and coordinated transcriptional responses to developmental and environmental cues. In bacteria such as Mycobacterium marinum, the mevalonate pathway is used for isoprenoid biosynthesis and supports metabolic flexibility during infection. In the apicomplexan parasite Plasmodium falciparum, the MEP pathway is essential and is regulated in a stage-specific manner. Understanding how these pathways are regulated is key to targeting isoprenoid metabolism in pathogens and to engineering isoprenoid production in plants and microbes.
Key Genes Involved in GO:0019747 regulation of isoprenoid metabolic process
The following genes and proteins are key players in the regulation of isoprenoid metabolic process, based on published literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| HMGCR | Rate-limiting enzyme of the mevalonate pathway; converts HMG-CoA to mevalonate | Target of statins; regulated by sterol feedback and post-translational mechanisms |
| HMGCS1 | Synthesizes HMG-CoA from acetyl-CoA and acetoacetyl-CoA in the mevalonate pathway | Transcriptional regulation by SREBP; relevant to cholesterol synthesis |
| MVK | Mevalonate kinase; phosphorylates mevalonate in the MVA pathway | Defects cause mevalonate kinase deficiency; regulated by feedback |
| PMVK | Phosphomevalonate kinase; converts mevalonate-5-phosphate to mevalonate-5-diphosphate | Part of the MVA pathway; potential regulatory node |
| MVD | Mevalonate diphosphate decarboxylase; produces IPP from mevalonate-5-diphosphate | Regulated in response to sterol demand |
| FDPS | Farnesyl diphosphate synthase; synthesizes FPP from IPP and DMAPP | Key branch point for sterols, prenylation, and other isoprenoids |
| GGPS1 | Geranylgeranyl diphosphate synthase; synthesizes GGPP | Provides substrate for protein geranylgeranylation |
| DXS | 1-deoxy-D-xylulose-5-phosphate synthase; first enzyme of the MEP pathway | Rate-limiting in plastidial isoprenoid biosynthesis; target for metabolic engineering |
| DXR | 1-deoxy-D-xylulose-5-phosphate reductoisomerase; second enzyme of the MEP pathway | Target of fosmidomycin; essential in Plasmodium |
| MCT | 2-C-methyl-D-erythritol 4-phosphate cytidylyltransferase; MEP pathway enzyme | Regulated in plants and microbes |
| CMK | 4-diphosphocytidyl-2-C-methyl-D-erythritol kinase; MEP pathway enzyme | Part of the MEP pathway; potential regulatory point |
| MCS | 2-C-methyl-D-erythritol 2,4-cyclodiphosphate synthase; MEP pathway enzyme | Involved in isoprenoid precursor synthesis |
| HDS | 4-hydroxy-3-methylbut-2-enyl diphosphate synthase; MEP pathway enzyme | Regulated in response to oxidative stress |
| HDR | 4-hydroxy-3-methylbut-2-enyl diphosphate reductase; MEP pathway enzyme | Produces IPP and DMAPP; regulatory node |
| FNTA | Farnesyltransferase alpha subunit; participates in protein prenylation | Regulates Ras and other proteins; cancer relevance |
| FNTB | Farnesyltransferase beta subunit; catalytic subunit of FTase | Target for cancer therapy |
| PGGT1B | Geranylgeranyltransferase type I beta subunit; prenylates Rho proteins | Regulates Rho GTPase signaling |
| RABGGTA | Rab geranylgeranyltransferase alpha subunit; prenylates Rab proteins | Regulates vesicular trafficking |
How Is regulation of isoprenoid metabolic process Regulated?
The regulation of isoprenoid metabolic process is itself subject to multiple layers of control. In mammalian cells, the SREBP (sterol regulatory element-binding protein) pathway senses sterol levels and controls the transcription of many mevalonate pathway genes, including HMGCR and HMGCS1. Post-translational regulation of HMGCR by AMPK-mediated phosphorylation and by Insig-mediated ubiquitination provides rapid control of enzyme stability and activity. Protein prenylation is regulated by the availability of FPP and GGPP, which in turn depends on the activity of FDPS and GGPS1, and by the expression and activity of prenyltransferases. In plants, transcriptional regulation of MVA and MEP pathway genes is coordinated with developmental and environmental signals, and network analysis has revealed complex regulatory interactions. In Plasmodium falciparum, the MEP pathway is regulated stage-specifically, and its inhibition leads to parasite death. In Mycobacterium marinum, the mevalonate pathway is regulated to support metabolic flexibility during infection. These examples illustrate that regulation of isoprenoid metabolic process operates at transcriptional, post-translational, and metabolic levels.
regulation of isoprenoid metabolic process and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| HMGCR | Cardiovascular disease, cancer | Knockout or point-mutation in cell lines; statin response assays |
| FDPS | Cancer, bone disease | Knockout in cancer cell lines; prenylation assays |
| GGPS1 | Cancer, developmental disorders | Knock-in of patient mutations; geranylgeranylation assays |
| DXS | Infectious disease (Plasmodium, Mycobacterium) | Knockout in P. falciparum or M. marinum; growth inhibition assays |
| DXR | Infectious disease (Plasmodium) | Knockout or point-mutation in P. falciparum; fosmidomycin sensitivity |
Cancer
Dysregulation of isoprenoid metabolism is implicated in cancer through multiple mechanisms. The mevalonate pathway provides precursors for cholesterol and for prenyl groups that modify Ras, Rho, and other oncogenic GTPases. Increased HMGCR activity and elevated protein prenylation can promote tumor cell proliferation and survival. Statins, which inhibit HMGCR, have been investigated for their potential anticancer effects, although results vary by cancer type. Targeting prenyltransferases, such as farnesyltransferase, has been explored as a therapeutic strategy, particularly for Ras-driven cancers. Thus, regulation of isoprenoid metabolic process is a relevant area for cancer research.
Cardiovascular disease
The mevalonate pathway is central to cholesterol biosynthesis, and its regulation directly impacts cardiovascular health. HMGCR is the target of statins, which lower LDL cholesterol and reduce cardiovascular risk. Beyond cholesterol, isoprenoid intermediates regulate endothelial function and vascular smooth muscle cell proliferation through protein prenylation. Dysregulated isoprenoid metabolism contributes to atherosclerosis and other cardiovascular conditions. Nutritional factors can modulate isoprenoid metabolism, as discussed in the context of nutritargeting.
Infectious disease
Isoprenoid biosynthesis is essential for many pathogens, making it a target for anti-infective therapies. Plasmodium falciparum relies on the MEP pathway for isoprenoid precursors, and inhibition of DXR by fosmidomycin kills the parasite. Mycobacterium marinum uses the mevalonate pathway to support metabolic flexibility during infection, and this pathway is required for survival in host cells. These findings highlight the importance of regulation of isoprenoid metabolic process in infectious disease and the potential for targeting regulatory enzymes.
Metabolic and developmental disorders
Inherited defects in isoprenoid metabolism cause rare metabolic disorders, such as mevalonate kinase deficiency, which presents with periodic fever and developmental abnormalities. Dysregulation of isoprenoid metabolism has also been linked to metabolic syndrome and insulin resistance, although the mechanisms are complex. Understanding the regulation of isoprenoid metabolic process may provide insights into these conditions.
From regulation of isoprenoid metabolic process-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of HMGCR affect isoprenoid flux and cell viability? | CRISPR knockout of HMGCR in human cell lines; lipidomics and viability assays |
| Does a specific point mutation in FDPS alter prenylation of Ras? | CRISPR point mutation of FDPS; prenylation and Ras localization assays |
| Can knock-in of a patient-derived MVK mutation recapitulate mevalonate kinase deficiency? | CRISPR knock-in of mutant MVK in cell lines; inflammatory cytokine profiling |
| Does overexpression of DXS increase isoprenoid production in plants? | CRISPR-mediated overexpression or transgenic Arabidopsis; terpenoid quantification |
| Does knockout of DXR in Plasmodium falciparum reduce isoprenoid biosynthesis? | CRISPR knockout in P. falciparum; metabolic labeling and growth assays |
| Does knockout of the mevalonate pathway in Mycobacterium marinum affect intracellular survival? | CRISPR knockout in M. marinum; macrophage infection assays |
How to Study the regulation of isoprenoid metabolic process Process
| Method | What It Measures | Typical Application |
|---|---|---|
| RNA-seq | Transcript levels of isoprenoid pathway genes | Identify transcriptional regulators and expression changes |
| Metabolomics (LC-MS/GC-MS) | Levels of isoprenoid intermediates and end products | Assess metabolic flux and pathway activity |
| Lipidomics | Cholesterol and other sterol species | Evaluate mevalonate pathway output |
| Prenylation assays (click chemistry, Western blot) | Prenylation status of target proteins | Measure FTase/GGTase activity and substrate prenylation |
| CRISPR knockout screens | Gene essentiality and effects on isoprenoid metabolism | Discover novel regulators and drug targets |
| CRISPR activation (CRISPRa) | Overexpression of pathway genes | Increase isoprenoid production for metabolic engineering |
| Metabolic labeling (13C-glucose, 13C-acetate) | Flux through isoprenoid pathways | Trace carbon flow in MVA and MEP pathways |
| Enzyme activity assays | Activity of HMGCR, FDPS, GGPS1, etc. | Measure direct effects of genetic perturbations |
Transcriptomics and RNA-seq
RNA sequencing (RNA-seq) is widely used to measure the expression of genes involved in isoprenoid metabolism under different conditions. In Arabidopsis, comprehensive transcriptomic analysis has revealed coordinated regulation of MVA and MEP pathway genes, facilitating metabolic engineering. In Plasmodium falciparum, stage-specific transcriptomics has shown that MEP pathway genes are expressed at specific points in the life cycle. RNA-seq can identify transcriptional regulatory networks and candidate regulators of GO:0019747.
Metabolomics and lipidomics
Mass spectrometry-based metabolomics and lipidomics quantify isoprenoid intermediates and end products, such as mevalonate, IPP, FPP, GGPP, cholesterol, and prenylated proteins. These methods are essential for assessing the functional impact of genetic perturbations on isoprenoid metabolic flux. In Mycobacterium marinum, metabolomics has been used to show that the mevalonate pathway supports metabolic flexibility. In plants, metabolomics guides metabolic engineering of terpenoid production.
Proteomics and prenylation assays
Proteomic approaches, including click-chemistry-based prenylation probes, can identify and quantify prenylated proteins and assess the activity of prenyltransferases. Western blotting with prenylation-specific antibodies and subcellular fractionation are also used to monitor protein prenylation. These methods help link regulation of isoprenoid metabolism to downstream signaling events.
CRISPR screening and functional genomics
CRISPR knockout and activation screens enable unbiased identification of genes that regulate isoprenoid metabolism. Libraries targeting metabolic enzymes, transcription factors, and signaling proteins can be screened for effects on isoprenoid flux or sensitivity to inhibitors such as statins. Such screens can reveal novel regulators of GO:0019747 and potential therapeutic targets.
How CRISPR Can Be Used to Study GO:0019747 regulation of isoprenoid metabolic process
Knockout
CRISPR knockout is used to create cell models lacking specific genes involved in the regulation of isoprenoid metabolic process. For example, knockout of HMGCR in human cell lines can reveal its essentiality and effects on cholesterol synthesis and prenylation. Knockout of DXR in Plasmodium falciparum can validate its role in the MEP pathway and parasite survival. Knockout of mevalonate pathway genes in Mycobacterium marinum can test their requirement for intracellular survival. These models are valuable for target validation and drug discovery.
Point Mutation
CRISPR point mutation introduces specific amino acid changes to study structure-function relationships or to model patient-derived mutations. For instance, point mutations in HMGCR can dissect its regulation by phosphorylation or sterol-induced degradation. Point mutations in FDPS or GGPS1 can alter substrate specificity or catalytic activity, affecting prenylation. Point mutations in MVK can model mevalonate kinase deficiency and its impact on isoprenoid metabolism. These models provide precise insights into regulatory mechanisms.
Knock-in
CRISPR knock-in allows the introduction of reporter tags, such as GFP or luciferase, or the replacement of a gene with a mutant allele. Tagged knock-in of HMGCR can enable live-cell imaging of its localization and turnover. Knock-in of patient mutations in MVK or other isoprenoid genes can create disease models for mechanistic studies. Knock-in of promoter-reporter constructs can monitor transcriptional regulation of isoprenoid pathway genes. These models are essential for understanding dynamic regulation.
Overexpression
CRISPR activation (CRISPRa) or traditional overexpression can increase the expression of genes that regulate isoprenoid metabolism. Overexpression of DXS or DXR in plants or microbes can enhance isoprenoid production for biotechnological applications. Overexpression of HMGCR or FDPS can increase flux through the mevalonate pathway and alter prenylation. These models are useful for metabolic engineering and for studying the consequences of pathway activation.
How EDITGENE Supports regulation of isoprenoid metabolic process Research
Researchers studying regulation of isoprenoid metabolic process-related genes often need to determine whether a candidate gene is causally involved in pathway control, and CRISPR-based models provide the most direct way to test this. EDITGENE offers a comprehensive suite of services to generate and characterize such models.
Contact EDITGENE today to design your custom CRISPR model for regulation of isoprenoid metabolic process research.
Frequently Asked Questions About regulation of isoprenoid metabolic process
What is GO:0019747?
GO:0019747 is the Gene Ontology term for regulation of isoprenoid metabolic process, defined as any process that modulates the frequency, rate or extent of the chemical reactions and pathways involving isoprenoids.
What are isoprenoids?
Isoprenoids, also called terpenoids, are a diverse class of natural products derived from the five-carbon precursors IPP and DMAPP, and they include sterols, carotenoids, and prenyl groups.
What genes are involved in regulation of isoprenoid metabolic process?
Key genes include HMGCR, HMGCS1, MVK, FDPS, GGPS1, DXS, DXR, and prenyltransferases such as FNTA and PGGT1B.
How is isoprenoid metabolism regulated?
It is regulated at transcriptional, post-translational, and metabolic levels, including SREBP-mediated transcription, HMGCR phosphorylation and degradation, and feedback by sterols and non-sterol intermediates.
What is the mevalonate pathway?
The mevalonate pathway is a major route for isoprenoid biosynthesis that produces cholesterol and prenyl groups, and it is regulated by HMGCR and other enzymes.
What is the MEP pathway?
The methylerythritol phosphate (MEP) pathway is an alternative route for isoprenoid precursor biosynthesis found in plants, algae, and many bacteria, and it is essential in Plasmodium falciparum.
How does protein prenylation relate to isoprenoid metabolism?
Protein prenylation is a post-translational modification that attaches farnesyl or geranylgeranyl groups from isoprenoid metabolism to proteins, regulating their membrane localization and function.
What diseases are linked to isoprenoid metabolism?
Dysregulated isoprenoid metabolism is linked to cancer, cardiovascular disease, infectious diseases, and metabolic disorders such as mevalonate kinase deficiency.
How can CRISPR be used to study isoprenoid metabolism?
CRISPR knockout, point mutation, knock-in, and overexpression models allow causal testing of genes that regulate isoprenoid metabolic processes.
What methods are used to study regulation of isoprenoid metabolic process?
Common methods include RNA-seq, metabolomics, lipidomics, prenylation assays, CRISPR screens, and metabolic labeling.
Conclusion
GO:0019747, regulation of isoprenoid metabolic process, is a fundamental biological process that controls the synthesis and utilization of a vast array of essential molecules. Its regulation occurs at multiple levels, from transcription to post-translational modification and feedback inhibition, and its dysregulation is implicated in cancer, cardiovascular disease, infectious disease, and metabolic disorders. Understanding these regulatory mechanisms is critical for developing therapeutic strategies and for metabolic engineering applications. CRISPR-based models and advanced omics technologies provide powerful tools to dissect the regulation of isoprenoid metabolism and to translate these insights into clinical and biotechnological advances.
References
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