GO:0052659 inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity: Mechanism, Genes and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0052659 defines the enzymatic activity that removes the 5-phosphate from 1D-myo-inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4), yielding 1D-myo-inositol 1,3,4-trisphosphate and inorganic phosphate.
• This activity is a key off-switch in the inositol tris/tetrakisphosphate pathway, which is initiated by Ins(1,4,5)P3 3-kinase converting Ins(1,4,5)P3 to Ins(1,3,4,5)P4.
• The SH2-domain-containing inositol 5-phosphatases SHIP1 and SHIP2 are established enzymes with Ins(1,3,4,5)P4 5-phosphatase activity, linking this reaction to phosphoinositide signaling and immune regulation.
• Ins(1,3,4,5)P4 metabolism is also influenced by a distinct 3-phosphatase activity that removes the 3-phosphate, and this competing route is inhibited by Ins(1,3,4,5,6)P5 and InsP6.
• Dysregulation of inositol polyphosphate 5-phosphatases such as SHIP1 and SHIP2 has been implicated in hematologic malignancies, metabolic disease, and immune disorders.
• CRISPR knockout, point-mutation, knock-in, and overexpression models enable precise dissection of GO:0052659-related enzymes in cell-based and disease-relevant systems.
Description
Inositol polyphosphates are versatile signaling molecules that control calcium mobilization, vesicle trafficking, and cell survival. The reaction defined by GO:0052659, inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity, specifically dephosphorylates 1D-myo-inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4) at the 5-position to produce 1D-myo-inositol 1,3,4-trisphosphate and phosphate. This activity is part of the inositol tris/tetrakisphosphate pathway, which begins when Ins(1,4,5)P3 3-kinase phosphorylates Ins(1,4,5)P3 to form Ins(1,3,4,5)P4. Because Ins(1,3,4,5)P4 can modulate calcium and phosphoinositide signaling, the enzymes that eliminate it are critical for signal termination and for maintaining the balance of inositol polyphosphate pools. The 5-phosphatase step is catalyzed by members of the inositol polyphosphate 5-phosphatase family, including the SH2-domain-containing proteins SHIP1 and SHIP2. SHIP2 was shown to hydrolyze both phosphatidylinositol 3,4,5-trisphosphate and Ins(1,3,4,5)P4, directly demonstrating its 5-phosphatase activity toward this soluble substrate. SHIP1, the founding member of the SHIP family, similarly acts on Ins(1,3,4,5)P4 and is a central regulator of immune cell signaling. These enzymes therefore connect GO:0052659 to broader phosphoinositide 3-kinase (PI3K) and immune pathways. For researchers, GO:0052659 provides a precise functional annotation to study how cells terminate Ins(1,3,4,5)P4 signals. The activity can be measured in vitro with synthetic or natural Ins(1,3,4,5)P4 analogues, and its regulation is intertwined with competing 3-phosphatase and 5-phosphatase routes that determine the fate of Ins(1,3,4,5)P4. Understanding this activity is essential for interpreting calcium signaling, phosphoinositide dynamics, and the pharmacological targeting of 5-phosphatases in disease.
inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity At A Glance
| GO ID | GO:0052659 |
|---|---|
| GO term | inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity |
| Ontology | molecular_function |
| Synonym | D-myo-inositol (1,3,4,5)-polyphosphate 5-phosphatase activity; inositol polyphosphate-5-phosphatase activity; Ins(1,3,4,5)P4 5-phosphatase activity; type II inositol polyphosphate 5-phosphatase activity; type I inositol-polyphosphate phosphatase activity |
| Definition | Catalysis of the reaction: 1D-myo-inositol 1,3,4,5-tetrakisphosphate + H2O = 1D-myo-inositol 1,3,4-trisphosphate + phosphate. |
| Major function | Termination of Ins(1,3,4,5)P4 signaling by hydrolytic removal of the 5-phosphate. |
| Substrate | 1D-myo-inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4) |
| Product | 1D-myo-inositol 1,3,4-trisphosphate and phosphate |
| Representative enzymes | SHIP1 (INPP5D), SHIP2 (INPPL1), and other inositol polyphosphate 5-phosphatases |
What Is GO:0052659?
GO:0052659 describes the catalytic activity that removes the 5-phosphate group from 1D-myo-inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4) in the presence of water, producing 1D-myo-inositol 1,3,4-trisphosphate and free phosphate. It is a molecular function term in the Gene Ontology and is synonymous with D-myo-inositol (1,3,4,5)-polyphosphate 5-phosphatase activity, inositol polyphosphate-5-phosphatase activity, Ins(1,3,4,5)P4 5-phosphatase activity, type II inositol polyphosphate 5-phosphatase activity, and type I inositol-polyphosphate phosphatase activity. The reaction is a hydrolytic dephosphorylation event and is distinct from 3-phosphatase activities that remove the 3-phosphate from the same substrate.
Why Is inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity Important in Cell Biology?
GO:0052659 is important because it defines a dedicated biochemical step that controls the lifetime of Ins(1,3,4,5)P4, a soluble inositol polyphosphate generated in the inositol tris/tetrakisphosphate pathway. By removing the 5-phosphate, this activity prevents excessive or prolonged Ins(1,3,4,5)P4 accumulation and helps shape calcium and phosphoinositide signals. The enzymes that carry this activity, notably SHIP1 and SHIP2, are central nodes in immune and metabolic signaling and are actively studied as drug targets. Consequently, measuring and manipulating this activity is relevant to cancer biology, immunology, and neurobiology.
• Provides a biochemical off-switch for Ins(1,3,4,5)P4, a product of Ins(1,4,5)P3 3-kinase in the inositol tris/tetrakisphosphate pathway.
• Links soluble inositol polyphosphate metabolism to phosphoinositide 3-kinase signaling through SHIP family enzymes.
• SHIP2 directly hydrolyzes Ins(1,3,4,5)P4, demonstrating that this activity is intrinsic to a major 5-phosphatase.
• Competes with a distinct 3-phosphatase route that also degrades Ins(1,3,4,5)P4, so the balance between these activities determines downstream inositol polyphosphate profiles.
• Inhibitors such as Ins(1,3,4,5,6)P5 and InsP6 can modulate the 3-phosphatase arm, indirectly influencing how much substrate is available for 5-phosphatase action.
• Synthetic Ins(1,3,4,5)P4 analogues enable controlled in vitro assays of 5-phosphatase activity.
• Dysregulated 5-phosphatase function has been associated with hematologic malignancies and immune disorders.
• The activity is relevant to calcium-mobilizing messenger systems that depend on precise Ins(1,4,5)P3 and Ins(1,3,4,5)P4 levels.
• Understanding GO:0052659 supports the development of selective modulators of inositol polyphosphate 5-phosphatases.
• CRISPR-based models allow causal testing of whether a candidate 5-phosphatase gene contributes to a given phenotype.
Molecular Mechanism of inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity
Substrate recognition and binding
In simple terms: The enzyme must first grab the correct inositol polyphosphate molecule.
The substrate for GO:0052659 is 1D-myo-inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4), a soluble inositol polyphosphate produced by Ins(1,4,5)P3 3-kinase. Enzymes with this activity, such as SHIP2, recognize the tetrakisphosphate headgroup and position the 5-phosphate for hydrolysis. Synthetic analogues of Ins(1,3,4,5)P4 have been used to probe substrate recognition and to assay 5-phosphatase activity in vitro.
Catalytic hydrolysis of the 5-phosphate
In simple terms: The enzyme cuts off the phosphate at the 5-position using water.
The catalytic step is a hydrolytic dephosphorylation: Ins(1,3,4,5)P4 + H2O yields 1D-myo-inositol 1,3,4-trisphosphate plus phosphate. SHIP2 was shown to display both phosphatidylinositol 3,4,5-trisphosphate and Ins(1,3,4,5)P4 5-phosphatase activity, confirming that the same enzyme can act on lipid and soluble inositol polyphosphate substrates. This reaction terminates the signaling potential of Ins(1,3,4,5)P4 at the 5-position.
Competition with 3-phosphatase activity
In simple terms: Another enzyme can remove a different phosphate from the same molecule, so the two routes compete.
Ins(1,3,4,5)P4 can also be dephosphorylated at the 3-position by a distinct salt-activated 3-phosphatase activity found at the inner surface of the human erythrocyte membrane. This 3-phosphatase is inhibited by Ins(1,3,4,5,6)P5 and InsP6 in rat parotid glands, indicating that cellular levels of higher inositol polyphosphates can steer Ins(1,3,4,5)P4 toward either the 3-phosphatase or the 5-phosphatase route. The balance between these activities shapes the downstream inositol polyphosphate landscape.
Enzymes and cofactors
In simple terms: Specific proteins carry this activity, and their regulation depends on protein domains and cellular context.
The SH2-domain-containing inositol 5-phosphatases SHIP1 and SHIP2 are established enzymes with Ins(1,3,4,5)P4 5-phosphatase activity. SHIP2 was biochemically characterized as a 5-phosphatase acting on both phosphatidylinositol 3,4,5-trisphosphate and Ins(1,3,4,5)P4. SHIP1 is a central regulator of immune cell signaling and also acts on Ins(1,3,4,5)P4. These enzymes require their catalytic 5-phosphatase domain, and their activity can be studied using synthetic Ins(1,3,4,5)P4 analogues.
Integration with calcium and phosphoinositide signaling
In simple terms: This activity helps keep calcium and lipid signals under control.
Ins(1,4,5)P3 is a calcium-mobilizing messenger, and its phosphorylation by 3-kinase produces Ins(1,3,4,5)P4. By removing the 5-phosphate from Ins(1,3,4,5)P4, the 5-phosphatase activity defined by GO:0052659 contributes to the termination of this branch of the inositol tris/tetrakisphosphate pathway. Because SHIP enzymes also act on phosphatidylinositol 3,4,5-trisphosphate, this activity is integrated with phosphoinositide 3-kinase signaling.
Key Genes Involved in GO:0052659 inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity
The following genes and proteins are directly or functionally linked to inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity (GO:0052659) based on published biochemical and genetic evidence.
| Gene | Major Role | Research Relevance |
|---|---|---|
| INPP5D (SHIP1) | SH2-domain-containing inositol 5-phosphatase that acts on Ins(1,3,4,5)P4 and phosphatidylinositol 3,4,5-trisphosphate | Immune cell signaling, hematologic malignancies, and regulation of phosphoinositide pools |
| INPPL1 (SHIP2) | Inositol 5-phosphatase with demonstrated Ins(1,3,4,5)P4 5-phosphatase activity | Metabolic signaling, insulin sensitivity, and phosphoinositide 3-kinase pathway crosstalk |
| ITPKA | Inositol-trisphosphate 3-kinase A that produces Ins(1,3,4,5)P4 from Ins(1,4,5)P3 | Upstream generator of the substrate for GO:0052659; actin targeting and neuronal signaling |
| ITPKB | Inositol-trisphosphate 3-kinase B that produces Ins(1,3,4,5)P4 | Immune and neuronal signaling; contributes to Ins(1,3,4,5)P4 pools |
| ITPKC | Inositol-trisphosphate 3-kinase C that produces Ins(1,3,4,5)P4 | Regulation of inositol polyphosphate levels in diverse tissues |
| INPP5A | Type I inositol polyphosphate 5-phosphatase | Related 5-phosphatase activity; contributes to inositol polyphosphate turnover |
| INPP5B | Inositol polyphosphate 5-phosphatase | Related 5-phosphatase family member; phosphoinositide signaling |
| OCRL | Inositol polyphosphate 5-phosphatase | Lowe syndrome biology; phosphoinositide metabolism |
| SYNJ1 | Synaptojanin 1, a polyphosphoinositide phosphatase | Synaptic vesicle trafficking and phosphoinositide turnover |
| SYNJ2 | Synaptojanin 2, a polyphosphoinositide phosphatase | Membrane trafficking and phosphoinositide signaling |
| INPP4A | Inositol polyphosphate 4-phosphatase | Related inositol polyphosphate turnover; indirect influence on substrate availability |
| INPP4B | Inositol polyphosphate 4-phosphatase | Phosphoinositide signaling and tumor suppression |
| PTEN | Lipid phosphatase that opposes phosphoinositide 3-kinase signaling | Indirectly affects phosphoinositide pools linked to SHIP enzymes |
| PIK3CA | Catalytic subunit of phosphoinositide 3-kinase | Upstream of phosphatidylinositol 3,4,5-trisphosphate and Ins(1,3,4,5)P4-related signaling |
| PIK3CD | Phosphoinositide 3-kinase delta catalytic subunit | Immune signaling context for SHIP1 function |
| PLCG1 | Phospholipase C gamma 1 | Generates Ins(1,4,5)P3, the precursor of Ins(1,3,4,5)P4 |
| PLCG2 | Phospholipase C gamma 2 | Generates Ins(1,4,5)P3 in immune cells |
| ITPR1 | Inositol 1,4,5-trisphosphate receptor | Mediates calcium release downstream of Ins(1,4,5)P3 signaling |
How Is inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity Regulated?
The activity defined by GO:0052659 is regulated at multiple levels. Substrate availability depends on Ins(1,4,5)P3 3-kinase, which produces Ins(1,3,4,5)P4 from Ins(1,4,5)P3. Competing 3-phosphatase activity can divert Ins(1,3,4,5)P4 away from the 5-phosphatase route, and this 3-phosphatase is inhibited by Ins(1,3,4,5,6)P5 and InsP6. The 5-phosphatase enzymes themselves, including SHIP1 and SHIP2, are regulated by their SH2 domains and by cellular context, allowing them to integrate phosphoinositide 3-kinase signaling with soluble inositol polyphosphate turnover. In addition, the 3-kinase isoenzymes that generate the substrate are targeted to actin and other cellular structures, which can influence local Ins(1,3,4,5)P4 concentrations.
inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| INPP5D (SHIP1) | Hematologic malignancies and immune disorders | Knockout and point-mutation models in immune cell lines |
| INPPL1 (SHIP2) | Metabolic disease and insulin signaling | Overexpression and knockout models in adipocytes or hepatocytes |
| ITPKA | Neuronal signaling and actin regulation | Knockout and tagged knock-in models in neuronal cells |
| ITPKB | Immune and neuronal signaling | Knockout models in T cells or neurons |
| ITPKC | Inositol polyphosphate imbalance | Point-mutation and overexpression models in epithelial cells |
Hematologic malignancies and immune disorders
SHIP1 (INPP5D) is a central regulator of immune cell signaling and acts on Ins(1,3,4,5)P4. Dysregulated SHIP1 function has been linked to hematologic malignancies and immune disorders, making the 5-phosphatase activity defined by GO:0052659 relevant to blood cancers and inflammatory disease.
Metabolic disease and insulin signaling
SHIP2 (INPPL1) displays both phosphatidylinositol 3,4,5-trisphosphate and Ins(1,3,4,5)P4 5-phosphatase activity. Because SHIP2 modulates phosphoinositide 3-kinase signaling, its 5-phosphatase activity is of interest in metabolic disease and insulin resistance research.
Neurological and calcium signaling disorders
Ins(1,4,5)P3 is a calcium-mobilizing messenger, and its conversion to Ins(1,3,4,5)P4 by 3-kinase is part of the inositol tris/tetrakisphosphate pathway. The 3-kinase isoenzymes are targeted to actin and are important for neuronal function, so enzymes that terminate Ins(1,3,4,5)P4 signals may influence calcium-dependent neuronal processes.
Inositol polyphosphate imbalance
The 3-phosphatase and 5-phosphatase routes compete for Ins(1,3,4,5)P4, and higher inositol polyphosphates such as Ins(1,3,4,5,6)P5 and InsP6 can inhibit the 3-phosphatase. This interplay suggests that diseases involving altered inositol polyphosphate levels could be studied through the lens of GO:0052659.
From inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of a candidate 5-phosphatase alter Ins(1,3,4,5)P4 levels? | CRISPR knockout cell line followed by inositol polyphosphate profiling |
| Does a specific catalytic residue mediate 5-phosphatase activity? | CRISPR point-mutation knock-in of the catalytic domain |
| Does tagging the endogenous enzyme affect its localization? | Tagged knock-in with fluorescent or affinity tag |
| Does overexpression of SHIP2 change phosphoinositide signaling? | CRISPR overexpression or cDNA overexpression cell model |
| Which genes modify the phenotype of 5-phosphatase loss? | CRISPR library screening with a focused or genome-wide library |
| Can a disease-associated variant change enzyme function? | Knock-in of the patient variant followed by biochemical assay |
How to Study the inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity Process
| Method | What It Measures | Typical Application |
|---|---|---|
| In vitro 5-phosphatase assay | Hydrolysis of Ins(1,3,4,5)P4 to Ins(1,3,4)P3 | Testing recombinant SHIP1 or SHIP2 activity |
| Mass spectrometry of inositol polyphosphates | Cellular levels of Ins(1,3,4,5)P4 and related species | Profiling pathway changes after gene editing |
| CRISPR knockout screening | Gene requirements for a phenotype | Identifying modifiers of 5-phosphatase loss |
| CRISPR point-mutation knock-in | Effect of a specific amino acid change | Testing catalytic residues or disease variants |
| Tagged knock-in | Protein localization and interactions | Visualizing endogenous 5-phosphatase enzymes |
| Overexpression | Gain-of-function effects | Testing SHIP2 or SHIP1 dosage |
| Calcium imaging | Downstream calcium signals | Linking Ins(1,3,4,5)P4 metabolism to calcium |
| Co-immunoprecipitation | Protein-protein interactions | Studying SH2-domain-mediated regulation |
Biochemical 5-phosphatase assays
Enzymatic activity toward Ins(1,3,4,5)P4 can be measured using synthetic or natural substrate analogues. Such assays allow direct testing of whether a candidate enzyme, such as SHIP2, hydrolyzes Ins(1,3,4,5)P4. They are typically performed with recombinant enzyme and radiolabeled or fluorescently labeled substrate.
Inositol polyphosphate profiling
Mass spectrometry or chromatographic methods can quantify Ins(1,3,4,5)P4 and its product 1D-myo-inositol 1,3,4-trisphosphate in cells. These measurements help determine whether a genetic perturbation shifts the balance between the 5-phosphatase and 3-phosphatase routes.
CRISPR-based genetic screens
Pooled CRISPR knockout or activation screens can identify genes that modify phenotypes linked to inositol polyphosphate 5-phosphatases. Hits can then be validated with individual knockout or point-mutation models to test causality.
Imaging and localization studies
Fluorescent tagging of 5-phosphatase enzymes or their substrates can reveal where the activity occurs in cells. Because 3-kinase isoenzymes are targeted to actin, localization studies can connect substrate production to 5-phosphatase action.
How CRISPR Can Be Used to Study GO:0052659 inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity
Knockout
CRISPR knockout of INPP5D or INPPL1 can eliminate the 5-phosphatase activity defined by GO:0052659 in a cell model. Such models are useful for measuring changes in Ins(1,3,4,5)P4 levels and downstream calcium or phosphoinositide signaling.
Point Mutation
Point-mutation knock-in can alter a single catalytic residue in a 5-phosphatase enzyme, allowing researchers to test whether the enzymatic activity is required for a specific phenotype. This approach is valuable for separating catalytic from scaffolding functions of SHIP proteins.
Knock-in
Knock-in of a fluorescent or affinity tag at the endogenous locus enables visualization and purification of the 5-phosphatase enzyme. This can reveal where Ins(1,3,4,5)P4 hydrolysis occurs and how the enzyme is regulated in its native context.
Overexpression
CRISPR activation or cDNA overexpression can increase the levels of a 5-phosphatase such as SHIP2, testing gain-of-function effects on Ins(1,3,4,5)P4 metabolism and phosphoinositide signaling. Overexpression models are also useful for drug-response studies.
How EDITGENE Supports inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity Research
Researchers studying inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity-related genes often need to determine whether a candidate gene is causally involved in a specific signaling or disease phenotype. EDITGENE provides the CRISPR tools and cell models required to move from correlation to causation.
Contact EDITGENE today to design your custom CRISPR model for inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity research.
Frequently Asked Questions About inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity
What is inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity?
It is the enzymatic activity defined by GO:0052659 that removes the 5-phosphate from 1D-myo-inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4), producing 1D-myo-inositol 1,3,4-trisphosphate and phosphate.
What genes are involved in inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity?
Key genes include INPP5D (SHIP1) and INPPL1 (SHIP2), which encode SH2-domain-containing inositol 5-phosphatases that act on Ins(1,3,4,5)P4. Upstream enzymes ITPKA, ITPKB, and ITPKC generate the substrate.
What is the reaction catalyzed by GO:0052659?
The reaction is: 1D-myo-inositol 1,3,4,5-tetrakisphosphate + H2O = 1D-myo-inositol 1,3,4-trisphosphate + phosphate.
How is Ins(1,3,4,5)P4 produced?
Ins(1,3,4,5)P4 is produced by Ins(1,4,5)P3 3-kinase, which phosphorylates Ins(1,4,5)P3 in the inositol tris/tetrakisphosphate pathway.
Which enzymes have Ins(1,3,4,5)P4 5-phosphatase activity?
SHIP2 (INPPL1) was shown to display Ins(1,3,4,5)P4 5-phosphatase activity, and SHIP1 (INPP5D) is also known to act on this substrate.
How is this activity measured experimentally?
It can be measured using synthetic Ins(1,3,4,5)P4 analogues in in vitro assays or by profiling inositol polyphosphates in cells.
Does a 3-phosphatase also act on Ins(1,3,4,5)P4?
Yes, a salt-activated 3-phosphatase at the inner surface of the human erythrocyte membrane removes the 3-phosphate from Ins(1,3,4,5)P4, competing with the 5-phosphatase route.
What inhibits the 3-phosphatase route?
Ins(1,3,4,5,6)P5 and inositol hexakisphosphate (InsP6) inhibit the inositol-1,3,4,5-tetrakisphosphate 3-phosphatase in rat parotid glands.
Why is this activity important in disease?
SHIP1 and SHIP2 are linked to hematologic malignancies, immune disorders, and metabolic disease, making the 5-phosphatase activity relevant to these conditions.
How can CRISPR help study GO:0052659?
CRISPR knockout, point-mutation, knock-in, and overexpression models allow causal testing of whether a specific 5-phosphatase gene or residue is required for Ins(1,3,4,5)P4 metabolism and downstream phenotypes.
Conclusion
GO:0052659, inositol-1,3,4,5-tetrakisphosphate 5-phosphatase activity, defines a precise biochemical step that terminates Ins(1,3,4,5)P4 signaling by removing the 5-phosphate. This activity is carried by SHIP family enzymes such as SHIP1 and SHIP2 and is integrated with the inositol tris/tetrakisphosphate pathway and phosphoinositide 3-kinase signaling. Understanding its regulation and its competition with 3-phosphatase routes is essential for interpreting calcium and phosphoinositide signaling in health and disease. CRISPR-based knockout, point-mutation, knock-in, and overexpression models provide the tools needed to test the causal role of specific genes and residues in this activity. EDITGENE supports these efforts with custom cell model generation, library screening, and bioinformatics services tailored to inositol polyphosphate research.
References
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