GO:1903963 arachidonate transport: Lipid Signaling Pathway, Genes, Functions and Research Methods

Research-grade guide for scientists and biopharma professionals

Key Takeaways

GO:1903963 (arachidonate transport) describes the directed movement of arachidonate into, out of, or within a cell, or between cells, via transporters or pores.
Arachidonate transport is mechanistically linked to endocannabinoid transport, as anandamide and arachidonic acid share uptake pathways.
Key proteins implicated include FAAH, NAPE-PLD, and membrane transporters such as those in the endocannabinoid system.
Dysregulated arachidonate transport contributes to inflammation, cancer, and ischemia-reperfusion injury through ferroptosis.
CRISPR knockout, knock-in, and overexpression models are essential for dissecting transporter function and lipid signaling.
EDITGENE provides custom cell models and library screening to study arachidonate transport genes in disease contexts.

Description

Arachidonate transport (GO:1903963) is a biological process defined as the directed movement of arachidonate into, out of, or within a cell, or between cells, by means of some agent such as a transporter or pore. Arachidonate, or arachidonic acid, is a polyunsaturated fatty acid that serves as a precursor for eicosanoids and endocannabinoids, and its transport is critical for lipid signaling. Understanding this process is essential for researchers studying inflammation, cancer, and neurological disorders, as arachidonate transport influences membrane dynamics and secretory vesicle exocytosis. The process is tightly linked to endocannabinoid transport, with shared mechanisms for anandamide and arachidonic acid uptake. Recent studies highlight the role of arachidonate transport in ferroptosis during ischemia-reperfusion injury, underscoring its clinical relevance. This article synthesizes authoritative QuickGO data and verified PubMed literature to provide a research-grade overview of GO:1903963, its genes, functions, and experimental approaches.

arachidonate transport At A Glance

GO ID GO:1903963
GO term arachidonate transport
Ontology biological_process
Synonym arachidonic acid transport
Major function Directed movement of arachidonate across cellular membranes via transporters or pores
Related process Endocannabinoid transport and anandamide uptake
Key tissues Brain, immune cells, endothelial cells
Disease relevance Inflammation, cancer, ischemia-reperfusion injury

What Is GO:1903963?

GO:1903963, arachidonate transport, is the directed movement of an arachidonate molecule into, out of, or within a cell, or between cells, mediated by agents such as transporters or pores. This process is synonymous with arachidonic acid transport and is a biological process essential for lipid signaling and membrane homeostasis.

Why Is arachidonate transport Important in Cell Biology?

Arachidonate transport is crucial because arachidonic acid is a precursor to eicosanoids and endocannabinoids, which regulate inflammation, pain, and cell survival. Disruptions in this process are implicated in cancer progression, where store-independent Orai1-mediated Ca2+ entry modulates lipid signaling, and in ischemia-reperfusion injury, where Piezo1 activation enhances ferroptosis via arachidonate transport. Understanding GO:1903963 provides insights into membrane trafficking and secretory vesicle exocytosis.
Regulates eicosanoid and endocannabinoid synthesis, impacting inflammation and pain.
Modulates ferroptosis in endothelial cells during ischemia-reperfusion injury.
Influences cancer cell proliferation through Ca2+ signaling and lipid uptake.
Essential for secretory vesicle exocytosis and neurotransmitter release.
Linked to neurodegenerative disorders via endocannabinoid transport dysfunction.
Potential target for anti-inflammatory and anticancer therapies.
Involved in membrane remodeling and lipid raft dynamics.
Provides a model for studying transporter-mediated lipid movement.

What Happens During arachidonate transport?

Arachidonate Release and Membrane Interaction
In simple terms: Arachidonate is first released from membrane lipids and interacts with the cell membrane.
Arachidonate is liberated from phospholipids by phospholipase A2 and then interacts with membrane transporters or pores for directed movement. This step is critical for initiating transport and is linked to endocannabinoid transport mechanisms.
Transporter-Mediated Uptake
In simple terms: Specific proteins help move arachidonate across the cell membrane.
Transporters such as those involved in anandamide uptake facilitate arachidonate movement into cells. The process is energy-dependent and can be regulated by calcium signaling.
Intracellular Trafficking
In simple terms: Once inside, arachidonate is moved to different cellular compartments.
Intracellular arachidonate transport involves binding proteins and membrane contact sites, enabling its delivery to enzymes like cyclooxygenases and lipoxygenases.
Regulation by Piezo1 and Ferroptosis
In simple terms: Mechanical stress can trigger arachidonate transport, leading to cell death in some contexts.
Piezo1 activation in endothelial cells enhances arachidonate transport, aggravating ferroptosis during ischemia-reperfusion injury. This highlights a mechanotransduction link to lipid transport.
Role in Secretory Vesicle Exocytosis
In simple terms: Arachidonate transport supports the release of signaling molecules from cells.
Lipids including arachidonate are essential for secretory vesicle exocytosis, influencing neurotransmitter release and hormone secretion.

Key Genes Involved in GO:1903963 arachidonate transport

The following genes and proteins are experimentally implicated in arachidonate transport and related lipid signaling pathways.
GeneMajor RoleResearch Relevance
FAAHDegrades anandamide and related lipidsRegulates endocannabinoid transport and arachidonate release
NAPE-PLDSynthesizes anandamide from NAPELinks arachidonate transport to endocannabinoid signaling
Piezo1Mechanosensitive cation channelActivation enhances arachidonate transport and ferroptosis
ORAI1Store-independent Ca2+ entry channelModulates lipid signaling and cancer progression
PLA2G4APhospholipase A2, releases arachidonateInitiates arachidonate transport from membranes
PTGS1Cyclooxygenase-1Converts arachidonate to prostaglandins
PTGS2Cyclooxygenase-2Inducible enzyme in inflammation
ALOX55-lipoxygenaseProduces leukotrienes from arachidonate
ALOX1212-lipoxygenaseGenerates eicosanoids in platelets
ALOX1515-lipoxygenaseInvolved in inflammation resolution
CYP2C9Cytochrome P450 epoxygenaseMetabolizes arachidonate to epoxyeicosatrienoic acids
CYP2J2Cytochrome P450 epoxygenaseProduces EETs with cardiovascular effects
SLC27A1Fatty acid transport proteinFacilitates arachidonate uptake
FABP3Fatty acid binding proteinIntracellular arachidonate trafficking
FABP5Fatty acid binding proteinModulates lipid signaling in cancer
TRPV1Capsaicin receptorActivated by arachidonate metabolites
CB1Cannabinoid receptor 1Mediates endocannabinoid effects linked to arachidonate transport

How Is arachidonate transport Regulated?

Arachidonate transport is regulated by calcium signaling, mechanical stress via Piezo1, and endocannabinoid system components. Store-independent Orai1-mediated Ca2+ entry modulates lipid uptake in cancer cells. Additionally, secretory vesicle exocytosis influences lipid transport dynamics.

arachidonate transport and Human Disease

GeneDisease / BiologyPotential Experimental Model
Piezo1Ischemia-reperfusion injury, ferroptosisEndothelial cell knockout
ORAI1Cancer, store-independent Ca2+ entryCancer cell line overexpression
FAAHNeurodegeneration, painKnockout mouse models
PTGS2Inflammation, cancerPoint mutation knock-in
ALOX5Asthma, inflammationOverexpression in immune cells
Arachidonate Transport in Cancer
Dysregulated arachidonate transport promotes cancer progression by supplying lipids for eicosanoid synthesis and membrane remodeling. Store-independent Orai1-mediated Ca2+ entry enhances arachidonate uptake, supporting tumor growth.
Ischemia-Reperfusion Injury and Ferroptosis
Piezo1 activation in endothelial cells aggravates microvascular ischemia-reperfusion injury by enhancing arachidonate transport and ferroptosis. This identifies arachidonate transport as a therapeutic target in ischemic diseases.
Neurodegeneration and Endocannabinoid Signaling
Impaired arachidonate transport affects endocannabinoid signaling, contributing to neurodegenerative disorders. Anandamide transport dysfunction is linked to altered synaptic lipid signaling.

From arachidonate transport-Related Genes to Experimental Models

Research QuestionSuitable Model
Does Piezo1 regulate arachidonate transport?Piezo1 knockout endothelial cells
How does ORAI1 affect lipid uptake in cancer?ORAI1 overexpression in cancer cell lines
What is the role of FAAH in endocannabinoid transport?FAAH knockout mice
Can point mutations in PTGS2 alter arachidonate metabolism?CRISPR point mutation knock-in
Does tagged FABP3 track intracellular arachidonate?Tagged knock-in with fluorescent protein
Is ALOX5 overexpression sufficient to drive inflammation?Overexpression cell models

How to Study the arachidonate transport Process

MethodWhat It MeasuresTypical Application
Lipidomics (LC-MS/MS)Arachidonate and metabolite levelsQuantifying transport in cells
Fluorescent fatty acid uptakeReal-time transport rateLive-cell imaging
CRISPR knockout screenGenes affecting transportIdentifying novel transporters
ProteomicsProtein interactions with transportersMapping transport complexes
RNA-seqExpression of transport-related genesTranscriptional profiling
Calcium imagingCa2+ signaling during transportOrai1 and Piezo1 studies
Vesicle exocytosis assaySecretory vesicle releaseNeurotransmitter release
Lipidomics and Mass Spectrometry
Mass spectrometry-based lipidomics quantifies arachidonate and its metabolites, enabling measurement of transport activity.
Fluorescent Fatty Acid Uptake Assays
Fluorescently labeled arachidonate analogs are used to monitor real-time transport in live cells.
CRISPR Screening for Transporters
Genome-wide CRISPR knockout screens identify genes required for arachidonate transport.
Imaging and Vesicle Trafficking
Live-cell imaging of secretory vesicles reveals arachidonate transport dynamics during exocytosis.

How CRISPR Can Be Used to Study GO:1903963 arachidonate transport

Knockout

CRISPR knockout of genes like Piezo1 or ORAI1 in cell models ablates arachidonate transport, revealing their essential roles.

Point Mutation

Point mutations in transport proteins such as FAAH or PTGS2 can dissect catalytic residues and regulatory sites.

Knock-in

Knock-in of tagged transporters (e.g., GFP-FABP3) enables live-cell tracking of arachidonate transport.

Overexpression

Overexpression of ALOX5 or ORAI1 in cell lines models enhanced arachidonate transport and downstream signaling.

How EDITGENE Supports arachidonate transport Research

Researchers studying arachidonate transport-related genes often need to determine whether a candidate gene is causally involved in lipid signaling, disease progression, or cellular metabolism. EDITGENE provides custom CRISPR cell models and screening services to accelerate this discovery.
Contact EDITGENE today to design your custom CRISPR model for arachidonate transport research.

Frequently Asked Questions About arachidonate transport

GO:1903963 is the Gene Ontology term for arachidonate transport, defined as the directed movement of arachidonate into, out of, or within a cell, or between cells, via transporters or pores.
Key genes include FAAH, NAPE-PLD, Piezo1, ORAI1, PLA2G4A, PTGS1/2, ALOX5, and fatty acid transporters like SLC27A1.
It is regulated by calcium signaling, mechanical stress via Piezo1, and endocannabinoid system components.
Cancer, ischemia-reperfusion injury, neurodegeneration, and inflammatory disorders.
The synonym is arachidonic acid transport.
It belongs to the biological_process ontology.
Use lipidomics, fluorescent uptake assays, CRISPR screens, and imaging of secretory vesicles.
Piezo1 activation enhances arachidonate transport and aggravates ferroptosis in endothelial cells.
Store-independent Orai1-mediated Ca2+ entry modulates lipid signaling and cancer progression.
Knockout, point mutation, knock-in, and overexpression models for genes like Piezo1, ORAI1, and FAAH.

Conclusion

GO:1903963 arachidonate transport is a fundamental biological process with broad implications for lipid signaling, inflammation, cancer, and ischemia-reperfusion injury. Understanding its molecular players and regulatory mechanisms provides opportunities for therapeutic intervention. EDITGENE offers comprehensive CRISPR solutions to study arachidonate transport genes in relevant disease models.

References

  1. 1. Nicolussi S et al.. 2015. Endocannabinoid transport revisited.. Vitam Horm 98:441-85 PMID: 25817877
  2. 2. McFarland MJ et al.. 2004. Anandamide transport.. Pharmacol Ther 104(2):117-35 PMID: 15518883
  3. 3. Palmer SL et al.. 2002. Cannabinergic ligands.. Chem Phys Lipids 121(1-2):3-19 PMID: 12505686
  4. 4. Fowler CJ. 2012. Anandamide uptake explained?. Trends Pharmacol Sci 33(4):181-5 PMID: 22297258
  5. 5. Glaser ST et al.. 2005. Anandamide transport: a critical review.. Life Sci 77(14):1584-604 PMID: 15979096
  6. 6. Chen FF et al.. 2026. Piezo1 activation in endothelial cells aggravates microvascular ischemia-reperfusion injury in limbs by enhancing ferroptosis.. Exp Mol Med 58(1):143-160 PMID: 41507309
  7. 7. Cantonero C et al.. 2019. Store-independent Orai1-mediated Ca(2+) entry and cancer.. Cell Calcium 80:1-7 PMID: 30921687
  8. 8. Akefe IO et al.. 2023. Lipids and Secretory Vesicle Exocytosis.. Adv Neurobiol 33:357-397 PMID: 37615874
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