GO:0001588 dopamine neurotransmitter receptor activity, coupled via Gs: Mechanism, Genes and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0001588 describes the molecular function of binding dopamine and activating adenylate cyclase through Gs coupling, a hallmark of D1-like dopamine receptors.
• The term encompasses dopamine D1 receptor activity and dopamine D5 receptor activity, which are the canonical Gs-coupled dopamine receptors.
• D1-like receptor signaling is essential for motor control, reward, cognition, and synaptic plasticity, and its dysfunction is implicated in Parkinson's disease, schizophrenia, and addiction.
• D1 and D2 receptors can form heterodimers that synergistically promote calcium signaling, revealing complex crosstalk beyond simple Gs coupling.
• Constitutive activity and chimeric receptor studies have shown that the D1 receptor can signal in a ligand-independent manner, which has implications for drug design.
• Studying GO:0001588 requires tools such as cAMP assays, calcium imaging, and CRISPR-based gene editing to dissect receptor-specific functions.
Description
Dopamine is a key neurotransmitter that regulates motor activity, motivation, reward, and cognition. Its actions are mediated by five G protein-coupled receptor subtypes, which are divided into D1-like (D1 and D5) and D2-like (D2, D3, and D4) families. The D1-like receptors are characterized by their ability to stimulate adenylate cyclase via Gs, a function captured by the Gene Ontology term GO:0001588, dopamine neurotransmitter receptor activity, coupled via Gs. This term is essential for annotating genes that encode receptors capable of binding dopamine and initiating a Gs-mediated signaling cascade. Researchers studying dopamine signaling rely on GO:0001588 to identify and classify receptors, understand their roles in physiology, and investigate their contributions to neurological and psychiatric disorders. The term also encompasses the D5 receptor, which shares the Gs-coupling mechanism but exhibits distinct expression patterns and pharmacological properties. As the primary molecular function of D1-like receptors, GO:0001588 is central to neurobiology and drug discovery.
dopamine neurotransmitter receptor activity, coupled via Gs At A Glance
| GO ID | GO:0001588 |
|---|---|
| GO term | dopamine neurotransmitter receptor activity, coupled via Gs |
| Ontology | molecular_function |
| Synonym | dopamine D1 receptor activity, dopamine D5 receptor activity |
| Major function | Binding dopamine and activating adenylate cyclase through Gs to initiate cellular responses |
| Receptor family | G protein-coupled receptors (GPCRs), class A rhodopsin-like |
| Endogenous ligand | Dopamine |
| G protein coupling | Gs (stimulatory G protein) |
| Downstream effector | Adenylate cyclase, leading to increased cAMP production |
What Is GO:0001588?
GO:0001588 is a molecular function term defined as the activity of combining with the neurotransmitter dopamine and activating adenylate cyclase via coupling to Gs, thereby initiating a change in cell activity. This definition captures the essential steps of ligand binding, G protein coupling, and downstream enzyme activation. The term is synonymous with dopamine D1 receptor activity and dopamine D5 receptor activity, reflecting the two known Gs-coupled dopamine receptor subtypes. It is distinct from other dopamine receptor activities that couple to Gi/Go (e.g., D2-like receptors) or that signal through different effectors.
Why Is dopamine neurotransmitter receptor activity, coupled via Gs Important in Cell Biology?
GO:0001588 is critical because it defines the molecular function of D1-like dopamine receptors, which are major mediators of dopaminergic neurotransmission in the brain. These receptors are involved in a wide range of physiological processes, including motor control, reward, learning, and memory. Dysregulation of D1-like receptor signaling is associated with numerous pathological conditions, such as Parkinson's disease, schizophrenia, attention-deficit hyperactivity disorder, and substance use disorders. Understanding the precise molecular mechanisms of Gs-coupled dopamine receptor activity is essential for developing targeted therapies that can modulate this pathway. Moreover, the term facilitates functional annotation of genes and proteins in genomic and proteomic studies, enabling researchers to identify novel components of dopamine signaling networks.
• Provides a standardized annotation for D1-like dopamine receptors in genomic and proteomic databases.
• Enables classification of dopamine receptors based on their G protein coupling specificity.
• Essential for studying motor control and basal ganglia function, as D1 receptors are highly expressed in the striatum.
• Implicated in reward processing and addiction, where D1 receptor signaling modulates reinforcement and motivation.
• Contributes to cognitive functions such as working memory and attention through prefrontal cortex D1 receptors.
• Dysfunction is linked to Parkinson's disease, where loss of dopaminergic neurons leads to altered D1 receptor signaling.
• Associated with schizophrenia and other psychiatric disorders, potentially due to imbalances in D1 and D2 receptor activity.
• Target for pharmacological interventions, including D1 agonists and antagonists used in clinical and preclinical research.
• Involved in synaptic plasticity and long-term potentiation, which are cellular correlates of learning and memory.
• Facilitates cross-talk with other neurotransmitter systems, such as adenosine and glutamate, through heteromerization.
Mechanism, Genes and Research Methods
Dopamine Binding and Receptor Activation
In simple terms: Dopamine binds to the receptor like a key in a lock, causing the receptor to change shape and become active.
The D1-like dopamine receptors (D1 and D5) are members of the class A GPCR family. They contain a seven-transmembrane domain architecture with an orthosteric binding site for dopamine. Upon dopamine binding, the receptor undergoes conformational changes that facilitate the exchange of GDP for GTP on the Gs alpha subunit. This activation step is highly specific and is the first committed step in the signaling cascade. The binding affinity and kinetics of dopamine to D1 versus D5 receptors can differ, influencing the duration and intensity of the signal.
Gs Protein Coupling and Adenylate Cyclase Activation
In simple terms: The activated receptor turns on a G protein, which then switches on an enzyme that produces a messenger molecule called cAMP.
Activated D1-like receptors act as guanine nucleotide exchange factors (GEFs) for the Gs heterotrimer. The Gs alpha subunit, once bound to GTP, dissociates from the beta-gamma dimer and directly binds to and activates adenylate cyclase. This enzyme catalyzes the conversion of ATP to cyclic AMP (cAMP), a second messenger that amplifies the signal. The resulting increase in intracellular cAMP activates protein kinase A (PKA) and other downstream effectors, such as EPAC, leading to diverse cellular responses including changes in ion channel activity, gene expression, and synaptic plasticity.
cAMP Signaling and Downstream Effectors
In simple terms: The messenger cAMP triggers a chain reaction inside the cell, altering many cellular activities.
Elevated cAMP levels activate PKA, which phosphorylates numerous substrates including ion channels, transcription factors (e.g., CREB), and other signaling proteins. This pathway is critical for D1 receptor-mediated modulation of neuronal excitability and gene expression. Additionally, cAMP can activate exchange proteins directly activated by cAMP (EPAC), which regulate small GTPases and contribute to synaptic remodeling. The D1 receptor also engages in crosstalk with other signaling pathways, such as calcium signaling, through mechanisms involving phospholipase C and IP3 receptors, as observed in heterologous expression systems.
Receptor Desensitization and Internalization
In simple terms: After signaling, the receptor is turned off and pulled inside the cell to prevent overstimulation.
Prolonged or repeated dopamine stimulation leads to desensitization of D1-like receptors. This process involves phosphorylation of the receptor by G protein-coupled receptor kinases (GRKs), followed by binding of beta-arrestin, which uncouples the receptor from Gs and promotes internalization via clathrin-coated pits. Internalized receptors can be either recycled back to the plasma membrane or targeted for degradation, depending on the cellular context. This regulatory mechanism is crucial for maintaining proper dopaminergic tone and preventing excitotoxicity.
Heteromerization and Functional Crosstalk
In simple terms: D1 receptors can pair with other receptors to change how they signal.
D1 receptors can form heteromers with other GPCRs, notably D2 receptors, adenosine A2A receptors, and others. D1-D2 heteromer formation leads to synergistic calcium signaling through Gq-mediated pathways, as demonstrated in transfected cells and striatal neurons. This crosstalk allows for integration of multiple neurotransmitter signals and fine-tuning of cellular responses. The existence of such heteromers has implications for understanding the complex pharmacology of dopamine-related disorders and for designing drugs that target specific receptor complexes.
Key Genes Involved in GO:0001588 dopamine neurotransmitter receptor activity, coupled via Gs
The following genes encode the receptors and key signaling molecules directly involved in GO:0001588, as well as related modulators that influence this activity.
| Gene | Major Role | Research Relevance |
|---|---|---|
| DRD1 | Encodes the D1 dopamine receptor, a primary Gs-coupled receptor for dopamine | Most studied D1-like receptor; target for Parkinson's disease, schizophrenia, and addiction research |
| DRD5 | Encodes the D5 dopamine receptor, a Gs-coupled receptor with high affinity for dopamine | Less abundant but important in limbic regions; potential role in hypertension and cognitive function |
| GNAS | Encodes the Gs alpha subunit that couples D1-like receptors to adenylate cyclase | Essential for signal transduction; mutations cause pseudohypoparathyroidism and related disorders |
| ADCY1 | Encodes adenylate cyclase 1, a calcium/calmodulin-stimulated isoform enriched in brain | Key effector for D1 receptor signaling in striatum and cortex |
| ADCY5 | Encodes adenylate cyclase 5, a major isoform in striatum | Critical for D1 receptor-mediated cAMP production and motor control |
| PRKACA | Encodes the catalytic subunit of PKA | Mediates many downstream effects of D1 receptor activation, including CREB phosphorylation |
| CREB1 | Encodes cAMP response element-binding protein | Transcription factor activated by D1 signaling; regulates genes involved in plasticity and survival |
| ARRB1 | Encodes beta-arrestin 1 | Regulates D1 receptor desensitization and internalization; also serves as a scaffold for alternative signaling |
| ARRB2 | Encodes beta-arrestin 2 | Similar to ARRB1; modulates D1 receptor trafficking and signaling |
| GRK2 | Encodes G protein-coupled receptor kinase 2 | Phosphorylates activated D1 receptors, promoting desensitization |
| GRK3 | Encodes G protein-coupled receptor kinase 3 | Another GRK involved in D1 receptor regulation |
| DRD2 | Encodes the D2 dopamine receptor, which couples to Gi/Go | Forms heteromers with D1; modulates D1 signaling via crosstalk |
| ADORA2A | Encodes adenosine A2A receptor | Forms heteromers with D1; antagonizes D1 signaling in striatum |
| PPP1R1B | Encodes DARPP-32, a key integrator of dopamine signaling | Phosphorylated by PKA; regulates phosphatase activity and downstream effects |
| CALY | Encodes calcyon, a D1 receptor-interacting protein | Enhances D1 receptor signaling to calcium and may link to Gq pathways |
| COMT | Encodes catechol-O-methyltransferase | Enzyme that degrades dopamine; influences receptor occupancy and signaling |
| SLC6A3 | Encodes the dopamine transporter (DAT) | Regulates extracellular dopamine levels; target of psychostimulants |
| TH | Encodes tyrosine hydroxylase | Rate-limiting enzyme in dopamine synthesis; determines dopamine availability |
How Is dopamine neurotransmitter receptor activity, coupled via Gs Regulated?
The activity of Gs-coupled dopamine receptors is tightly regulated at multiple levels. Receptor expression levels are controlled by transcription factors and epigenetic mechanisms. Post-translational modifications, including phosphorylation by GRKs and PKC, modulate receptor desensitization and internalization. Beta-arrestins not only desensitize the receptor but also initiate G protein-independent signaling pathways. Additionally, the availability of dopamine is regulated by synthesis (TH), packaging (VMAT2), reuptake (DAT), and degradation (COMT, MAO). Heteromerization with other GPCRs, such as D2 and A2A receptors, provides an additional layer of regulation, altering ligand binding and downstream signaling. Finally, the cAMP pathway itself is subject to feedback regulation by phosphodiesterases and phosphatases, including DARPP-32, which integrates signals from multiple neurotransmitters.
dopamine neurotransmitter receptor activity, coupled via Gs and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| DRD1 | Parkinson's disease, schizophrenia, addiction | DRD1 knockout mice, point-mutation knock-in mice, overexpression in striatal neurons |
| DRD5 | ADHD, hypertension, cognitive disorders | DRD5 knockout mice, conditional knock-in, CRISPRa overexpression |
| GNAS | Pseudohypoparathyroidism, Albright hereditary osteodystrophy | Gs alpha knockout cell lines, patient-derived iPSCs with point mutations |
| ADCY5 | Dyskinesia, movement disorders | ADCY5 knockout mice, knock-in of hyperactive variants |
| ARRB1 | Addiction, schizophrenia | Beta-arrestin 1 knockout mice, tagged knock-in for imaging |
Parkinson's Disease and Motor Dysfunction
Parkinson's disease is characterized by the degeneration of dopaminergic neurons in the substantia nigra, leading to reduced dopamine levels in the striatum. This results in altered D1 receptor signaling, which contributes to motor symptoms such as bradykinesia and rigidity. Studies in animal models have shown that D1 receptor agonists can improve motor function, and brain region-specific changes in dopamine receptors, including D1, have been linked to tau pathology through CDK5 in Alzheimer's disease models, suggesting shared mechanisms. The loss of D1-mediated cAMP signaling in striatal neurons is a key factor in the pathophysiology of Parkinson's disease.
Schizophrenia and Psychosis
Schizophrenia is associated with dysregulated dopamine neurotransmission, particularly in the prefrontal cortex and striatum. While D2 receptor hyperactivity is a well-established hypothesis, D1 receptor hypofunction in the prefrontal cortex is thought to contribute to cognitive deficits and negative symptoms. Post-mortem studies have shown altered D1 receptor binding in schizophrenia patients. The balance between D1 and D2 signaling is critical for normal cognition, and disruptions in this balance may underlie psychotic symptoms. Targeting D1 receptors has been proposed as a therapeutic strategy for cognitive impairment in schizophrenia.
Addiction and Reward Processing
D1 receptors play a central role in reward learning and reinforcement. Drugs of abuse, such as cocaine and amphetamines, increase extracellular dopamine, leading to excessive D1 receptor activation in the nucleus accumbens and other reward-related regions. This aberrant signaling contributes to the development of addiction and long-lasting neuroadaptations. Studies using D1 receptor antagonists or knockout mice have shown reduced drug-seeking behavior. The D1 receptor is therefore a potential target for medications development for substance use disorders.
Neurodevelopmental and Psychiatric Disorders
Alterations in D1 receptor signaling have been implicated in attention-deficit hyperactivity disorder (ADHD), bipolar disorder, and major depression. For example, the D5 receptor (DRD5) has been associated with ADHD in genetic studies. Additionally, D1 receptor dysfunction may contribute to cognitive deficits in these conditions. The role of D1 receptors in modulating prefrontal cortical circuits makes them relevant to executive function and emotional regulation. Further research using CRISPR models can help elucidate the specific contributions of D1 and D5 receptors to these disorders.
From dopamine neurotransmitter receptor activity, coupled via Gs-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does DRD1 mediate specific aspects of reward learning? | DRD1 knockout mice or conditional knockout in nucleus accumbens |
| How does a point mutation in DRD1 affect ligand binding affinity? | CRISPR point-mutation knock-in of DRD1 in cell lines or mice |
| What is the role of D1-D2 heteromers in calcium signaling? | Knock-in mice expressing tagged DRD1 and DRD2 for FRET or BRET studies |
| Can overexpression of DRD5 rescue cognitive deficits? | Viral-mediated overexpression of DRD5 in prefrontal cortex of animal models |
| How does Gs alpha mutation affect D1 receptor signaling? | GNAS knockout or point-mutation knock-in cell lines |
| What are the downstream targets of D1 receptor activation? | CRISPR knockout of candidate genes followed by RNA-seq and phosphoproteomics |
How to Study the dopamine neurotransmitter receptor activity, coupled via Gs Process
| Method | What It Measures | Typical Application |
|---|---|---|
| cAMP assay (ELISA, luminescence) | Intracellular cAMP levels | Quantifying D1/D5 receptor activation by agonists |
| Calcium imaging | Intracellular calcium transients | Detecting D1-mediated calcium signaling and heteromer crosstalk |
| FRET/BRET | Protein-protein interactions and conformational changes | Visualizing D1-D2 heteromer formation in live cells |
| CRISPR knockout | Loss of gene function | Abolishing DRD1 or DRD5 to study specific roles |
| CRISPR point mutation | Specific amino acid changes | Modeling disease-associated variants or altering ligand binding |
| CRISPR knock-in (tagged) | Endogenous protein labeling | Imaging receptor localization and trafficking |
| RNA-seq | Transcriptome-wide gene expression | Identifying downstream targets of D1 receptor activation |
| Phosphoproteomics | Phosphorylation sites on proteins | Mapping signaling networks activated by D1 receptors |
cAMP Assays for Receptor Activity
The most direct way to measure GO:0001588 activity is to quantify intracellular cAMP levels following dopamine stimulation. Common methods include radioimmunoassays, ELISA, and luminescence-based assays (e.g., GloSensor). These assays can be performed in cell lines expressing recombinant D1 or D5 receptors, or in primary neuronal cultures. Dose-response curves with dopamine agonists and antagonists allow determination of potency and efficacy. Such assays are essential for characterizing receptor function and for screening pharmacological compounds.
Calcium Imaging and Heteromer Studies
D1 receptors can also signal through calcium, particularly when forming heteromers with D2 receptors or when co-expressing calcyon. Calcium imaging using fluorescent indicators (e.g., Fura-2, Fluo-4) can detect D1-mediated calcium transients in response to dopamine or selective agonists. This method is useful for studying crosstalk between Gs and Gq pathways. Additionally, FRET or BRET biosensors can visualize heteromer formation and conformational changes in live cells. These techniques provide spatial and temporal resolution of receptor signaling.
Genetic Manipulation with CRISPR
CRISPR-Cas9 genome editing enables the creation of knockout, point-mutation, and knock-in models to study D1-like receptor function. Knockout of DRD1 or DRD5 in cell lines or mice abolishes specific signaling pathways, allowing attribution of function. Point mutations can mimic disease-associated variants or alter ligand binding. Knock-in of tagged receptors (e.g., HA or GFP) facilitates imaging and biochemical purification. Overexpression via CRISPR activation (CRISPRa) or viral vectors can enhance receptor levels to study gain-of-function effects. These approaches are indispensable for dissecting the molecular mechanisms of GO:0001588.
Transcriptomics and Proteomics
RNA sequencing (RNA-seq) can reveal changes in gene expression downstream of D1 receptor activation, identifying target genes regulated by cAMP/PKA/CREB. Phosphoproteomics can map the signaling network activated by D1 receptors, including phosphorylation of ion channels, kinases, and transcription factors. Proteomic approaches can also identify novel interacting partners of D1 receptors. Combining these methods with CRISPR-based perturbations provides a systems-level view of D1 receptor function in health and disease.
How CRISPR Can Be Used to Study GO:0001588 dopamine neurotransmitter receptor activity, coupled via Gs
Knockout
CRISPR knockout of DRD1 or DRD5 completely eliminates receptor expression, providing a clean background to study the specific contributions of each receptor to dopamine signaling. Knockout cell lines can be used for cAMP assays, calcium imaging, and transcriptomics. In vivo, conditional knockout mice allow spatial and temporal control of gene deletion, enabling studies of receptor function in specific brain regions or developmental stages. Knockout models have been instrumental in linking D1 receptors to motor control, reward, and cognition.
Point Mutation
CRISPR point mutation introduces precise single-nucleotide changes to alter specific amino acids in the receptor. This can be used to mimic naturally occurring polymorphisms associated with disease or to probe the functional importance of key residues in ligand binding, G protein coupling, or desensitization. For example, mutating serine/threonine residues in the C-terminal tail can prevent phosphorylation and impair beta-arrestin recruitment. Point-mutation models are valuable for understanding structure-function relationships and for validating drug targets.
Knock-in
CRISPR knock-in allows the insertion of tags (e.g., GFP, HA, HiBiT) or reporter genes into the endogenous DRD1 or DRD5 locus. Tagged receptors can be visualized in live cells for trafficking studies, immunoprecipitated for interaction proteomics, or used in BRET/FRET biosensors. Knock-in of a luciferase reporter downstream of the DRD1 promoter can monitor receptor expression in real time. These models preserve endogenous regulatory elements, ensuring physiological expression levels.
Overexpression
CRISPR activation (CRISPRa) or viral vector-mediated overexpression can increase D1 receptor levels beyond endogenous. This is useful for gain-of-function studies, such as assessing whether elevated D1 signaling enhances synaptic plasticity or rescues deficits in disease models. Overexpression in cell lines is also common for biochemical and pharmacological assays. However, careful controls are needed to avoid artifacts from supraphysiological expression. Overexpression models complement knockout and knock-in approaches to provide a comprehensive understanding of receptor function.
How EDITGENE Supports dopamine neurotransmitter receptor activity, coupled via Gs Research
Researchers studying dopamine neurotransmitter receptor activity, coupled via Gs-related genes often need to determine whether a candidate gene is causally involved in a specific signaling pathway or disease phenotype. This requires robust, reproducible genetic models that can precisely manipulate gene expression or sequence. EDITGENE provides a comprehensive suite of CRISPR-based services to accelerate such investigations, from knockout and point-mutation cell lines to knock-in reporters and overexpression systems. By leveraging these tools, scientists can dissect the molecular mechanisms of D1-like receptor signaling and translate findings into therapeutic strategies.
Contact EDITGENE today to design your custom CRISPR model for dopamine neurotransmitter receptor activity, coupled via Gs research.
Frequently Asked Questions About dopamine neurotransmitter receptor activity, coupled via Gs
What is GO:0001588?
GO:0001588 is a Gene Ontology molecular function term that describes the activity of binding dopamine and activating adenylate cyclase via Gs coupling, characteristic of D1-like dopamine receptors.
What genes are involved in dopamine neurotransmitter receptor activity, coupled via Gs?
The primary genes are DRD1 and DRD5, which encode the D1 and D5 receptors, respectively. Other genes such as GNAS, ADCY1, and ADCY5 encode downstream signaling components.
Which dopamine receptors are coupled to Gs?
The D1 and D5 dopamine receptors (encoded by DRD1 and DRD5) are the canonical Gs-coupled receptors that stimulate adenylate cyclase.
How does D1 receptor signaling work?
Dopamine binds to the D1 receptor, causing it to activate Gs, which in turn stimulates adenylate cyclase to produce cAMP, leading to activation of PKA and downstream cellular responses.
What diseases are associated with D1 dopamine receptor dysfunction?
Dysfunction of D1 receptors is implicated in Parkinson's disease, schizophrenia, addiction, ADHD, and other neurological and psychiatric disorders.
Can D1 and D2 receptors interact?
Yes, D1 and D2 receptors can form heteromers that exhibit synergistic calcium signaling, revealing complex crosstalk beyond simple Gs coupling.
What research methods are used to study Gs-coupled dopamine receptors?
Common methods include cAMP assays, calcium imaging, FRET/BRET for heteromer studies, and CRISPR-based genetic manipulation.
How can CRISPR be used to study DRD1 function?
CRISPR can create knockout, point-mutation, knock-in, and overexpression models to dissect the specific roles of DRD1 in signaling and behavior.
What is the role of D5 dopamine receptor?
The D5 receptor (DRD5) is a Gs-coupled receptor with high affinity for dopamine, expressed in limbic regions, and has been linked to ADHD and cognitive function.
Are there drugs that target D1 receptors?
Yes, D1 receptor agonists and antagonists are used in research and some are in clinical trials for Parkinson's disease and other conditions.
Conclusion
GO:0001588, dopamine neurotransmitter receptor activity, coupled via Gs, defines the molecular function of D1-like dopamine receptors, which are central to dopaminergic signaling in the brain. These receptors regulate motor control, reward, cognition, and emotion, and their dysfunction contributes to major neurological and psychiatric disorders. Understanding the precise mechanisms of Gs coupling, cAMP signaling, and receptor regulation is essential for developing targeted therapies. Advances in CRISPR-based gene editing and high-throughput screening are accelerating discoveries in this field, offering new hope for treating dopamine-related diseases.
References
- 1. Jaber M et al.. 1996. Dopamine receptors and brain function.. Neuropharmacology 35(11):1503-19 PMID: 9025098
- 3. Singh S et al.. 2025. Brain region-specific dopamine receptor changes and astrocyte activation influence tau pathology through CDK5 in Alzheimer's disease models.. J Alzheimers Dis 108(4):1696-1716 PMID: 41160462
- 4. Chun LS et al.. 2013. D1-D2 dopamine receptor synergy promotes calcium signaling via multiple mechanisms.. Mol Pharmacol 84(2):190-200 PMID: 23680635
- 6. Kozell LB et al.. 1997. Constitutive activity of a chimeric D2/D1 dopamine receptor.. Mol Pharmacol 52(6):1137-49 PMID: 9396784
- 7. Kim H et al.. 2022. Visualization of differential GPCR crosstalk in DRD1-DRD2 heterodimer upon different dopamine levels.. Prog Neurobiol 213:102266 PMID: 35364139
- 8. Kitayama E et al.. 2023. Functional Expression of IP, 5-HT(4), D(1), A(2A), and VIP Receptors in Human Odontoblast Cell Line.. Biomolecules 13(6) PMID: 37371459
