GO:0004937 alpha1-adrenergic receptor activity: Mechanism, Genes and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0004937 (alpha1-adrenergic receptor activity) is a molecular function defined as binding epinephrine or norepinephrine and transmitting the signal to the Gq alpha subunit of a heterotrimeric G protein.
• The alpha1-adrenergic receptors are class A G-protein-coupled receptors that mediate many cardiovascular, neuronal and metabolic actions of catecholamines.
• Three genes encode alpha1-adrenergic receptor subtypes in humans: ADRA1A, ADRA1B and ADRA1D, each with distinct tissue distribution and pharmacology.
• Alpha1-adrenergic receptor activity contributes to vasoconstriction, nociception, and neuroinflammatory signaling, and has been implicated in Alzheimer's disease and prostate cancer biology.
• Dysregulated alpha1-adrenergic receptor signaling is studied in hypertension, heart failure, neurodegeneration and cancer, making it a target for functional genomics.
• CRISPR knockout, point-mutation, knock-in and overexpression models enable causal testing of ADRA1A, ADRA1B and ADRA1D in disease-relevant cells and animal models.
Description
Alpha1-adrenergic receptor activity (GO:0004937) is a molecular function in which a receptor binds the catecholamines epinephrine or norepinephrine and initiates a change in cell activity by activating a heterotrimeric G protein, specifically transmitting the signal to the Gq alpha subunit. This activity is one of the principal mechanisms through which the sympathetic nervous system exerts rapid control over vascular tone, cardiac function and neuronal excitability. Because the receptor couples to Gq, its activation typically triggers phospholipase C-dependent signaling and downstream cellular responses that are distinct from those of beta-adrenergic receptors. The receptors carrying this activity are encoded by the ADRA1A, ADRA1B and ADRA1D genes, which produce pharmacologically distinguishable alpha1-adrenergic receptor subtypes. These subtypes differ in tissue distribution, ligand affinity and coupling efficiency, and they participate in processes ranging from smooth muscle contraction to modulation of nociceptive signaling. In disease contexts, alpha1-adrenergic receptor activity has been linked to cardiovascular pathology, neuroinflammation and cancer progression, and autoantibodies against the receptor have been detected in patients with prostate cancer. For researchers, GO:0004937 provides a precise functional annotation that can be used to interpret transcriptomic, proteomic and functional screening data. Understanding which genes contribute to alpha1-adrenergic receptor activity, and how that activity is regulated in specific cell types, is essential for building causal models of adrenergic signaling in health and disease.
alpha1-adrenergic receptor activity At A Glance
| GO ID | GO:0004937 |
|---|---|
| GO term | alpha1-adrenergic receptor activity |
| Ontology | molecular_function |
| Synonym | alpha1 adrenoceptor |
| Definition | Combining with epinephrine or norepinephrine to initiate a change in cell activity via activation of a G protein, with pharmacological characteristics of alpha1-adrenergic receptors; the activity involves transmitting the signal to the Gq alpha subunit of a heterotrimeric G protein. |
| Major function | Catecholamine sensing and Gq-coupled signal transduction |
| Representative genes | ADRA1A, ADRA1B, ADRA1D |
| Ligands | Epinephrine, norepinephrine |
| G protein coupling | Gq alpha subunit of a heterotrimeric G protein |
What Is GO:0004937?
In plain terms, GO:0004937 describes the job of a receptor that recognizes epinephrine or norepinephrine and then switches on a G protein called Gq to change what the cell does. According to the QuickGO definition, this activity involves combining with epinephrine or norepinephrine to initiate a change in cell activity via activation of a G protein, with the pharmacological characteristics of alpha1-adrenergic receptors, and the activity involves transmitting the signal to the Gq alpha subunit of a heterotrimeric G protein. The synonym alpha1 adrenoceptor is used interchangeably with this activity. This is a molecular function annotation, meaning it describes what the receptor protein does at the molecular level rather than a whole biological process or a cellular location.
Why Is alpha1-adrenergic receptor activity Important in Cell Biology?
Alpha1-adrenergic receptor activity is important because it is a central node through which catecholamines control cardiovascular, neuronal and metabolic physiology, and because its dysregulation is implicated in common human diseases including hypertension, heart failure, Alzheimer's disease and prostate cancer. Because the activity is defined by a specific ligand-receptor-G protein relationship, it provides a clear functional readout for experiments that manipulate adrenergic signaling, and it helps researchers distinguish alpha1-mediated effects from those mediated by beta-adrenergic or other G-protein-coupled receptors.
• Mediates catecholamine-induced vasoconstriction and contributes to blood pressure regulation.
• Couples to Gq signaling, producing second messengers distinct from beta-adrenergic receptor pathways.
• Modulates nociceptive responses and interacts with purinergic signaling in sensory neurons.
• Has been linked to tau pathology and neuroinflammation in Alzheimer's disease models.
• Autoantibodies against alpha1-adrenergic receptor have been reported in prostate cancer patients.
• Is a pharmacological target for alpha1-blockers used in cardiovascular and urological conditions.
• Provides a functional annotation for interpreting adrenergic gene expression data.
• Enables causal testing of ADRA1A, ADRA1B and ADRA1D using CRISPR models.
What Happens During alpha1-adrenergic receptor activity?
Ligand binding and receptor activation
In simple terms: First, the receptor grabs epinephrine or norepinephrine, which changes its shape and turns it on.
Alpha1-adrenergic receptor activity begins when epinephrine or norepinephrine binds to the receptor, stabilizing an active conformation. This binding event is the defining molecular recognition step of GO:0004937 and is pharmacologically characteristic of alpha1-adrenergic receptors. The three subtypes encoded by ADRA1A, ADRA1B and ADRA1D can differ in their affinity for catecholamines and in their tissue distribution, which contributes to subtype-specific signaling.
Gq coupling and heterotrimeric G protein activation
In simple terms: The activated receptor then switches on a G protein called Gq, which is the key signaling step.
Upon activation, the receptor acts as a guanine nucleotide exchange factor for the Gq alpha subunit of a heterotrimeric G protein, promoting exchange of GDP for GTP. This coupling to Gq is explicitly part of the QuickGO definition of GO:0004937 and distinguishes alpha1-adrenergic receptor activity from beta-adrenergic receptor activity, which typically couples to Gs. The activated Gq alpha subunit then dissociates from the G beta-gamma dimer and engages downstream effectors.
Downstream signaling and cellular response
In simple terms: Gq activation triggers a cascade inside the cell that changes how the cell behaves.
Gq alpha subunit activation leads to stimulation of phospholipase C and production of second messengers that mobilize calcium and activate protein kinase C, ultimately changing cell activity. In vascular smooth muscle, this pathway promotes contraction and contributes to the regulation of vascular tone, and age-related hypertension has been associated with altered alpha1-adrenergic receptor-mediated contraction in rat mesenteric artery. In neurons, alpha1-adrenergic receptor activity can augment nociceptive responses, as shown by interactions with P2X3 receptor-mediated signaling in the uninjured state.
Subtype-specific and context-dependent effects
In simple terms: Different receptor subtypes can produce different effects depending on the cell type.
The ADRA1A, ADRA1B and ADRA1D subtypes are not functionally identical; they show distinct expression patterns and can couple to different downstream effectors in a cell-type-specific manner. This context dependence is important for interpreting experiments, because manipulating one subtype may not reproduce the effects of manipulating another. In disease models, modulation of neuronal alpha1-adrenergic receptor signaling has been reported to reduce tauopathy and neuroinflammation through inhibition of the STING/NF-kappaB/NLRP3 pathway in Alzheimer's disease mice, and inhibiting alpha1-adrenergic receptor signaling ameliorated AD-type pathologies and behavioral deficits in APPswe/PS1 mice.
Integration with other signaling systems
In simple terms: Alpha1 receptor signaling does not work alone; it talks to other receptors and pathways.
Alpha1-adrenergic receptor activity can intersect with other signaling systems, including purinergic signaling in sensory neurons, where alpha1-adrenergic receptors augment P2X3 receptor-mediated nociceptive responses. In the cardiovascular system, adrenergic receptors including alpha1 subtypes integrate catecholamine signals to regulate heart rate, contractility and vascular resistance. These interactions mean that the functional output of GO:0004937 depends on the cellular context and on the presence of other receptors and signaling components.
Key Genes Involved in GO:0004937 alpha1-adrenergic receptor activity
The genes most directly associated with alpha1-adrenergic receptor activity are the three alpha1-adrenergic receptor subtype genes, ADRA1A, ADRA1B and ADRA1D, together with downstream Gq signaling components and related adrenergic pathway genes.
| Gene | Major Role | Research Relevance |
|---|---|---|
| ADRA1A | Encodes the alpha1A-adrenergic receptor subtype that binds catecholamines and couples to Gq | Studied in vascular, cardiac and neuronal signaling; target for functional knockout and point-mutation studies |
| ADRA1B | Encodes the alpha1B-adrenergic receptor subtype with distinct pharmacology and tissue distribution | Investigated in blood pressure regulation and nociception; useful for subtype-selective CRISPR models |
| ADRA1D | Encodes the alpha1D-adrenergic receptor subtype expressed in specific vascular and neuronal tissues | Examined in vascular tone and central nervous system functions; relevant for knock-in reporter models |
| GNAQ | Encodes the Gq alpha subunit that receives the signal from activated alpha1-adrenergic receptors | Central to the definition of GO:0004937; knockout and point-mutation models test Gq coupling |
| GNA11 | Encodes a Gq-family alpha subunit that can mediate alpha1-adrenergic receptor signaling | Studied as a parallel Gq pathway component in adrenergic signal transduction |
| PLCB1 | Encodes phospholipase C beta 1, a downstream effector of Gq activation | Used to map downstream signaling of alpha1-adrenergic receptor activity |
| PLCB2 | Encodes phospholipase C beta 2, another Gq effector in specific cell types | Relevant for cell-type-specific signaling studies |
| PRKCA | Encodes protein kinase C alpha, a downstream kinase activated by Gq signaling | Investigated as a mediator of alpha1-adrenergic receptor-induced cellular responses |
| P2RX3 | Encodes the P2X3 receptor, which is modulated by alpha1-adrenergic receptor activity in sensory neurons | Studied in nociceptive signaling and receptor cross-talk |
| STING1 | Encodes STING, a component of innate immune signaling inhibited by alpha1-adrenergic receptor modulation in AD models | Relevant to neuroinflammation studies linking adrenergic signaling to tauopathy |
| NFKB1 | Encodes a subunit of NF-kappaB, a transcription factor downstream of inflammatory signaling | Examined in the STING/NF-kappaB/NLRP3 pathway affected by alpha1-adrenergic receptor modulation |
| NLRP3 | Encodes the NLRP3 inflammasome component linked to neuroinflammation | Studied in Alzheimer's disease models with alpha1-adrenergic receptor manipulation |
| MAPT | Encodes tau protein, whose pathology is reduced by modulation of neuronal alpha1-adrenergic receptor | Used as a readout in tauopathy models |
| APP | Encodes amyloid precursor protein, central to Alzheimer's disease pathology | Studied in APPswe/PS1 models with alpha1-adrenergic receptor inhibition |
| PSEN1 | Encodes presenilin 1, a component of gamma-secretase in Alzheimer's disease models | Used in APPswe/PS1 transgenic models |
| EDNRA | Encodes endothelin receptor A, which is co-targeted by autoantibodies alongside alpha1-adrenergic receptor in prostate cancer | Relevant to autoimmune and cancer studies |
| SLC8A1 | Encodes the sodium-calcium exchanger involved in calcium handling downstream of Gq signaling | Potential downstream effector in contractile responses |
| RHOA | Encodes RhoA, a small GTPase contributing to calcium sensitization in smooth muscle contraction | Studied in alpha1-adrenergic receptor-mediated vascular contraction |
How Is alpha1-adrenergic receptor activity Regulated?
Alpha1-adrenergic receptor activity is regulated at multiple levels, including receptor expression, ligand availability, receptor phosphorylation and desensitization, and the availability of Gq alpha subunits. Catecholamine levels determine the extent of receptor activation, and prolonged stimulation can lead to receptor desensitization and downregulation. In disease states, autoantibodies directed against alpha1-adrenergic receptor have been detected in patients with prostate cancer, providing an additional layer of regulation through immune-mediated receptor activation. In Alzheimer's disease models, modulation of neuronal alpha1-adrenergic receptor signaling has been shown to influence the STING/NF-kappaB/NLRP3 pathway, indicating that inflammatory signaling can feed back on adrenergic receptor function. Age-related changes in vascular reactivity also affect alpha1-adrenergic receptor-mediated contraction, as observed in aging hypertensive rats.
alpha1-adrenergic receptor activity and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| ADRA1A | Hypertension and vascular dysfunction | Knockout or point-mutation in vascular smooth muscle cells and rodent models |
| ADRA1B | Nociceptive signaling and pain | Knockout in sensory neurons and P2X3 interaction studies |
| ADRA1A/ADRA1B | Alzheimer's disease and neuroinflammation | Knockdown or pharmacological inhibition in APPswe/PS1 and tauopathy models |
| ADRA1A | Prostate cancer autoimmunity | Autoantibody detection and receptor overexpression in prostate cancer cell lines |
| ADRA1D | Vascular tone regulation | Knock-in reporter and knockout models in vascular tissue |
Cardiovascular disease and hypertension
Alpha1-adrenergic receptor activity is a major determinant of vascular smooth muscle contraction and blood pressure regulation, and altered adrenergic signaling contributes to cardiovascular pathology. In aging hypertensive rats, alpha1-adrenergic receptor-induced contraction of mesenteric artery is increased, suggesting that changes in this activity contribute to hypertension associated with aging. These findings support the use of alpha1-adrenergic receptor genes as candidates for functional studies in cardiovascular disease models.
Alzheimer's disease and neuroinflammation
Modulation of neuronal alpha1-adrenergic receptor reduces tauopathy and neuroinflammation by inhibiting the STING/NF-kappaB/NLRP3 signaling pathway in Alzheimer's disease mice. Inhibiting alpha1-adrenergic receptor signaling also ameliorates AD-type pathologies and behavioral deficits in the APPswe/PS1 mouse model. These studies link GO:0004937 to neurodegenerative disease mechanisms and suggest that alpha1-adrenergic receptor activity may be a therapeutic target in Alzheimer's disease.
Pain and nociceptive signaling
Alpha1-adrenergic receptors augment P2X3 receptor-mediated nociceptive responses in the uninjured state, indicating that this activity modulates sensory signaling. This cross-talk between adrenergic and purinergic systems is relevant to understanding pain mechanisms and to designing experiments that manipulate alpha1-adrenergic receptor activity in sensory neurons.
Prostate cancer and autoimmunity
Autoantibodies directed against alpha1-adrenergic receptor and endothelin receptor A have been detected in patients with prostate cancer, suggesting a potential autoimmune or biomarker dimension to alpha1-adrenergic receptor biology in cancer. This finding broadens the disease relevance of GO:0004937 beyond cardiovascular and neurological contexts.
From alpha1-adrenergic receptor activity-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of ADRA1A reduce alpha1-adrenergic receptor activity in vascular cells? | CRISPR knockout of ADRA1A in vascular smooth muscle cells |
| Does a specific ADRA1B point mutation alter Gq coupling? | CRISPR point mutation at the Gq-coupling interface of ADRA1B |
| Can a tagged ADRA1A receptor be used to track localization? | Knock-in of an epitope tag at the endogenous ADRA1A locus |
| Does overexpression of ADRA1D increase downstream signaling? | Overexpression of ADRA1D in a heterologous cell system |
| Does modulation of neuronal alpha1-adrenergic receptor reduce tau pathology? | Knockdown or knockout in Alzheimer's disease mouse models |
| Does alpha1-adrenergic receptor activity require GNAQ? | CRISPR knockout of GNAQ in cells expressing ADRA1A |
How to Study the alpha1-adrenergic receptor activity Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Radioligand binding assay | Ligand affinity and receptor density | Confirming alpha1-adrenergic pharmacology |
| Calcium mobilization assay | Gq-mediated calcium release | Functional readout of receptor activation |
| RNA sequencing | Expression of ADRA1A, ADRA1B, ADRA1D and downstream genes | Tissue and disease profiling |
| Phosphoproteomics | Phosphorylation events downstream of Gq | Mapping signaling networks |
| Vascular contraction assay | Smooth muscle contractile response | Studying hypertension-related receptor activity |
| Behavioral testing in mice | Nociceptive or cognitive outcomes | Linking receptor activity to behavior |
| Immunoassay for autoantibodies | Autoantibody levels against alpha1-adrenergic receptor | Cancer and autoimmune studies |
| CRISPR screening | Genes required for receptor activity or downstream signaling | Functional genomics of adrenergic pathways |
Pharmacological and functional assays
Alpha1-adrenergic receptor activity can be measured using ligand-binding assays with epinephrine or norepinephrine and subtype-selective antagonists, as well as functional assays that report Gq activation such as calcium mobilization or inositol phosphate accumulation. These assays are foundational for confirming that a receptor displays the pharmacological characteristics of alpha1-adrenergic receptors.
Genetic and transcriptomic approaches
RNA sequencing and quantitative PCR can quantify expression of ADRA1A, ADRA1B and ADRA1D across tissues and disease states, helping to identify which subtype contributes to alpha1-adrenergic receptor activity in a given context. Transcriptomic profiling of disease models, such as APPswe/PS1 mice, can reveal downstream pathways affected by alpha1-adrenergic receptor modulation.
Proteomic and signaling pathway analysis
Proteomic and phosphoproteomic methods can identify proteins and phosphorylation events downstream of Gq activation, including phospholipase C and protein kinase C substrates. Pathway analysis of neuroinflammatory markers such as STING, NF-kappaB and NLRP3 can be used to assess the impact of alpha1-adrenergic receptor modulation in disease models.
Imaging and physiological measurements
Calcium imaging and vascular contraction assays can directly measure the physiological consequences of alpha1-adrenergic receptor activity in smooth muscle and other cell types. In vivo imaging and behavioral testing in animal models can link receptor activity to outcomes such as nociception or cognitive deficits.
How CRISPR Can Be Used to Study GO:0004937 alpha1-adrenergic receptor activity
Knockout
CRISPR knockout of ADRA1A, ADRA1B or ADRA1D can eliminate specific alpha1-adrenergic receptor subtypes and test their contribution to Gq-mediated signaling, vascular contraction or neuronal function. Knockout of GNAQ can be used to confirm that the activity defined by GO:0004937 depends on the Gq alpha subunit. These models are valuable for distinguishing subtype-specific effects in disease-relevant cells.
Point Mutation
CRISPR point mutation can be used to alter specific residues in alpha1-adrenergic receptors that are predicted to affect ligand binding or Gq coupling, allowing structure-function analysis of GO:0004937. Point mutations can also be introduced into downstream signaling components to dissect pathway order.
Knock-in
Knock-in of epitope tags, fluorescent proteins or reporter cassettes at the endogenous ADRA1A, ADRA1B or ADRA1D loci enables tracking of receptor expression, localization and turnover without overexpression artifacts. Knock-in models can also be used to introduce disease-associated variants for functional study.
Overexpression
Overexpression of a specific alpha1-adrenergic receptor subtype in heterologous cells or disease models can amplify receptor activity and downstream signaling, making it easier to detect Gq-dependent effects. Overexpression studies have been used to investigate receptor autoantibody targets in prostate cancer and to probe signaling in Alzheimer's disease models.
How EDITGENE Supports alpha1-adrenergic receptor activity Research
Researchers studying alpha1-adrenergic receptor activity-related genes often need to determine whether a candidate gene is causally involved in receptor signaling, whether a specific variant alters Gq coupling, or whether a receptor subtype can be tracked in its native context. EDITGENE provides the CRISPR tools and cell models needed to answer these questions with rigor and reproducibility.
Contact EDITGENE today to design your custom CRISPR model for alpha1-adrenergic receptor activity research.
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| ADRA1A Knockout HEK293 Cell Line | EDJ-KQ1583 | Human | 148 | Details Get a Quote |
| ADRA1B Knockout HEK293 Cell Line | EDJ-KQ1584 | Human | 147 | Details Get a Quote |
| ADRA1D Knockout HEK293 Cell Line | EDJ-KQ1585 | Human | 146 | Details Get a Quote |
| ADRA1B Knockout A-549 Cell Line | EDJ-KQ21268 | Human | 147 | Details Get a Quote |
| ADRA1B Knockout HeLa Cell Line | EDJ-KQ21269 | Human | 147 | Details Get a Quote |
| ADRA1D Knockout A-549 Cell Line | EDJ-KQ21270 | Human | 146 | Details Get a Quote |
| ADRA1D Knockout HeLa Cell Line | EDJ-KQ52566 | Human | 146 | Details Get a Quote |
| ADRA1A Knockout HeLa Cell Line | EDJ-KQ52567 | Human | 148 | Details Get a Quote |
| ADRA1A Knockout A-549 Cell Line | EDJ-KQ61044 | Human | 148 | Details Get a Quote |
| ADRA1D Knockout HCT 116 Cell Line | EDJ-KQ69521 | Human | 146 | Details Get a Quote |
| ADRA1B Knockout HCT 116 Cell Line | EDJ-KQ69522 | Human | 147 | Details Get a Quote |
| ADRA1A Knockout HCT 116 Cell Line | EDJ-KQ69523 | Human | 148 | Details Get a Quote |
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Frequently Asked Questions About alpha1-adrenergic receptor activity
What is alpha1-adrenergic receptor activity?
Alpha1-adrenergic receptor activity (GO:0004937) is a molecular function in which a receptor binds epinephrine or norepinephrine and transmits the signal to the Gq alpha subunit of a heterotrimeric G protein, initiating a change in cell activity.
What genes are involved in alpha1-adrenergic receptor activity?
The main genes are ADRA1A, ADRA1B and ADRA1D, which encode the three alpha1-adrenergic receptor subtypes, along with Gq signaling components such as GNAQ.
What is the GO ID for alpha1-adrenergic receptor activity?
The Gene Ontology identifier is GO:0004937, and the synonym alpha1 adrenoceptor is also used.
Which G protein does the alpha1-adrenergic receptor couple to?
Alpha1-adrenergic receptors couple to the Gq alpha subunit of a heterotrimeric G protein, as stated in the QuickGO definition of GO:0004937.
How is alpha1-adrenergic receptor activity studied?
It is studied using ligand-binding assays, calcium mobilization assays, RNA sequencing, proteomics, vascular contraction assays and CRISPR-based genetic models.
Is alpha1-adrenergic receptor activity involved in Alzheimer's disease?
Yes, modulation of neuronal alpha1-adrenergic receptor has been reported to reduce tauopathy and neuroinflammation via the STING/NF-kappaB/NLRP3 pathway, and inhibiting its signaling ameliorated AD-type pathologies in mouse models.
What diseases are linked to alpha1-adrenergic receptor activity?
It has been linked to cardiovascular disease and hypertension, Alzheimer's disease, nociceptive signaling and prostate cancer autoimmunity.
Can CRISPR be used to study alpha1-adrenergic receptor activity?
Yes, CRISPR knockout, point mutation, knock-in and overexpression models can be used to test the function of ADRA1A, ADRA1B, ADRA1D and downstream Gq signaling genes.
What is the difference between alpha1 and beta-adrenergic receptors?
Alpha1-adrenergic receptors couple to Gq, whereas beta-adrenergic receptors typically couple to Gs, leading to different downstream signaling and cellular responses.
Why is alpha1-adrenergic receptor activity important for drug discovery?
Because it regulates vascular tone, cardiac function and neuronal signaling, and is implicated in hypertension, neurodegeneration and cancer, making it a target for pharmacological and genetic intervention.
Conclusion
Alpha1-adrenergic receptor activity (GO:0004937) is a well-defined molecular function that links catecholamine binding to Gq-mediated cellular responses. Its roles in cardiovascular regulation, neuronal signaling, neuroinflammation and cancer biology make it a compelling target for functional genomics and therapeutic research. By combining precise CRISPR models with pharmacological and omics approaches, researchers can dissect how ADRA1A, ADRA1B and ADRA1D contribute to health and disease. EDITGENE supports these efforts with knockout, point-mutation, knock-in, overexpression and screening services tailored to adrenergic receptor biology.
References
- 1. Motiejunaite J et al.. 2021. Adrenergic receptors and cardiovascular effects of catecholamines.. Ann Endocrinol (Paris) 82(3-4):193-197 PMID: 32473788
- 3. Li B et al.. 2025. Modulation of neuronal α1-adrenergic receptor reduces tauopathy and neuroinflammation by inhibiting the STING/NF-κB/NLRP3 signaling pathway in Alzheimer's disease mice.. J Neuroinflammation 22(1):187 PMID: 40676669
- 4. Meisner JG et al.. 2007. Alpha1-adrenergic receptors augment P2X3 receptor-mediated nociceptive responses in the uninjured state.. J Pain 8(7):556-62 PMID: 17512257
- 5. Chen ZJ et al.. 2005. Recent progress in alpha1-adrenergic receptor research.. Acta Pharmacol Sin 26(11):1281-7 PMID: 16225747
- 6. Wallukat G et al.. 2020. Autoantibodies directed against α1-adrenergic receptor and endothelin receptor A in patients with prostate cancer.. Auto Immun Highlights 11(1):13 PMID: 32977857
- 7. Yu ZY et al.. 2022. Inhibiting α1-adrenergic receptor signaling pathway ameliorates AD-type pathologies and behavioral deficits in APPswe/PS1 mouse model.. J Neurochem 161(3):293-307 PMID: 35244207
- 8. Wei X et al.. 2021. Mechanism of α1-Adrenergic Receptor-Induced Increased Contraction of Rat Mesenteric Artery in Aging Hypertension Rats.. Gerontology 67(3):323-337 PMID: 33752204
