GO:0030546 signaling receptor activator activity: Mechanism, Genes and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0030546 signaling receptor activator activity describes the molecular function of directly or indirectly interacting with a receptor to increase the proportion of active receptors.
• This activity is central to intercellular communication and is exemplified by ligands such as BDNF, IGF-1, adiponectin, and H2S-related factors that activate their cognate receptors [1,6,7,4].
• Dysregulation of signaling receptor activator activity contributes to metabolic, cardiovascular, and neurological diseases, including vascular aging and neuroinflammation [4,7].
• Exercise and other physiological stimuli modulate receptor activator activity through pathways involving PGC-1α, FNDC5/BDNF, IGF-1/IGF-1R, and adiponectin/AdipoR1 [1,6,7].
• CRISPR-based models (knockout, point mutation, knock-in, overexpression) enable causal dissection of receptor activator genes in disease and therapy [2,8].
• EDITGENE provides end-to-end services for functional studies of signaling receptor activator activity, from cell model generation to CRISPR library screening and bioinformatics.
Description
GO:0030546 signaling receptor activator activity is a molecular function term in the Gene Ontology that defines the ability of a molecule to interact directly or indirectly with a receptor and increase the proportion of receptors in their active form. This activity is fundamental to signal transduction, as it initiates cascades that regulate cell growth, metabolism, differentiation, and survival. Unlike receptor binding alone, signaling receptor activator activity specifically requires a functional consequence: receptor activation. This distinction is critical for annotating ligands, cofactors, and accessory proteins that modulate receptor signaling in physiological and pathological contexts. Researchers study signaling receptor activator activity to understand how extracellular cues are translated into cellular responses. For example, exercise-induced BDNF activation of TrkB receptors in the hippocampus requires the PGC-1α/FNDC5 pathway, illustrating how a signaling receptor activator (BDNF) is regulated by upstream metabolic coactivators. Similarly, IGF-1 activates IGF-1R to alleviate skeletal muscle atrophy through PI3K/Akt signaling, demonstrating the therapeutic relevance of this activity in muscle wasting conditions. Adiponectin activates AdipoR1 to shift microglial polarization and reduce neuroinflammation, further highlighting the broad impact of receptor activator activity in disease. Given its central role in cell signaling, GO:0030546 is a key term for functional genomics, drug discovery, and CRISPR-based disease modeling. Understanding which genes encode receptor activators, how their activity is regulated, and how mutations alter receptor activation can reveal new therapeutic targets. This article provides a comprehensive overview of the mechanisms, key genes, research methods, and CRISPR models relevant to signaling receptor activator activity, based on published literature [2,8].
signaling receptor activator activity At A Glance
| GO ID | GO:0030546 |
|---|---|
| GO term | signaling receptor activator activity |
| Ontology | molecular_function |
| Synonym | receptor activator activity, signalling receptor activator activity |
| Definition | The function of interacting (directly or indirectly) with receptors such that the proportion of receptors in the active form is increased. |
| Major function | Initiating or enhancing receptor-mediated signal transduction |
| Examples | BDNF, IGF-1, adiponectin, H2S-related factors |
| Related diseases | Vascular aging, neuroinflammation, muscle atrophy, metabolic disorders |
| Research methods | CRISPR knockout, point mutation, knock-in, overexpression, signaling assays |
What Is GO:0030546?
In our own words, GO:0030546 signaling receptor activator activity is the function of a molecule that binds to or indirectly influences a receptor, leading to an increase in the fraction of receptors that are in an active state. This activity is not merely about binding; it requires a positive effect on receptor activation, which may occur through direct ligand-receptor interaction or via accessory proteins that facilitate receptor activation. The term is used to annotate gene products that act as agonists or co-activators of receptor signaling, distinguishing them from receptor antagonists or neutral binders.
Why Is signaling receptor activator activity Important in Cell Biology?
Signaling receptor activator activity is essential for understanding how cells respond to their environment. It governs processes ranging from neuronal plasticity and metabolic homeostasis to immune regulation and tissue repair [1,6,7]. Dysregulation of this activity is implicated in a wide array of diseases, including cardiovascular aging, neurodegeneration, and cancer [4,7]. Because receptor activators are often secreted or membrane-associated proteins, they represent attractive drug targets and biomarkers. Moreover, the ability to precisely edit genes encoding receptor activators using CRISPR technologies allows researchers to establish causal links between specific activators and disease phenotypes, accelerating the development of targeted therapies [2,8].
• Controls fundamental signaling pathways such as PI3K/Akt, MAPK, and cAMP, influencing cell survival, proliferation, and metabolism.
• Mediates exercise-induced benefits in the brain, muscle, and cardiovascular system through activation of BDNF/TrkB, IGF-1/IGF-1R, and adiponectin/AdipoR1 axes [1,6,7].
• Plays a protective role in vascular aging via the endothelial NAD+-H2S signaling network.
• Modulates neuroinflammation by shifting microglial polarization from M1 to M2 through adiponectin/AdipoR1 activation.
• Is implicated in clonal hematopoiesis and its response to lifestyle interventions such as exercise and sleep.
• Provides a mechanistic basis for understanding how maternal exercise benefits offspring health via placental SOD3.
• Serves as a target for therapeutic intervention in muscle atrophy, myocardial infarction, and metabolic syndrome.
• Enables the development of CRISPR-based disease models to study gene function and validate drug targets.
• Facilitates the discovery of novel receptor activators through functional genomics and high-throughput screening.
• Underpins the rationale for exercise mimetics and lifestyle interventions in disease prevention.
Molecular Mechanism of signaling receptor activator activity
Direct Ligand-Receptor Interaction
In simple terms: A signaling molecule binds directly to its receptor, flipping a switch that turns the receptor on.
The most straightforward mechanism of signaling receptor activator activity involves a ligand binding directly to the extracellular domain of a receptor, inducing conformational changes that lead to receptor dimerization, autophosphorylation, and activation of downstream signaling cascades. For example, BDNF binds to TrkB receptors, triggering autophosphorylation and activation of PI3K/Akt and MAPK pathways, which promote neuronal survival and plasticity. Similarly, IGF-1 binds to IGF-1R, leading to receptor autophosphorylation and activation of PI3K/Akt signaling, which alleviates skeletal muscle atrophy. This direct interaction is highly specific and is often regulated by ligand availability, receptor expression levels, and post-translational modifications.
Indirect Activation via Accessory Proteins
In simple terms: Sometimes a helper protein assists the receptor in turning on, without binding the receptor itself.
Signaling receptor activator activity can also occur indirectly, where an accessory protein facilitates receptor activation without directly binding the receptor. For instance, the endothelial NAD+-H2S signaling network involves enzymes that produce H2S, which then modifies receptor proteins or their partners to enhance receptor activation. In this context, the activator may modulate the receptor's environment, such as by altering redox state or providing necessary cofactors, thereby increasing the proportion of active receptors. This indirect mechanism expands the repertoire of signaling receptor activators beyond classical ligands and highlights the importance of cellular context.
Regulation by Metabolic Coactivators
In simple terms: Proteins like PGC-1α act as master regulators that boost the production of receptor activators.
The expression and activity of signaling receptor activators are often controlled by transcriptional coactivators such as PGC-1α. Exercise induces hippocampal BDNF through a PGC-1α/FNDC5 pathway, where PGC-1α upregulates FNDC5, which is cleaved to release irisin, and ultimately increases BDNF levels. This cascade demonstrates how metabolic coactivators can indirectly enhance signaling receptor activator activity by increasing the availability of the activator ligand. Similarly, PGC-1α regulates exercise intensity-dependent atrial remodeling, potentially through modulation of receptor activator pathways. Such regulation ensures that receptor activation is coupled to cellular energy status and physiological demand.
Receptor Activation and Signal Amplification
In simple terms: Once activated, receptors amplify the signal by turning on many downstream molecules.
Upon activation by a signaling receptor activator, receptors typically undergo conformational changes that enable them to activate intracellular signaling proteins. For example, activated IGF-1R phosphorylates insulin receptor substrate (IRS) proteins, leading to PI3K/Akt activation and downstream effects on protein synthesis and muscle hypertrophy. Adiponectin binding to AdipoR1 activates AMPK and PPARα pathways, which shift microglial polarization and reduce neuroinflammation. The strength and duration of receptor activation are tightly controlled by negative feedback mechanisms, including receptor internalization, dephosphorylation, and degradation, ensuring that signaling is transient and appropriate.
Integration with Cellular Stress and Aging Pathways
In simple terms: Receptor activator activity is linked to how cells handle stress and aging.
Signaling receptor activator activity intersects with cellular stress responses and aging. The endothelial NAD+-H2S signaling network, which includes receptor activator components, is impaired during vascular aging, and its restoration reverses age-related vascular dysfunction. Maternal exercise enhances placental superoxide dismutase 3 (SOD3), which may act as a signaling receptor activator to improve offspring health. These examples illustrate that receptor activator activity is not isolated but is integrated with redox balance, mitochondrial function, and systemic metabolism. Understanding these connections may reveal new targets for interventions that delay aging and prevent disease.
Key Genes Involved in GO:0030546 signaling receptor activator activity
The following genes encode proteins that exhibit signaling receptor activator activity or regulate it, based on published literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| BDNF | Activates TrkB receptors to promote neuronal survival and plasticity | Exercise-induced hippocampal neurogenesis; neuropsychiatric disorders |
| FNDC5 | Precursor of irisin, which induces BDNF expression | Mediates benefits of exercise on brain function |
| PGC-1α (PPARGC1A) | Transcriptional coactivator that upregulates FNDC5 and BDNF | Master regulator of exercise-induced adaptations [1,5] |
| IGF-1 | Activates IGF-1R to stimulate PI3K/Akt signaling | Muscle atrophy, myocardial infarction, growth disorders |
| IGF-1R | Receptor tyrosine kinase activated by IGF-1 | Target for muscle wasting and cancer |
| Adiponectin | Activates AdipoR1 to modulate microglial polarization | Neuroinflammation, depression, metabolic syndrome |
| AdipoR1 | Receptor for adiponectin, activates AMPK and PPARα | Anti-inflammatory and insulin-sensitizing effects |
| SOD3 | Extracellular superoxide dismutase, may act as a signaling modulator | Maternal exercise benefits on offspring health |
| H2S-producing enzymes (CBS, CSE, 3-MST) | Generate H2S that modulates receptor signaling | Vascular aging and endothelial function |
| NAD+ biosynthetic enzymes (NAMPT, NMNAT) | Maintain NAD+ levels for H2S signaling | Vascular aging and metabolic regulation |
| TrkB (NTRK2) | Receptor for BDNF, mediates neurotrophic signaling | Neurodegeneration, mood disorders |
| IRS-1 | Docking protein downstream of IGF-1R | Insulin resistance, muscle atrophy |
| AMPK | Energy sensor activated by adiponectin/AdipoR1 | Metabolic homeostasis, neuroinflammation |
| PPARα | Nuclear receptor activated by adiponectin signaling | Lipid metabolism, inflammation |
| PI3K | Kinase activated by IGF-1R and BDNF/TrkB | Cell survival, proliferation, metabolism [1,6] |
| Akt | Serine/threonine kinase downstream of PI3K | Muscle hypertrophy, neuronal survival [1,6] |
| MAPK/ERK | Kinase cascade activated by BDNF/TrkB | Neuronal plasticity, cell proliferation |
| SOD3 | Extracellular antioxidant enzyme | Placental function and offspring health |
How Is signaling receptor activator activity Regulated?
Signaling receptor activator activity is regulated at multiple levels. Transcriptional control by PGC-1α modulates the expression of ligands such as FNDC5 and BDNF in response to exercise [1,5]. Post-translational modifications, including proteolytic cleavage of FNDC5 to irisin, determine the availability of active receptor activators. Receptor availability and sensitivity are also regulated by feedback mechanisms, such as receptor internalization and degradation. Metabolic cues, including NAD+ levels and H2S production, influence the activity of receptor activators in the vasculature. Additionally, adiponectin/AdipoR1 signaling is regulated by adiponectin multimerization and receptor expression levels, which are altered in obesity and inflammation. These regulatory layers ensure that receptor activation is tightly coupled to physiological state and can be disrupted in disease.
signaling receptor activator activity and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| BDNF | Neurodegeneration, depression, cognitive decline | Knockout mice, overexpression in hippocampus |
| IGF-1 | Muscle atrophy, myocardial infarction, metabolic syndrome | Muscle-specific knockout, knock-in of human IGF-1 |
| AdipoR1 | Neuroinflammation, depression, insulin resistance | AdipoR1 knockout mice, overexpression in microglia |
| SOD3 | Placental dysfunction, offspring metabolic health | SOD3 knockout mice, maternal exercise models |
| H2S-producing enzymes | Vascular aging, endothelial dysfunction | Endothelial-specific knockout, NAD+ supplementation |
Signaling Receptor Activator Activity in Vascular Aging
Impaired signaling receptor activator activity contributes to vascular aging. The endothelial NAD+-H2S signaling network, which includes receptor activator components, is downregulated with age, leading to endothelial dysfunction and increased oxidative stress. Restoration of this network reverses age-related vascular phenotypes, suggesting that targeting receptor activator activity could be a therapeutic strategy for cardiovascular aging. Key genes involved include H2S-producing enzymes and NAD+ biosynthetic enzymes, which modulate receptor activation through redox-dependent mechanisms.
Role in Neuroinflammation and Depression
Adiponectin/AdipoR1 signaling exhibits receptor activator activity that shifts microglial polarization from pro-inflammatory M1 to anti-inflammatory M2, reducing neuroinflammation in chronic stress models. Running exercise alleviates hippocampal neuroinflammation through this pathway, highlighting the therapeutic potential of activating AdipoR1 in depression and other neuroinflammatory conditions. BDNF/TrkB signaling, another receptor activator axis, is also critical for hippocampal function and is induced by exercise via PGC-1α/FNDC5.
Muscle Atrophy and Metabolic Disorders
IGF-1 acts as a signaling receptor activator for IGF-1R, stimulating PI3K/Akt signaling to prevent skeletal muscle atrophy in myocardial infarction models. Both aerobic and resistance exercise alleviate muscle atrophy through this pathway, underscoring the importance of receptor activator activity in muscle maintenance. Dysregulation of IGF-1/IGF-1R signaling is also implicated in insulin resistance and metabolic syndrome, making it a target for therapeutic intervention.
Clonal Hematopoiesis and Exercise Response
Mutation-dependent responses to sleep and exercise in clonal hematopoiesis suggest that signaling receptor activator activity may influence the behavior of mutant hematopoietic clones. Exercise and sleep are known to modulate systemic signaling, potentially through receptor activators such as IGF-1 and adiponectin, which could affect clonal expansion and disease progression. Understanding these interactions may inform lifestyle interventions for individuals with clonal hematopoiesis.
From signaling receptor activator activity-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of BDNF reduce exercise-induced hippocampal neurogenesis? | BDNF knockout mice with running wheel access |
| Can point mutation in IGF-1R alter ligand specificity? | Knock-in mice expressing mutant IGF-1R |
| Does overexpression of AdipoR1 protect against neuroinflammation? | Transgenic mice with microglial AdipoR1 overexpression |
| What is the role of SOD3 in maternal exercise benefits? | SOD3 knockout mice subjected to maternal exercise |
| How does H2S signaling affect vascular aging? | Endothelial-specific CSE knockout mice |
| Does clonal hematopoiesis alter response to exercise? | Bone marrow transplant models with Tet2 or Dnmt3a mutations |
How to Study the signaling receptor activator activity Process
| Method | What It Measures | Typical Application |
|---|---|---|
| CRISPR knockout screen | Loss-of-function effects on receptor activation | Identify negative regulators of signaling |
| CRISPR activation screen | Gain-of-function effects on receptor activation | Discover enhancers of signaling |
| Phosphoproteomics | Global phosphorylation changes upon receptor activation | Map downstream signaling networks |
| Western blot | Phosphorylation of specific receptors and kinases | Validate receptor activation [1,6] |
| RNA-seq | Transcriptional changes induced by receptor activators | Identify target genes and pathways |
| ChIP-seq | Transcription factor binding at receptor activator loci | Study PGC-1α-mediated regulation |
| Behavioral assays | Cognitive and affective outcomes of receptor activation | Assess neurotrophic effects in vivo [1,7] |
| Vascular reactivity assay | Endothelial function and vascular tone | Evaluate H2S signaling in aging |
CRISPR-Based Genetic Screens
CRISPR knockout and activation screens can identify genes that regulate signaling receptor activator activity. For example, a genome-wide knockout screen in cells treated with a receptor activator can reveal negative regulators of the pathway, while an activation screen can identify enhancers. These screens are powerful for discovering novel components of receptor signaling networks and have been applied to study exercise mimetics and metabolic pathways.
Phosphoproteomics and Signaling Assays
Phosphoproteomics allows comprehensive mapping of receptor-activated signaling cascades. By stimulating cells with a receptor activator (e.g., IGF-1 or BDNF) and quantifying phosphorylation changes, researchers can identify downstream effectors and feedback mechanisms. Western blotting for phosphorylated receptors (e.g., p-IGF-1R, p-TrkB) and downstream kinases (p-Akt, p-ERK) provides direct evidence of receptor activation [1,6].
Transcriptomics and Epigenomics
RNA sequencing (RNA-seq) and chromatin immunoprecipitation sequencing (ChIP-seq) can reveal how receptor activator genes are transcriptionally regulated. For instance, PGC-1α ChIP-seq has been used to identify target genes such as FNDC5 in response to exercise. ATAC-seq can assess chromatin accessibility at loci encoding receptor activators, providing insights into epigenetic regulation.
In Vivo Models and Behavioral Assays
Animal models, including knockout and transgenic mice, are essential for studying the physiological roles of signaling receptor activators. Exercise paradigms, such as treadmill running or voluntary wheel running, combined with behavioral tests (e.g., forced swim test, novel object recognition) can assess the impact of receptor activator activity on brain function and behavior [1,7]. Similarly, muscle function tests and vascular reactivity assays can evaluate cardiovascular and skeletal muscle phenotypes [4,6].
How CRISPR Can Be Used to Study GO:0030546 signaling receptor activator activity
Knockout
CRISPR knockout of genes encoding signaling receptor activators (e.g., BDNF, IGF-1, adiponectin) can abolish receptor activation and reveal essential functions. For example, BDNF knockout mice exhibit impaired exercise-induced hippocampal neurogenesis, demonstrating the requirement for this receptor activator in brain plasticity. Knockout of AdipoR1 in microglia exacerbates neuroinflammation, highlighting its protective role. These models are invaluable for establishing causality and identifying compensatory mechanisms.
Point Mutation
Point mutations can be introduced to dissect specific residues required for receptor activator function. For instance, mutating the cleavage site in FNDC5 prevents irisin release, allowing researchers to test whether irisin is necessary for BDNF induction by exercise. Similarly, point mutations in IGF-1 that alter receptor binding affinity can clarify structure-function relationships. Such models provide precise mechanistic insights beyond simple knockouts.
Knock-in
Knock-in of reporter tags (e.g., GFP, luciferase) or human orthologs enables real-time tracking of receptor activator expression and function. A BDNF-GFP knock-in mouse allows visualization of BDNF secretion and transport in vivo. Knock-in of human IGF-1 into the mouse Igf1 locus can model human-specific regulation and facilitate drug testing. These models are particularly useful for studying dynamic changes in receptor activator activity during development or disease.
Overexpression
Overexpression of signaling receptor activators via CRISPR activation (CRISPRa) or transgenic approaches can enhance receptor signaling and test therapeutic potential. For example, overexpression of AdipoR1 in microglia reduces neuroinflammation and depressive-like behaviors in mice. Overexpression of SOD3 in placenta mimics maternal exercise benefits, suggesting a protective role. CRISPRa allows tunable, reversible overexpression, making it ideal for studying dose-dependent effects.
How EDITGENE Supports signaling receptor activator activity Research
Researchers studying signaling receptor activator activity-related genes often need to determine whether a candidate gene is causally involved in receptor activation and downstream phenotypes. This requires precise genetic manipulation, which can be achieved through CRISPR-based knockout, point mutation, knock-in, or overexpression models. EDITGENE specializes in providing these services, along with CRISPR library screening and bioinformatics support, to accelerate discovery in this field.
Contact EDITGENE today to design your custom CRISPR model for signaling receptor activator activity research.
Frequently Asked Questions About signaling receptor activator activity
What is GO:0030546 signaling receptor activator activity?
GO:0030546 is a Gene Ontology molecular function term defined as the function of interacting directly or indirectly with receptors such that the proportion of receptors in the active form is increased.
What genes are involved in signaling receptor activator activity?
Key genes include BDNF, FNDC5, PGC-1α, IGF-1, IGF-1R, adiponectin, AdipoR1, SOD3, and H2S-producing enzymes such as CBS and CSE [1,3,4,6,7].
How is signaling receptor activator activity regulated?
It is regulated transcriptionally by coactivators like PGC-1α, post-translationally by proteolytic cleavage, and through feedback mechanisms such as receptor internalization [1,2,5].
What diseases are associated with signaling receptor activator activity?
Dysregulation is linked to vascular aging, neuroinflammation, depression, muscle atrophy, metabolic syndrome, and clonal hematopoiesis [4,6,7,8].
How can I study signaling receptor activator activity in the lab?
Common methods include CRISPR knockout/activation screens, phosphoproteomics, Western blot for phosphorylated receptors, RNA-seq, and in vivo behavioral assays [1,2,6].
What is the role of BDNF in signaling receptor activator activity?
BDNF acts as a signaling receptor activator by binding to TrkB receptors, inducing autophosphorylation and activating PI3K/Akt and MAPK pathways to promote neuronal survival and plasticity.
How does exercise affect signaling receptor activator activity?
Exercise induces PGC-1α, which upregulates FNDC5 and BDNF, and also stimulates IGF-1 and adiponectin signaling, thereby enhancing receptor activator activity in brain, muscle, and vasculature [1,6,7].
Can CRISPR be used to study signaling receptor activator activity?
Yes, CRISPR knockout, point mutation, knock-in, and overexpression models allow precise manipulation of genes encoding receptor activators to test their causal roles in signaling and disease [2,8].
What is the connection between adiponectin and neuroinflammation?
Adiponectin activates AdipoR1, which shifts microglial polarization from M1 to M2, reducing neuroinflammation in chronic stress models.
How does H2S signaling relate to vascular aging?
The endothelial NAD+-H2S signaling network, which includes receptor activator components, is impaired during aging; restoring it reverses vascular dysfunction.
Conclusion
GO:0030546 signaling receptor activator activity is a fundamental molecular function that governs how cells respond to external and internal cues. Through direct ligand-receptor interactions or indirect modulation, receptor activators such as BDNF, IGF-1, and adiponectin initiate signaling cascades critical for neuronal, metabolic, and cardiovascular health [1,6,7]. Dysregulation of these activities contributes to a range of diseases, including vascular aging, neuroinflammation, and muscle atrophy [4,6,7]. Advances in CRISPR-based gene editing and functional genomics have made it possible to dissect the causal roles of receptor activators with unprecedented precision [2,8]. By leveraging knockout, point mutation, knock-in, and overexpression models, researchers can uncover new therapeutic targets and biomarkers. EDITGENE's comprehensive services in cell model generation, CRISPR library screening, and bioinformatics empower discovery in this dynamic field, ultimately accelerating the translation of basic findings into clinical applications.
References
- 1. Wrann CD et al.. 2013. Exercise induces hippocampal BDNF through a PGC-1α/FNDC5 pathway.. Cell Metab 18(5):649-59 PMID: 24120943
- 2. Walzik D et al.. 2024. Molecular insights of exercise therapy in disease prevention and treatment.. Signal Transduct Target Ther 9(1):138 PMID: 38806473
- 3. Kusuyama J et al.. 2021. Placental superoxide dismutase 3 mediates benefits of maternal exercise on offspring health.. Cell Metab 33(5):939-956.e8 PMID: 33770509
- 4. Das A et al.. 2018. Impairment of an Endothelial NAD(+)-H(2)S Signaling Network Is a Reversible Cause of Vascular Aging.. Cell 173(1):74-89.e20 PMID: 29570999
- 5. Xiao J et al.. 2025. PGC-1α Regulates Exercise Intensity-Dependent Atrial Remodeling and Fibrillation in Rats.. Aging Dis 17(5):2767-2779 PMID: 40956965
- 6. Feng L et al.. 2022. Aerobic exercise and resistance exercise alleviate skeletal muscle atrophy through IGF-1/IGF-1R-PI3K/Akt pathway in mice with myocardial infarction.. Am J Physiol Cell Physiol 322(2):C164-C176 PMID: 34852207
- 7. Liu L et al.. 2024. Running exercise alleviates hippocampal neuroinflammation and shifts the balance of microglial M1/M2 polarization through adiponectin/AdipoR1 pathway activation in mice exposed to chronic unpredictable stress.. Mol Psychiatry 29(7):2031-2042 PMID: 38361125
- 8. Gerhardt T et al.. 2026. Mutation-dependent responses to sleep and exercise in clonal haematopoiesis.. Nature 655(8125):1309-1319 PMID: 42271062
