GO:1900143 positive regulation of oligodendrocyte apoptotic process: Apoptosis Signaling Pathway, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:1900143 describes any process that activates or increases the frequency, rate or extent of oligodendrocyte apoptotic process, a biological_process annotation in the Gene Ontology.
• Oligodendrocyte apoptosis is a developmentally regulated event that removes excess oligodendrocyte lineage cells and shapes the final myelinated architecture of the central nervous system.
• Positive regulation of this process is mechanistically coupled to transcriptional control of differentiation, since factors that block oligodendrocyte differentiation can indirectly favor apoptosis of improperly differentiated cells.
• The p53-MDM2 axis is a validated node in oligodendrocyte lineage cell death, and pharmacological MDM2 inhibition with navtemadlin modulates this pathway in recurrent glioblastoma.
• MicroRNAs such as miR-219a-5p and transcription factors including SOX17 and CREB5 influence oligodendrocyte precursor survival, differentiation and apoptotic susceptibility.
• CRISPR knockout, point-mutation, knock-in and overexpression models are the standard tools for causally testing whether a candidate gene positively regulates oligodendrocyte apoptosis.
Description
GO:1900143, positive regulation of oligodendrocyte apoptotic process, is a Gene Ontology biological_process term defined as any process that activates or increases the frequency, rate or extent of oligodendrocyte apoptotic process. Oligodendrocytes are the myelinating cells of the central nervous system, and their programmed death is a normal developmental event that matches the number of myelinating cells to the number of axons requiring myelin. Because oligodendrocyte apoptosis is tightly regulated, the Gene Ontology separates the apoptotic process itself from the positive and negative regulators that control it, and GO:1900143 captures the positive-regulatory arm of that control system. For researchers, GO:1900143 matters because it provides a controlled vocabulary for annotating genes and pathways that promote oligodendrocyte death. Studies of oligodendrocyte differentiation have shown that the balance between differentiation and apoptosis is controlled by transcriptional elongation machinery, including the PAF1 complex and p-TEFb, so perturbations of these complexes can shift cells toward or away from apoptosis. Similarly, transcription factors such as SOX17 negatively regulate oligodendrocyte precursor cell differentiation, and when differentiation is blocked, precursor cells may become susceptible to apoptotic elimination. The term is also clinically relevant. In recurrent glioblastoma, the MDM2 inhibitor navtemadlin engages the p53 pathway and modulates apoptosis in tumor and neural lineage cells, illustrating how positive regulation of apoptotic processes in oligodendrocyte lineage cells can be pharmacologically targeted. Chemogenetic activation of oligodendrocytes delays postnatal myelination by promoting progenitor proliferation and inhibiting maturation, a phenotype that indirectly affects the size of the apoptotic-susceptible oligodendrocyte pool. Thus GO:1900143 sits at the intersection of developmental myelination, transcriptional control, microRNA regulation and therapeutic modulation of cell death.
positive regulation of oligodendrocyte apoptotic process At A Glance
| GO ID | GO:1900143 |
|---|---|
| GO term | positive regulation of oligodendrocyte apoptotic process |
| Ontology | biological_process |
| Synonym | activation of oligodendrocyte apoptosis; activation of oligodendrocyte apoptotic process; positive regulation of oligodendrocyte apoptosis; up regulation of oligodendrocyte apoptosis; up-regulation of oligodendrocyte apoptosis; upregulation of oligodendrocyte apoptosis; up regulation of oligodendrocyte apoptotic process; up-regulation of oligodendrocyte apoptotic process; upregulation of oligodendrocyte apoptotic process |
| Major function | Increases the frequency, rate or extent of apoptotic death of oligodendrocytes and their precursors |
| Biological context | Developmental myelination, oligodendrocyte precursor differentiation and central nervous system homeostasis |
| Key regulatory nodes | PAF1C and p-TEFb transcriptional elongation complexes, SOX17, miR-219a-5p, CREB5 and the p53-MDM2 axis |
| Disease relevance | Glioblastoma response and resistance to MDM2 inhibition, demyelinating and neurodegenerative conditions |
| Research methods | CRISPR knockout, point mutation, knock-in, overexpression, RNA-seq, imaging and pharmacological perturbation |
What Is GO:1900143?
In plain terms, GO:1900143 describes any molecular or cellular process that turns up the rate of programmed cell death specifically in oligodendrocytes. The QuickGO definition states that it is any process that activates or increases the frequency, rate or extent of oligodendrocyte apoptotic process. It is a positive regulatory term, meaning it does not describe the execution of apoptosis itself but rather the upstream signals, transcription factors, microRNAs and pharmacological agents that increase the likelihood or extent of oligodendrocyte apoptosis.
Why Is positive regulation of oligodendrocyte apoptotic process Important in Cell Biology?
GO:1900143 is important because oligodendrocyte apoptosis is a decisive event in central nervous system development and repair, and the positive regulators annotated to this term determine how many oligodendrocytes survive to myelinate axons. When positive regulation is excessive, myelin deficits and demyelinating pathology can result; when it is insufficient, surplus or dysfunctional oligodendrocyte lineage cells may persist. The term therefore provides a structured way to annotate genes, microRNAs and drugs that shift the survival-death balance in oligodendrocyte lineage cells, which is directly relevant to developmental biology, regenerative medicine and neuro-oncology.
• Defines the positive-regulatory arm of oligodendrocyte apoptosis, separating it from the apoptotic execution machinery itself.
• Links transcriptional elongation control by PAF1C and p-TEFb to oligodendrocyte differentiation and survival decisions.
• Provides an annotation framework for transcription factors such as SOX17 that block oligodendrocyte precursor differentiation and can indirectly affect apoptotic susceptibility.
• Connects microRNA regulation, including miR-219a-5p, to oligodendrogenesis and the survival of oligodendrocyte lineage cells.
• Supports mechanistic interpretation of p53-MDM2-targeted therapies such as navtemadlin in recurrent glioblastoma.
• Helps explain how chemogenetic activation of oligodendrocytes alters progenitor proliferation, maturation and the size of the apoptotic-susceptible pool.
• Guides CRISPR model design for causal testing of candidate positive regulators.
• Provides a vocabulary bridge between developmental myelination studies and disease-focused apoptosis research.
• Supports biomarker and target discovery in demyelinating and neurodegenerative disease research.
• Enables reproducible Gene Ontology-based enrichment analysis of oligodendrocyte death pathways.
What Happens During positive regulation of oligodendrocyte apoptotic process?
Initiation by differentiation-coupled transcriptional signals
In simple terms: When an oligodendrocyte precursor fails to differentiate properly, transcriptional signals can push it toward apoptosis.
Positive regulation of oligodendrocyte apoptotic process begins with signals that couple differentiation status to survival. The PAF1 complex and p-TEFb act antagonistically during oligodendrocyte differentiation, and perturbation of this balance alters the differentiation program that determines whether cells survive or die. Because differentiation and apoptosis are coordinated, factors that block precursor differentiation, such as SOX17, can shift cells into a state in which apoptotic elimination is more likely. In this initiation phase, the cell integrates transcriptional elongation signals, transcription factor activity and developmental cues before committing to apoptosis.
MicroRNA and post-transcriptional modulation
In simple terms: Small RNA molecules can raise or lower the threshold for oligodendrocyte death.
Post-transcriptional regulation by microRNAs modulates the sensitivity of oligodendrocyte lineage cells to apoptotic stimuli. Neutralization of nerve growth factor promotes oligodendrogenesis by increasing miR-219a-5p levels, linking a specific microRNA to the expansion and survival of oligodendrocyte lineage cells. Developmental profiling of microRNA expression in Schwann cells, the peripheral myelinating cells, provides a comparative framework for understanding how microRNA programs are deployed in myelinating lineages. Together, these studies indicate that microRNA networks can act upstream of the apoptotic decision and thereby contribute to positive or negative regulation of oligodendrocyte apoptosis.
Transcription factor control of precursor fate
In simple terms: Transcription factors decide whether precursor cells mature or are eliminated.
Transcription factors set the fate of oligodendrocyte precursor cells and thereby influence how many cells become susceptible to apoptosis. SOX17 negatively regulates oligodendrocyte precursor cell differentiation, and blocking differentiation can redirect precursors toward alternative fates or death. CREB5 promotes proliferation of neural stem and progenitor cells in the rat subventricular zone via regulation of NFIX expression, showing that CREB-family factors control the size of progenitor pools from which oligodendrocyte lineage cells arise. These findings place transcription factor networks upstream of the positive regulation of oligodendrocyte apoptotic process.
Pharmacological and p53-dependent modulation
In simple terms: Drugs that activate p53 can push oligodendrocyte lineage and tumor cells toward apoptosis.
The p53-MDM2 axis is a well-established regulator of apoptosis, and pharmacological MDM2 inhibition with navtemadlin engages this axis in patients with recurrent glioblastoma. A window-of-opportunity trial revealed mechanisms of response and resistance to navtemadlin, demonstrating that p53 pathway activation has measurable effects on cell death programs in neural lineage contexts. Because p53 activation can promote apoptosis in multiple cell types, MDM2 inhibitors provide a tractable experimental system for probing positive regulation of apoptotic processes in oligodendrocyte lineage cells.
Activity-dependent and chemogenetic modulation of the apoptotic pool
In simple terms: Changing oligodendrocyte activity changes how many precursors proliferate, mature or die.
Chemogenetic activation of oligodendrocytes delays postnatal myelination by promoting progenitor proliferation and inhibiting maturation. This manipulation changes the size and composition of the oligodendrocyte lineage pool, which in turn affects how many cells are subject to apoptotic regulation. The study illustrates that activity-dependent signals can indirectly modulate the positive regulation of oligodendrocyte apoptotic process by altering the number of cells that reach the apoptotic-susceptible stage.
Key Genes Involved in GO:1900143 positive regulation of oligodendrocyte apoptotic process
The following genes and proteins have been experimentally linked to oligodendrocyte lineage survival, differentiation and apoptotic regulation in the cited literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| PAF1C complex components | Transcriptional elongation control during oligodendrocyte differentiation | Antagonism with p-TEFb determines differentiation and survival outcomes |
| p-TEFb (CDK9/Cyclin T) | Transcriptional elongation kinase complex | Balances PAF1C activity to regulate oligodendrocyte differentiation |
| SOX17 | Negative regulator of oligodendrocyte precursor cell differentiation | Blocks differentiation and can shift precursors toward apoptotic susceptibility |
| miR-219a-5p | MicroRNA promoting oligodendrogenesis | Increased by NGF neutralization and linked to oligodendrocyte lineage expansion |
| NGF (nerve growth factor) | Neurotrophic factor whose neutralization raises miR-219a-5p | Modulates oligodendrogenesis and survival signaling |
| CREB5 | Promotes neural stem/progenitor proliferation via NFIX | Controls progenitor pool size upstream of oligodendrocyte lineage commitment |
| NFIX | Transcription factor regulated by CREB5 | Influences neural stem/progenitor proliferation in the subventricular zone |
| MDM2 | Negative regulator of p53 | Pharmacological target of navtemadlin in recurrent glioblastoma |
| TP53 | Tumor suppressor and apoptosis regulator | Central node in p53-dependent apoptotic responses |
| Navtemadlin (drug) | MDM2 inhibitor | Clinical tool for probing p53-dependent apoptosis in neural lineage cells |
| Dcx (chemogenetic marker context) | Activity-dependent modulation of oligodendrocytes | Chemogenetic activation delays myelination and alters progenitor dynamics |
| Oligodendrocyte lineage cells | Myelinating cells of the central nervous system | Target population for apoptosis regulation studies |
| Schwann cell microRNA program | Peripheral myelinating cell microRNA regulation | Comparative framework for myelinating lineage microRNA studies |
| Apelin/APJ system | Energy metabolism and water homeostasis regulator | Context for systemic metabolic influences on neural cell survival |
How Is positive regulation of oligodendrocyte apoptotic process Regulated?
Positive regulation of oligodendrocyte apoptotic process is controlled at multiple levels. Transcriptional elongation is a key node, because the PAF1 complex and p-TEFb act antagonistically during oligodendrocyte differentiation, and their balance influences whether cells complete differentiation or undergo apoptosis. Transcription factors such as SOX17 negatively regulate oligodendrocyte precursor cell differentiation, thereby indirectly shaping the apoptotic-susceptible pool. Post-transcriptional regulation by microRNAs, including miR-219a-5p, modulates oligodendrogenesis and survival signaling. At the pharmacological level, the p53-MDM2 axis can be engaged by MDM2 inhibitors such as navtemadlin, which activate p53-dependent apoptosis programs. Finally, activity-dependent and chemogenetic manipulations of oligodendrocytes alter progenitor proliferation and maturation, changing the number of cells subject to apoptotic regulation.
positive regulation of oligodendrocyte apoptotic process and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| MDM2 | Recurrent glioblastoma response and resistance to navtemadlin | Patient-derived glioblastoma cells with MDM2 inhibition and p53 readouts |
| TP53 | p53-dependent apoptosis in neural lineage cells | TP53 knockout and point-mutation isogenic cell lines |
| SOX17 | Oligodendrocyte precursor differentiation block | SOX17 overexpression and knockout in oligodendrocyte precursor cultures |
| miR-219a-5p | Oligodendrogenesis and oligodendrocyte lineage survival | microRNA mimic and inhibitor transfection in oligodendrocyte lineage cells |
| PAF1C / p-TEFb | Differentiation-coupled apoptotic regulation | Knockdown or knockout of PAF1C and p-TEFb components in differentiating oligodendrocytes |
Glioblastoma and p53-pathway therapeutics
Recurrent glioblastoma is treated with agents that engage the p53 pathway, and the MDM2 inhibitor navtemadlin has been evaluated in a window-of-opportunity trial that revealed mechanisms of response and resistance. Because p53 activation can promote apoptosis in neural lineage cells, positive regulation of oligodendrocyte apoptotic process is mechanistically relevant to understanding both tumor cell death and potential effects on normal oligodendrocyte lineage cells during therapy.
Demyelinating and developmental myelination disorders
Oligodendrocyte apoptosis is a normal developmental event that matches myelinating cell number to axonal demand, and perturbations of this balance can contribute to myelin deficits. Chemogenetic activation of oligodendrocytes delays postnatal myelination by promoting progenitor proliferation and inhibiting maturation, demonstrating that altering oligodendrocyte lineage dynamics has direct consequences for myelin formation. Genes that regulate differentiation, such as SOX17, can therefore influence disease-relevant myelination outcomes.
MicroRNA-linked oligodendrocyte dysfunction
MicroRNAs such as miR-219a-5p regulate oligodendrogenesis, and changes in their levels can alter the survival and expansion of oligodendrocyte lineage cells. Comparative studies of microRNA expression in Schwann cells provide additional context for how microRNA programs control myelinating lineages. Dysregulation of these programs may contribute to oligodendrocyte loss in neurological disease.
From positive regulation of oligodendrocyte apoptotic process-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is a candidate gene required for positive regulation of oligodendrocyte apoptosis? | CRISPR knockout in oligodendrocyte lineage cells followed by apoptosis assays |
| Does a specific point mutation alter apoptotic susceptibility? | CRISPR point-mutation knock-in of the variant and comparison with isogenic wild-type cells |
| Does a disease-associated variant change protein function? | Knock-in of the variant allele with functional and survival readouts |
| Where and when is the protein expressed during oligodendrocyte lineage progression? | Tagged knock-in with fluorescent or epitope tag and imaging |
| Does overexpression of a candidate gene increase oligodendrocyte apoptosis? | Doxycycline-inducible overexpression in oligodendrocyte precursor cells |
| Does pharmacological p53 activation modulate oligodendrocyte lineage apoptosis? | MDM2 inhibitor treatment of neural lineage cultures with apoptosis readouts |
How to Study the positive regulation of oligodendrocyte apoptotic process Process
| Method | What It Measures | Typical Application |
|---|---|---|
| RNA sequencing | Transcriptome changes during oligodendrocyte differentiation and apoptosis | Identifying positive regulators of oligodendrocyte apoptosis |
| microRNA profiling | Expression of microRNAs such as miR-219a-5p | Linking post-transcriptional regulators to oligodendrogenesis |
| Caspase activity assay | Apoptotic execution in oligodendrocyte lineage cells | Quantifying positive regulation of apoptosis |
| Viability and cell death staining | Frequency of dying cells under perturbation | Testing pharmacological modulators such as MDM2 inhibitors |
| Live-cell imaging | Progenitor proliferation, maturation and myelination dynamics | Connecting apoptotic regulation to myelination outcomes |
| Immunohistochemistry | Protein expression and localization in tissue | Validating candidate regulators in vivo |
| CRISPR knockout screening | Gene requirement for oligodendrocyte apoptosis | Identifying novel positive regulators |
| Pharmacological inhibition | Acute pathway modulation | Probing p53-dependent apoptosis with navtemadlin |
Transcriptional and transcriptomic profiling
RNA sequencing of oligodendrocyte lineage cells at different differentiation stages can identify transcriptional programs associated with positive regulation of apoptosis. Because PAF1C and p-TEFb control transcriptional elongation during oligodendrocyte differentiation, profiling of nascent transcripts and elongation factors helps define the regulatory network. Comparative microRNA profiling, as performed in Schwann cells, provides a complementary view of post-transcriptional regulation.
Apoptosis and survival assays
Apoptosis assays, including caspase activity measurements and viability staining, are used to quantify the frequency of oligodendrocyte death under different genetic or pharmacological conditions. These assays are essential for testing whether a candidate gene positively regulates oligodendrocyte apoptotic process. Pharmacological perturbation with MDM2 inhibitors provides a positive control for p53-dependent apoptosis.
Imaging of myelination and oligodendrocyte dynamics
Imaging approaches, including live-cell and tissue imaging, are used to track oligodendrocyte progenitor proliferation, maturation and myelination in vivo. Chemogenetic activation of oligodendrocytes has been combined with imaging to show delayed postnatal myelination and altered progenitor dynamics. These methods connect cellular apoptotic decisions to tissue-level myelination outcomes.
Pharmacological and genetic perturbation
Pharmacological tools such as navtemadlin allow acute modulation of the p53-MDM2 axis, while genetic tools such as CRISPR knockout and overexpression allow sustained perturbation of candidate regulators. Combining both approaches helps distinguish direct effects on apoptosis from indirect effects on differentiation and proliferation.
How CRISPR Can Be Used to Study GO:1900143 positive regulation of oligodendrocyte apoptotic process
Knockout
CRISPR knockout of candidate genes in oligodendrocyte lineage cells is used to test whether the gene is required for positive regulation of oligodendrocyte apoptotic process. For example, knocking out components of the PAF1 complex or p-TEFb alters oligodendrocyte differentiation and can change apoptotic outcomes. Knockout of transcription factors such as SOX17 can also shift precursor differentiation and survival.
Point Mutation
CRISPR point-mutation knock-in allows precise testing of disease-associated or functional variants in genes linked to oligodendrocyte apoptosis. Isogenic cell lines carrying a specific point mutation can be compared with wild-type cells to determine whether the variant alters apoptotic susceptibility. This approach is particularly useful for dissecting p53-pathway variants relevant to MDM2 inhibitor response.
Knock-in
Knock-in of reporter tags or disease alleles enables tracking of protein expression and function during oligodendrocyte lineage progression. Tagged knock-in models can reveal when and where a candidate regulator is expressed relative to apoptotic events. Knock-in of microRNA target sites or regulatory elements can also test post-transcriptional control mechanisms.
Overexpression
Overexpression of candidate genes in oligodendrocyte precursor cells tests whether increased dosage is sufficient to promote apoptosis. Inducible overexpression systems allow temporal control, which is important because differentiation stage influences apoptotic susceptibility. Overexpression of microRNAs such as miR-219a-5p can also be used to probe post-transcriptional regulation of oligodendrogenesis.
How EDITGENE Supports positive regulation of oligodendrocyte apoptotic process Research
Researchers studying positive regulation of oligodendrocyte apoptotic process-related genes often need to determine whether a candidate gene is causally involved in oligodendrocyte death, differentiation or survival. Observational expression data alone cannot establish causality, so isogenic CRISPR models are typically required to link a specific gene or variant to the apoptotic phenotype. EDITGENE provides the full range of CRISPR cell model services needed to build and validate such causal models.
Contact EDITGENE today to design your custom CRISPR model for positive regulation of oligodendrocyte apoptotic process research.
Frequently Asked Questions About positive regulation of oligodendrocyte apoptotic process
What is GO:1900143 positive regulation of oligodendrocyte apoptotic process?
GO:1900143 is a Gene Ontology biological_process term defined as any process that activates or increases the frequency, rate or extent of oligodendrocyte apoptotic process.
What genes are involved in positive regulation of oligodendrocyte apoptotic process?
Genes and proteins linked to this process include PAF1C and p-TEFb components, SOX17, miR-219a-5p, CREB5, NFIX, MDM2 and TP53.
How is oligodendrocyte apoptosis regulated during development?
Oligodendrocyte apoptosis is coupled to differentiation, and transcriptional elongation complexes such as PAF1C and p-TEFb act antagonistically to control differentiation and survival decisions.
What is the role of p53 in oligodendrocyte apoptosis?
The p53-MDM2 axis regulates apoptosis, and MDM2 inhibition with navtemadlin engages p53-dependent cell death programs in recurrent glioblastoma.
Which microRNAs regulate oligodendrocyte survival?
miR-219a-5p is increased by nerve growth factor neutralization and promotes oligodendrogenesis, linking microRNA regulation to oligodendrocyte lineage survival.
How do transcription factors affect oligodendrocyte precursor apoptosis?
SOX17 negatively regulates oligodendrocyte precursor cell differentiation, and blocking differentiation can shift precursors toward apoptotic susceptibility.
Can chemogenetic activation of oligodendrocytes affect myelination?
Yes, chemogenetic activation of oligodendrocytes delays postnatal myelination by promoting progenitor proliferation and inhibiting maturation.
What research methods are used to study positive regulation of oligodendrocyte apoptotic process?
Common methods include RNA sequencing, microRNA profiling, caspase activity assays, viability staining, live-cell imaging and CRISPR knockout screening.
How are CRISPR models used to study oligodendrocyte apoptosis?
CRISPR knockout, point-mutation, knock-in and overexpression models allow causal testing of whether a candidate gene positively regulates oligodendrocyte apoptosis.
Why is positive regulation of oligodendrocyte apoptotic process important for disease research?
It is relevant to glioblastoma therapy response, demyelinating conditions and developmental myelination disorders, where oligodendrocyte survival decisions affect myelin integrity.
Conclusion
GO:1900143 positive regulation of oligodendrocyte apoptotic process provides a precise Gene Ontology framework for annotating the signals, transcription factors, microRNAs and pharmacological agents that increase oligodendrocyte death. Experimental evidence links this process to transcriptional elongation control by PAF1C and p-TEFb, transcription factor regulation by SOX17 and CREB5, microRNA modulation by miR-219a-5p, and p53-pathway engagement by MDM2 inhibitors such as navtemadlin. Because oligodendrocyte apoptosis shapes developmental myelination and is relevant to neurological disease and neuro-oncology, causal models are essential for moving from correlation to mechanism. CRISPR knockout, point-mutation, knock-in and overexpression cell models, combined with transcriptomic, imaging and pharmacological methods, provide the experimental toolkit needed to dissect this pathway.
References
- 1. Kim S et al.. 2012. Antagonistic regulation of PAF1C and p-TEFb is required for oligodendrocyte differentiation.. J Neurosci 32(24):8201-7 PMID: 22699901
- 2. Rendo V et al.. 2025. A window-of-opportunity trial reveals mechanisms of response and resistance to navtemadlin in patients with recurrent glioblastoma.. Sci Transl Med 17(786):eadn6274 PMID: 39970230
- 3. Cheli VT et al.. 2026. Chemogenetic Activation of Oligodendrocytes Delays Postnatal Myelination by Promoting Progenitor Proliferation and Inhibiting Maturation.. Glia 74(2):e70094 PMID: 41102947
- 4. Fauveau M et al.. 2018. SOX17 transcription factor negatively regulates oligodendrocyte precursor cell differentiation.. Glia 66(10):2221-2232 PMID: 30152028
- 5. Brandi R et al.. 2021. Nerve Growth Factor Neutralization Promotes Oligodendrogenesis by Increasing miR-219a-5p Levels.. Cells 10(2) PMID: 33669304
- 6. Yu T et al.. 2025. CREB5 Promotes the Proliferation of Neural Stem/Progenitor Cells in the Rat Subventricular Zone via the Regulation of NFIX Expression.. Cells 14(16) PMID: 40862718
- 7. Gokey NG et al.. 2012. Developmental regulation of microRNA expression in Schwann cells.. Mol Cell Biol 32(2):558-68 PMID: 22064487
- 8. Hu G et al.. 2021. The Role of Apelin/Apelin Receptor in Energy Metabolism and Water Homeostasis: A Comprehensive Narrative Review.. Front Physiol 12:632886 PMID: 33679444
