GO:0045663 positive regulation of myoblast differentiation: Signaling Mechanisms, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0045663 (positive regulation of myoblast differentiation) describes any process that activates or increases the frequency, rate or extent of myoblast differentiation, the transition of mononucleate myoblasts toward fusion-competent myocytes that form myotubes and skeletal muscle fibers.
• Positive regulation is achieved by secreted and intracellular signals, including sialidase-mediated ganglioside remodeling, microRNA networks such as miR-27a, and kinase feedback loops such as Akt2-MyoD.
• The process is conserved from fish to mammals: medaka Neu3b sialidase positively regulates myoblast differentiation through ganglioside desialylation, while in mammals Disabled-2 promotes early myoblast differentiation.
• Ubiquitin-proteasome and Wnt/β-catenin signaling intersect with myoblast differentiation; RNF138 modulates skeletal muscle differentiation via Wnt/β-catenin, and SOCS2 regulates Hu sheep myoblast differentiation through STAT3/PSMB9.
• Myoblast differentiation is a tractable experimental system: C2C12 myoblasts are widely used, and C2C12-derived exosomes can be engineered to carry therapeutic miRNAs such as miR-92a-3p.
• CRISPR knockout, point mutation, knock-in and overexpression models allow causal testing of candidate positive regulators in myoblast differentiation and muscle regeneration [1,2,6].
Description
GO:0045663, positive regulation of myoblast differentiation, is a biological process term that captures any signal or molecular event that activates or increases the frequency, rate or extent of myoblast differentiation. Myoblasts are mononucleate muscle precursor cells that withdraw from the cell cycle, express muscle-specific transcription factors, and ultimately fuse into multinucleated myotubes that mature into skeletal muscle fibers. Because the size and regenerative capacity of skeletal muscle depend on the efficiency of this transition, positive regulators of myoblast differentiation are central to developmental biology, regenerative medicine, and the study of muscle-wasting conditions [6,7]. Mechanistically, positive regulation is not a single pathway but a convergence of extracellular cues, intracellular signaling cascades, microRNAs, and metabolic enzymes. For example, the medaka sialidase Neu3b positively regulates myoblast differentiation by desialylating gangliosides, while in mammals the endocytic adaptor Disabled-2 acts as a positive regulator of early myoblast differentiation. MicroRNA-27a has been shown to play a role in myoblast differentiation, and a positive feedback loop between Akt2 and MyoD reinforces the differentiated state. More recently, SOCS2 was reported to regulate Hu sheep myoblast differentiation via the STAT3/PSMB9 pathway, and RNF138 was shown to regulate skeletal muscle differentiation through Wnt/β-catenin signaling. For researchers, GO:0045663 provides a standardized annotation target for functional genomics, CRISPR screens, and transcriptomic or proteomic studies of muscle biology. Understanding which genes positively regulate myoblast differentiation, and how, informs the design of cell models for muscle disease, the interpretation of single-cell muscle atlases, and the development of exosome- or miRNA-based interventions, such as C2C12-derived exosomes acting through miR-92a-3p/PTEN/AKT signaling. This article summarizes the definition, mechanisms, key genes, disease links, and experimental methods relevant to GO:0045663.
positive regulation of myoblast differentiation At A Glance
| GO ID | GO:0045663 |
|---|---|
| GO term | positive regulation of myoblast differentiation |
| Ontology | biological_process |
| Definition | Any process that activates or increases the frequency, rate or extent of myoblast differentiation; a myoblast is a mononucleate cell that fuses with other myoblasts to form myotubes that develop into skeletal muscle fibers. |
| Synonyms | activation of myoblast differentiation; stimulation of myoblast differentiation; up regulation of myoblast differentiation; up-regulation of myoblast differentiation; upregulation of myoblast differentiation |
| Major function | Promotes the transition of mononucleate myoblasts into fusion-competent myocytes and multinucleated myotubes during skeletal muscle development and regeneration. |
| Biological context | Skeletal muscle development, postnatal muscle growth, and muscle regeneration after injury. |
| Representative positive regulators | Neu3b sialidase, Disabled-2, microRNA-27a, Akt2-MyoD feedback, SOCS2-STAT3/PSMB9, RNF138-Wnt/β-catenin. |
| Experimental models | C2C12 myoblasts, primary myoblasts, and exosome-based systems such as C2C12-derived exosomes. |
What Is GO:0045663?
GO:0045663 is defined by QuickGO as any process that activates or increases the frequency, rate or extent of myoblast differentiation. A myoblast is a mononucleate cell type that, by fusion with other myoblasts, gives rise to the myotubes that eventually develop into skeletal muscle fibers. In practical terms, annotating a gene or treatment to GO:0045663 means that experimental evidence shows enhanced myoblast differentiation, for example increased expression of myogenic markers, increased fusion index, or accelerated formation of multinucleated myotubes [4,6,8].
Why Is positive regulation of myoblast differentiation Important in Cell Biology?
Positive regulation of myoblast differentiation is fundamental to building and repairing skeletal muscle. Defects in the timing or efficiency of myoblast differentiation contribute to impaired muscle regeneration, muscle atrophy, and congenital myopathies, whereas excessive or misregulated differentiation can deplete the muscle stem cell pool [6,7]. Because the process is controlled by diverse and druggable nodes, including sialidases, microRNAs, kinases, ubiquitin-related factors, and cytokine signaling, it offers multiple entry points for therapeutic intervention. Standardized annotation to GO:0045663 also enables computational biologists to compare muscle differentiation programs across species and datasets, and helps experimentalists choose validated positive regulators as controls or targets in CRISPR screens.
• Skeletal muscle development depends on timely myoblast differentiation and fusion into myotubes.
• Muscle regeneration after injury requires activation, proliferation, and subsequent differentiation of myogenic precursors.
• Positive regulators such as Disabled-2 control the early steps of myoblast differentiation and are required for normal myotube formation.
• MicroRNA-27a is involved in myoblast differentiation, illustrating post-transcriptional control of this process.
• The Akt2-MyoD positive feedback loop reinforces the differentiated muscle phenotype and links metabolism to myogenesis.
• Sialidase-mediated ganglioside desialylation by Neu3b positively regulates myoblast differentiation, showing a role for glycosphingolipid remodeling.
• SOCS2 modulates myoblast differentiation via STAT3/PSMB9, connecting cytokine signaling and proteasome function to muscle cell fate.
• RNF138 regulates skeletal muscle differentiation through Wnt/β-catenin signaling, linking ubiquitin-related processes to myogenesis.
• C2C12-derived exosomes can modulate bone and muscle-related signaling through miR-92a-3p/PTEN/AKT, highlighting crosstalk between muscle and other tissues.
• GO:0045663 provides a standardized annotation for functional genomics and CRISPR screening in muscle biology [1,2,6].
What Happens During positive regulation of myoblast differentiation?
Initiation of myogenic commitment
In simple terms: This is the step where muscle precursor cells decide to become muscle.
Positive regulation of myoblast differentiation begins with signals that commit mononucleate myoblasts to the myogenic program. Disabled-2 acts as a positive regulator of early myoblast differentiation, promoting the initial steps that precede fusion. At the transcriptional level, myogenic factors such as MyoD are stabilized and amplified; a positive feedback loop between Akt2 and MyoD reinforces this commitment and sustains the differentiated state. Extracellular cues, including ganglioside remodeling by sialidases, can also bias cells toward differentiation.
Transcriptional amplification of the myogenic program
In simple terms: Once cells commit, they switch on a set of muscle genes that lock in the muscle identity.
After commitment, positive regulators increase the frequency and extent of differentiation by amplifying myogenic transcription. The Akt2-MyoD feedback loop is a clear example: Akt2 promotes MyoD activity, and MyoD in turn supports Akt2 expression, creating a self-reinforcing circuit. MicroRNAs such as miR-27a participate in this stage by modulating the availability of transcripts that either promote or restrain differentiation. In Hu sheep myoblasts, SOCS2 influences differentiation through STAT3 and PSMB9, indicating that cytokine signaling and proteasome-related processes can tune the transcriptional output.
Membrane remodeling and fusion competence
In simple terms: Cells change their surface so they can stick to and fuse with neighboring muscle cells.
A critical step in positive regulation is the acquisition of fusion competence. Sialidase Neu3b in medaka positively regulates myoblast differentiation by desialylating gangliosides, which alters membrane glycolipid composition and facilitates the fusion reaction. The myoblast fusion reaction itself is a tightly regulated process that requires recognition, adhesion, and membrane merger events, and positive regulators act at these steps to increase the rate and extent of myotube formation. Disabled-2 also contributes to early differentiation events that set the stage for fusion.
Signaling integration and feedback
In simple terms: Multiple signals are combined so that differentiation proceeds only when conditions are right.
Positive regulation of myoblast differentiation integrates several signaling pathways. RNF138 regulates skeletal muscle differentiation via Wnt/β-catenin signaling, showing that ubiquitin-related modulation of a canonical developmental pathway can promote differentiation. SOCS2 acts through STAT3/PSMB9, linking cytokine signaling and proteasomal activity to the differentiation program. The Akt2-MyoD loop provides positive feedback that stabilizes the differentiated state. These examples illustrate that GO:0045663 encompasses diverse molecular mechanisms that converge on increased differentiation efficiency.
Myotube formation and maturation
In simple terms: The final step is the creation of long, multinucleated muscle fibers.
The endpoint of positive regulation is the formation of myotubes, which eventually develop into skeletal muscle fibers. Increased differentiation frequency or rate manifests as larger, more numerous myotubes and higher expression of late myogenic markers. Experimental systems such as C2C12 myoblasts are commonly used to quantify this endpoint, and C2C12-derived exosomes can carry signals such as miR-92a-3p that influence related pathways. Positive regulators identified in fish, sheep, and mammalian cells all converge on this morphological outcome [1,2,4,6,8].
Key Genes Involved in GO:0045663 positive regulation of myoblast differentiation
The following genes and proteins have been experimentally linked to positive regulation of myoblast differentiation or closely related myogenic processes in the cited literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| Neu3b | Sialidase that desialylates gangliosides and positively regulates myoblast differentiation in medaka | Model for glycosphingolipid control of muscle differentiation; conserved sialidase biology |
| DAB2 (Disabled-2) | Positive regulator of early myoblast differentiation | Endocytic adaptor linking membrane trafficking to myogenic commitment |
| miR-27a | MicroRNA with a role in myoblast differentiation | Post-transcriptional regulator; candidate for miRNA-based modulation |
| AKT2 | Kinase in a positive feedback loop with MyoD during muscle differentiation | Links metabolism and survival signaling to myogenic transcription |
| MYOD1 | Myogenic transcription factor that participates in Akt2-MyoD feedback | Core myogenic determination factor; benchmark for differentiation assays |
| SOCS2 | Regulates Hu sheep myoblast differentiation via STAT3/PSMB9 | Connects cytokine signaling and proteasome function to myogenesis |
| STAT3 | Transcription factor in the SOCS2-STAT3/PSMB9 axis | Signal transducer modulating myoblast differentiation |
| PSMB9 | Proteasome subunit implicated in SOCS2-dependent myoblast differentiation | Links proteostasis to muscle cell differentiation |
| RNF138 | Regulates skeletal muscle differentiation via Wnt/β-catenin signaling | Ubiquitin-related modulator of a canonical developmental pathway |
| CTNNB1 (β-catenin) | Effector of Wnt signaling through which RNF138 regulates differentiation | Central node in Wnt-dependent myogenesis |
| PTEN | Target of miR-92a-3p in C2C12-derived exosome studies | Phosphatase controlling AKT signaling in muscle-related contexts |
| AKT (AKT1/AKT2) | Kinase pathway modulated by miR-92a-3p/PTEN in C2C12 exosome studies | Central survival and differentiation signaling node |
| Myogenin (MYOG) | Downstream myogenic marker typically assessed in differentiation assays [6,8] | Readout of differentiation progression |
| MyHC (MYH) | Late myogenic marker used to quantify myotube formation [6,8] | Endpoint marker for fusion and maturation |
| miR-92a-3p | Exosomal microRNA acting through PTEN/AKT in C2C12-derived exosomes | Candidate therapeutic cargo for muscle-bone crosstalk |
| C2C12 myoblasts | Common cell model for studying positive regulation of myoblast differentiation | Standard in vitro system for KO, overexpression, and imaging |
| Hu sheep myoblasts | Primary myoblast model used to study SOCS2-STAT3/PSMB9 | Relevant for livestock muscle growth and comparative biology |
| Medaka myoblasts | Model system for Neu3b sialidase function in differentiation | Comparative developmental model for sialidase-dependent myogenesis |
How Is positive regulation of myoblast differentiation Regulated?
Positive regulation of myoblast differentiation is controlled by multiple layers of regulation. At the signaling level, the Akt2-MyoD positive feedback loop ensures that once differentiation begins, it is reinforced and maintained. Wnt/β-catenin signaling is modulated by RNF138, which regulates skeletal muscle differentiation and can influence the balance between proliferation and differentiation. Cytokine signaling through SOCS2 and STAT3, coupled to the proteasome subunit PSMB9, provides another regulatory axis in myoblasts. Post-transcriptional control by microRNAs such as miR-27a adds further tuning, and glycosphingolipid remodeling by sialidases such as Neu3b can act as a positive regulatory input at the membrane. Exosome-mediated communication, exemplified by C2C12-derived exosomes acting through miR-92a-3p/PTEN/AKT, represents an additional layer by which extracellular vesicles can influence muscle-related signaling. Together, these mechanisms determine the frequency, rate, and extent of myoblast differentiation.
positive regulation of myoblast differentiation and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| DAB2 | Impaired early myoblast differentiation; muscle regeneration defects | DAB2 knockout and rescue in C2C12 myoblasts |
| RNF138 | Skeletal muscle differentiation defects via Wnt/β-catenin | RNF138 knockout and point-mutation myoblast lines |
| SOCS2 | Altered myoblast differentiation via STAT3/PSMB9 | SOCS2 overexpression and knockout in primary myoblasts |
| AKT2 | Metabolic and differentiation signaling in muscle | AKT2 knockout and knock-in C2C12 models |
| PTEN | Muscle-bone crosstalk; osteoporosis-related signaling | PTEN knockout and miR-92a-3p mimic studies in C2C12 |
Impaired muscle regeneration and atrophy
Efficient myoblast differentiation is required for skeletal muscle regeneration after injury, and positive regulators such as Disabled-2 promote the early steps of this process. When positive regulation is insufficient, myotube formation is reduced, which can contribute to muscle atrophy and poor recovery. The myoblast fusion reaction itself is essential for muscle development, regeneration, and adaptations, and its dysregulation is linked to muscle pathology. Studying GO:0045663 helps identify nodes that could be targeted to enhance regeneration.
Muscle-bone crosstalk and osteoporosis
C2C12-derived exosomes have been shown to exert therapeutic effects on glucocorticoid-induced osteoporosis through the miR-92a-3p/PTEN/AKT signaling pathway. This illustrates that factors associated with myoblast biology can influence bone homeostasis, and that exosomal cargo from muscle cells may be harnessed for therapeutic purposes. Positive regulation of myoblast differentiation is therefore relevant not only to muscle disease but also to musculoskeletal crosstalk.
Cancer cachexia and metabolic stress
Signaling pathways that positively regulate myoblast differentiation, such as Akt2-MyoD feedback and SOCS2-STAT3/PSMB9, intersect with metabolic and inflammatory signaling that is often perturbed in cancer cachexia. Although direct evidence linking GO:0045663 to cachexia requires further study, the molecular nodes identified in myoblast models provide candidate mechanisms for muscle wasting in systemic disease.
Congenital and genetic muscle disorders
Because myoblast differentiation and fusion are fundamental to skeletal muscle formation, genetic defects that impair positive regulation can contribute to congenital myopathies and other muscle disorders. Model organisms such as medaka have revealed conserved requirements for sialidase activity in myoblast differentiation, suggesting that similar mechanisms may be relevant to human muscle disease. Functional annotation to GO:0045663 aids in prioritizing candidate genes from patient sequencing data.
From positive regulation of myoblast differentiation-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is a candidate gene required for myoblast differentiation? | CRISPR knockout in C2C12 myoblasts followed by differentiation assays |
| Does a specific amino acid change alter positive regulatory activity? | Point-mutation knock-in in myoblasts |
| Does a disease-associated variant affect myotube formation? | Knock-in of the variant into the endogenous locus in C2C12 cells |
| Where and when is the protein expressed during differentiation? | Tagged knock-in (e.g., fluorescent or epitope tag) and imaging |
| Does increased dosage of a candidate gene enhance differentiation? | Overexpression of the gene in myoblasts |
| Can exosomal cargo modulate differentiation-related signaling? | C2C12-derived exosome treatment of target cells |
How to Study the positive regulation of myoblast differentiation Process
| Method | What It Measures | Typical Application |
|---|---|---|
| RNA-seq | Global transcript changes during differentiation | Identify positive regulators and downstream targets |
| Western blot | Protein levels and activation of signaling nodes | Assess Akt2-MyoD feedback and myogenic markers |
| Immunofluorescence | Myotube formation and fusion index | Quantify positive regulation of differentiation |
| CRISPR knockout | Loss-of-function effects on differentiation | Test requirement for candidate genes |
| Overexpression | Gain-of-function effects on differentiation | Test sufficiency of candidate genes |
| Exosome isolation and treatment | Extracellular vesicle-mediated signaling | Study C2C12-derived exosome effects |
| Proteasome activity assay | Proteolytic capacity linked to PSMB9 | Investigate SOCS2-STAT3/PSMB9 axis |
| Live-cell imaging | Dynamics of myoblast fusion | Resolve fusion reaction steps |
Transcriptomic profiling of differentiation
RNA sequencing of myoblasts before and after induction of differentiation can identify genes whose expression correlates with positive regulation of myoblast differentiation. This approach is useful for validating candidates such as SOCS2 and its downstream STAT3/PSMB9 axis, and for comparing wild-type and knockout cells. Time-course designs capture the transition from proliferation to fusion-competent myocytes.
Protein and phosphoprotein analysis
Western blotting and phosphoproteomics can measure the activation state of signaling nodes such as Akt and MyoD, which form a positive feedback loop during muscle differentiation. Proteasome-related proteins such as PSMB9 can also be monitored in the context of SOCS2 regulation. These methods complement transcriptomic data by capturing post-translational regulation.
Imaging of fusion and myotube formation
Immunofluorescence for myogenic markers such as myogenin and myosin heavy chain allows quantification of differentiation and fusion indices. This is a direct readout of positive regulation of myoblast differentiation and is widely used in C2C12 studies [6,8]. Live-cell imaging can further resolve the dynamics of myoblast fusion.
Functional perturbation with CRISPR and overexpression
CRISPR knockout, point mutation, knock-in, and overexpression enable causal testing of candidate positive regulators. For example, RNF138 has been studied using loss-of-function approaches in the context of Wnt/β-catenin signaling, and overexpression of Akt2 or MyoD can enhance differentiation. These perturbation methods are essential for moving from correlation to causation.
How CRISPR Can Be Used to Study GO:0045663 positive regulation of myoblast differentiation
Knockout
CRISPR knockout of candidate positive regulators in myoblasts can determine whether a gene is required for differentiation. For example, knocking out RNF138 or DAB2 would test their roles in skeletal muscle differentiation and early myoblast differentiation, respectively [2,6]. Knockout models are also useful for validating hits from screens and for identifying compensatory pathways.
Point Mutation
Point mutations can be introduced to dissect domain-specific functions of positive regulators. For instance, mutating residues in RNF138 or Akt2 could reveal which domains are required for Wnt/β-catenin or Akt2-MyoD signaling during differentiation [2,8]. Point-mutation models are valuable for studying disease-associated variants.
Knock-in
Knock-in of tags or reporters allows visualization and quantification of positive regulators in live myoblasts. Tagged knock-in of myogenic factors or signaling proteins can reveal their localization and dynamics during differentiation. Knock-in of disease variants can also model their impact on myotube formation.
Overexpression
Overexpression of candidate genes can test whether increased dosage is sufficient to enhance myoblast differentiation. Overexpression of Akt2 or MyoD has been used to study the positive feedback loop that reinforces muscle differentiation. Overexpression of SOCS2 or its downstream effectors can similarly probe the STAT3/PSMB9 axis.
How EDITGENE Supports positive regulation of myoblast differentiation Research
Researchers studying positive regulation of myoblast differentiation-related genes often need to determine whether a candidate gene is causally involved in the differentiation process, and CRISPR-based models provide the most direct way to test this. EDITGENE offers a suite of services to generate and characterize such models in myoblast and other cell systems.
Contact EDITGENE today to design your custom CRISPR model for positive regulation of myoblast differentiation research.
Frequently Asked Questions About positive regulation of myoblast differentiation
What is GO:0045663?
GO:0045663 is the Gene Ontology term for positive regulation of myoblast differentiation, defined as any process that activates or increases the frequency, rate or extent of myoblast differentiation, where myoblasts fuse to form myotubes that develop into skeletal muscle fibers.
What genes are involved in positive regulation of myoblast differentiation?
Genes and factors experimentally linked to this process include Neu3b sialidase, Disabled-2 (DAB2), microRNA-27a, Akt2 and MyoD, SOCS2 with STAT3/PSMB9, and RNF138 with Wnt/β-catenin signaling.
How is myoblast differentiation positively regulated?
Positive regulation occurs through transcriptional amplification of the myogenic program, membrane remodeling for fusion competence, and signaling feedback loops such as Akt2-MyoD, as well as modulation by microRNAs and sialidases [4,5,8].
What is the role of Akt2 in myoblast differentiation?
Akt2 participates in a positive feedback loop with MyoD during muscle differentiation, reinforcing the differentiated state.
How does Disabled-2 affect myoblasts?
Disabled-2 acts as a positive regulator of early myoblast differentiation, promoting the initial steps of the differentiation program.
What is the role of microRNA-27a in myoblast differentiation?
MicroRNA-27a has been reported to play a role in myoblast differentiation, illustrating post-transcriptional control of this process.
How does SOCS2 regulate myoblast differentiation?
SOCS2 regulates Hu sheep myoblast differentiation via the STAT3/PSMB9 pathway, linking cytokine signaling and proteasome function to myogenesis.
What is the connection between RNF138 and muscle differentiation?
RNF138 regulates skeletal muscle differentiation through the Wnt/β-catenin signaling pathway.
Can exosomes influence myoblast differentiation?
C2C12-derived exosomes have been shown to act through miR-92a-3p/PTEN/AKT signaling, indicating that exosomal cargo can modulate muscle-related pathways.
What methods are used to study positive regulation of myoblast differentiation?
Common methods include RNA-seq, western blotting, immunofluorescence for myotube formation, CRISPR knockout and overexpression, exosome treatment, and live-cell imaging of fusion [1,2,3,6,7,8].
Conclusion
GO:0045663, positive regulation of myoblast differentiation, is a central biological process for skeletal muscle development and regeneration. Research across fish, sheep, and mammalian cell models has identified diverse positive regulators, including sialidases, endocytic adaptors, microRNAs, kinases, and ubiquitin-related proteins [1,2,4,5,6,8]. These findings provide a rich set of candidate genes and pathways for functional studies. CRISPR-based knockout, point-mutation, knock-in, and overexpression models, combined with transcriptomic, proteomic, and imaging methods, offer a rigorous path to establish causality and to translate these insights into therapeutic strategies for muscle disease and musculoskeletal crosstalk [1,2,3,6,8].
References
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- 2. Wang W et al.. 2025. RNF138 regulates skeletal muscle differentiation via the Wnt/β-catenin signaling pathway.. Theranostics 15(10):4446-4464 PMID: 40225576
- 3. Xu N et al.. 2023. Therapeutic Effects of Mechanical Stress-Induced C2C12-Derived Exosomes on Glucocorticoid-Induced Osteoporosis Through miR-92a-3p/PTEN/AKT Signaling Pathway.. Int J Nanomedicine 18:7583-7603 PMID: 38106447
- 4. Shiozaki K et al.. 2016. Positive regulation of myoblast differentiation by medaka Neu3b sialidase through gangliosides desialylation.. Biochimie 123:65-72 PMID: 26805383
- 5. Chen X et al.. 2014. Role of microRNA-27a in myoblast differentiation.. Cell Biol Int 38(2):266-71 PMID: 24123794
- 6. Shang N et al.. 2020. Disabled-2: a positive regulator of the early differentiation of myoblasts.. Cell Tissue Res 381(3):493-508 PMID: 32607799
- 7. Millay DP. 2022. Regulation of the myoblast fusion reaction for muscle development, regeneration, and adaptations.. Exp Cell Res 415(2):113134 PMID: 35367215
- 8. Kaneko S et al.. 2002. Positive feedback regulation between Akt2 and MyoD during muscle differentiation. Cloning of Akt2 promoter.. J Biol Chem 277(26):23230-5 PMID: 11948187
