MEF2C Antibodies

Structure of MEF2C

MEF2C is a transcription factor with a molecular weight of approximately 53 kDa, and its precise molecular weight varies slightly among different species due to differences in amino acid composition. This protein is composed of 467 amino acids and has typical MADS-box and MEF2 domains, forming a functional dimer structure. Its tertiary structure shows a highly conserved DNA binding interface, mainly binding to the CAT sequence in the promoter of the target gene through an α -helix. The key residues include basic amino acids that directly interact with DNA, as well as hydrophobic residues that mediate cofactor binding. The nuclear localization signal (NLS) of this protein is located at the carboxyl terminus and is crucial for its transcriptional activation function.

The activity of this protein is regulated by phosphorylation, and key phosphorylation sites (such as Ser396) affect its nuclear translocation and transcriptional activity. Mutations often occur in its DNA binding region, leading to neurodevelopmental disorders and congenital heart disease.

Fig. 1 Schematic overview of MEF2C activity in muscle cells.¹

Key structural properties of MEF2C:

• N-terminal MADS-box and MEF2 domains jointly mediate DNA binding and dimerization
• The C-terminal transcriptional activation domain is rich in proline, serine and glutamic acid residues
• Conserved nuclear localization signaling (NLS) ensures that proteins are located within the cell nucleus

Functions of MEF2C

The core function of the MEF2C gene-encoded protein is to regulate the development and differentiation of muscle and nerve cells. In addition, it is also involved in a variety of physiological and pathological processes, including heart formation, synaptic plasticity and inflammatory responses.

MEF2C activates or inhibits the transcription of target genes by binding to conserved DNA sequences (C/TTA(A/T)4TAG/A) and recruiting histone modification enzymes (such as p300, HDACs), and its activity is regulated by multi-level phosphorylation such as the MAPK signaling pathway.

Applications of MEF2C and MEF2C Antibody in Literature

1. Wang, Shanshan, et al. "MEF 2 C Alleviates Postoperative Cognitive Dysfunction by Repressing Ferroptosis." CNS Neuroscience & Therapeutics 30.10 (2024): e70066. https://doi.org/10.1111/cns.70066

This study explores the mechanism by which the transcription factor MEF2C inhibits ferroptosis by regulating the transcription of GPX4, thereby improving postoperative cognitive dysfunction. Experiments have shown that the decreased expression of MEF2C in the hippocampus can promote lipid peroxidation and iron accumulation, while its overexpression can alleviate cognitive impairment, providing a new target for the treatment of POCD.

2. Zhang, Zhikun, and Yongxiang Zhao. "Progress on the roles of MEF2C in neuropsychiatric diseases." Molecular brain 15.1 (2022): 8. https://doi.org/10.1186/s13041-021-00892-6

The article indicates that MEF2C is a MADS-BOX family transcription factor and plays a key role in embryonic and postnatal brain development, neuronal differentiation and synaptic formation. This article reviews the regulation of gene expression by MEF2C through alternative splicing and post-translational modification, as well as its relationship with the pathogenesis of neuropsychiatric disorders such as autism, epilepsy, and Alzheimer's disease.

3. Ward, Claire, Lucas Sjulson, and Renata Batista-Brito. "The function of Mef2c toward the development of excitatory and inhibitory cortical neurons." Frontiers in Cellular Neuroscience 18 (2024): 1465821. https://doi.org/10.3389/fncel.2024.1465821

The article indicates that MEF2C is a common risk gene for neurodevelopmental disorders (NDDs), influencing the assembly of cerebral cortex circuits and the excitation/inhibition balance. This article takes the loss of MEF2C function as an example to explore the mechanism by which it leads to abnormal brain connections and various NDDs behavioral disorders through regulating gene programs during the critical perinatal period.

4. Piasecka, Agnieszka, et al. "MEF2C shapes the microtranscriptome during differentiation of skeletal muscles." Scientific Reports 11.1 (2021): 3476. https://doi.org/10.1038/s41598-021-82706-2

The article indicates that MEF2C is a key transcription factor regulating muscle differentiation. Research has found that the deletion of MEF2C not only affects the transcription of multiple muscle-specific mirnas but also alters the 3' -terminal oligosylation modification of mirnas, thereby regulating the stability and expression dynamics of the microRNA group and playing an important dual quality regulatory role in muscle cell differentiation.

5. Canté-Barrett, Kirsten, et al. "MEF2C opposes Notch in lymphoid lineage decision and drives leukemia in the thymus." JCI insight 7.13 (2022): e150363. https://doi.org/10.1172/jci.insight.150363

The article indicates that abnormally high expression of MEF2C can impede the differentiation of early thymocyte T lines and promote the occurrence of B-line programmed and biphenotypic lymphocyte tumors. SIK inhibitors (such as dasatinib) can inhibit MEF2C activity, relieve T cell development arrest and enhance sensitivity to glucocorticoids, providing a new strategy for the treatment of ETP-ALL.

Creative Biolabs: MEF2C Antibodies for Research

Creative Biolabs specializes in the production of high-quality MEF2C antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

• Custom MEF2C Antibody Development: Tailor-made solutions to meet specific research requirements.
• Bulk Production: Large-scale antibody manufacturing for industry partners.
• Technical Support: Expert consultation for protocol optimization and troubleshooting.
• Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our MEF2C antibodies, custom preparations, or technical support, contact us at email.