MEF-2C CRISPR Activation Plasmid (h): sc-416594-ACT

MEF2C encodes the human transcription factor MEF-2C, a MADS-box/MEF2 family regulator that integrates calcium-dependent signaling with chromatin and transcriptional control. MEF-2C coordinates gene expression programs involved in muscle differentiation, neuronal development, synaptic remodeling, and immune cell lineage specification through pathways such as CaMK/Calcineurin–NFAT, MAPK, and interactions with class IIa HDACs. In the nucleus, MEF-2C binds MEF2 response elements to modulate activity-dependent transcription and cell-state transitions across multiple tissues. Dysregulated MEF2C expression or regulatory circuitry has been linked to neurodevelopmental phenotypes, altered excitatory/inhibitory balance, and cancer-associated transcriptional reprogramming, supporting its use as a node for mechanistic studies.

MEF-2C CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MEF2C expression without altering the underlying DNA sequence.

MEF-2C CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MEF2C locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.

Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the MEF2C transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MEF-2C expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MEF2C locus and enabling the study of MEF-2C-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MEF-2C pathway restoration in tumor cells with silenced or reduced MEF2C expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.