MEF-2A Lentiviral Activation Particles (h): sc-400484-LAC

MEF2A encodes the transcription factor MEF-2A, a MADS-box/MEF2 family regulator that integrates calcium-dependent signaling and MAPK inputs to control gene programs governing myogenesis, neuronal differentiation, synaptic remodeling, and cellular stress responses. MEF-2A activity is shaped by post-translational modifications and cofactor interactions, linking it to chromatin remodeling and stimulus-dependent transcription in muscle, immune, and neural lineages. Altered MEF2A expression or regulatory control has been associated with vascular biology and cardiac function, and broader MEF2 pathway dysregulation is implicated in neurodevelopmental and neurodegenerative contexts. As a node in CREB/HDAC- and calcineurin-dependent transcriptional networks, MEF-2A is frequently studied for its role in lineage specification, metabolic adaptation, and activity-dependent gene expression.

MEF-2A Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient MEF2A upregulation across a broader range of human cell types.

MEF-2A Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the MEF2A transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MEF-2A expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native MEF2A genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

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