
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MEF-2C Lentiviral Activation Particles (h) | sc-416594-LAC | 200 µl | $455.00 |
MEF2C encodes the transcription factor MEF-2C, a MADS-box/MEF2 family member that integrates calcium-dependent signaling to regulate gene programs controlling cell fate, differentiation, and survival. MEF-2C activity is modulated by pathways such as CaMK/Calcineurin and MAPK signaling, and it cooperates with chromatin regulators (including class IIa HDACs) to tune context-specific transcriptional outputs. In human biology, MEF2C is central to neurodevelopmental and cardiac gene networks, and altered regulation has been linked to congenital developmental phenotypes and dysregulated lineage specification in disease-relevant cellular models. These features make MEF2C a widely used node for studying transcriptional control, enhancer logic, and activity-dependent gene expression.
MEF-2C 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 MEF2C upregulation across a broader range of human cell types.
MEF-2C 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 MEF2C transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MEF-2C expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native MEF2C 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.