Myocardin Lentiviral Activation Particles (m): sc-431931-LAC

Myocd encodes myocardin, a potent transcriptional coactivator that partners with serum response factor (SRF) to control smooth muscle and cardiac muscle gene programs, including contractile and cytoskeletal components. By integrating signals from actin dynamics and RhoA/MRTF-related pathways, myocardin helps coordinate myogenic differentiation, vascular smooth muscle maturation, and maintenance of the contractile phenotype. Dysregulated MYOCD activity is linked to abnormal vascular remodeling and altered smooth muscle plasticity, making it relevant to studies of cardiovascular development and disease-associated gene expression changes. Mouse myocardin is therefore widely used as a model for transcriptional control of muscle lineage identity and stress-responsive remodeling networks.

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

Myocardin Lentiviral Activation Particles (m) 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 Myocd transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Myocardin expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Myocd 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.