MyoD Lentiviral Activation Particles (h): sc-400092-LAC

Human MYOD1 encodes MyoD, a basic helix–loop–helix transcription factor that functions as a master regulator of skeletal myogenic commitment and differentiation. MyoD binds E-box motifs to activate muscle gene programs and cooperates with chromatin remodelers and lineage factors to drive cell-cycle exit and myotube formation, integrating signals from myogenic regulatory factor networks and epigenetic control of transcription. MYOD1 activity intersects with pathways governing muscle development, regeneration, and lineage plasticity, and its dysregulation has been implicated in altered differentiation states and tumor-associated myogenic programs in certain cancers. As a node in transcriptional circuitry, MYOD1 is widely used to interrogate gene regulatory networks, chromatin accessibility changes, and myogenesis-associated phenotypes in human cell models.

MyoD 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 MYOD1 upregulation across a broader range of human cell types.

MyoD 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 MYOD1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MyoD expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native MYOD1 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.