SMARCA4/Brg1 Lentiviral Activation Particles (h): sc-400168-LAC

SMARCA4 (BRG1) encodes the ATPase catalytic subunit of the SWI/SNF (BAF) chromatin remodeling complex, which mobilizes nucleosomes to regulate DNA accessibility and transcriptional programs. Through ATP-dependent chromatin remodeling, SMARCA4 influences lineage specification, cell-cycle control, DNA damage responses, and enhancer activity, integrating signaling cues with epigenetic state. SMARCA4 functions across pathways governing chromatin organization and transcriptional regulation, including interactions with tumor suppressor and developmental regulators. Genetic alteration or dysregulated expression of SMARCA4 is implicated in multiple cancer-associated chromatin remodeling defects and serves as a key node for investigating epigenetic mechanisms of disease biology.

SMARCA4/Brg1 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 SMARCA4 upregulation across a broader range of human cell types.

SMARCA4/Brg1 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 SMARCA4 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous SMARCA4/Brg1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SMARCA4 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.