Lsh Lentiviral Activation Particles (h): sc-402466-LAC

Human HELLS encodes lymphoid-specific helicase (Lsh), an SNF2-family ATP-dependent chromatin remodeler that cooperates with DNA methyltransferases to establish and maintain DNA methylation patterns and repressive chromatin states. Lsh supports heterochromatin organization, transposon silencing, and replication-coupled chromatin assembly, linking ATP-driven nucleosome remodeling to genome stability and epigenetic inheritance. It participates in pathways governing DNA repair, cell-cycle progression, and lineage-specific transcriptional programs through regulation of chromatin accessibility. Dysregulated HELLS activity and altered Lsh expression have been associated with epigenome instability and aberrant gene silencing programs reported across multiple tumor contexts and developmental disorders, making it a useful node for mechanistic studies of epigenetic control.

Lsh 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 HELLS upregulation across a broader range of human cell types.

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