RASL11A Lentiviral Activation Particles (h): sc-409106-LAC

RASL11A encodes a small Ras-like GTP-binding protein within the RAS superfamily that is thought to modulate signal transduction by coupling guanine nucleotide cycling to downstream pathway dynamics. By influencing Ras-related molecular switches, RASL11A is implicated in processes such as proliferation control, cytoskeletal organization, and vesicle-associated trafficking that shape cell state and stress responsiveness. Altered expression patterns of RASL11A have been reported across multiple cancer and tissue remodeling contexts, supporting its use as a mechanistic node for studying oncogenic signaling rewiring and differentiation-associated phenotypes. Investigating RASL11A regulation can therefore inform how Ras-family networks integrate cues that impact growth control and cellular plasticity.

RASL11A 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 RASL11A upregulation across a broader range of human cell types.

RASL11A 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 RASL11A transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous RASL11A expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native RASL11A 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.