Slfn11 Lentiviral Activation Particles (h): sc-401137-LAC

Human SLFN11 encodes Schlafen family member 11 (Slfn11), a DNA damage response–associated factor that influences replication stress tolerance and cell fate following genotoxic insult. SLFN11 is linked to regulation of stalled replication forks, transcription–replication conflicts, and checkpoint signaling, integrating with pathways that shape S-phase progression and genome integrity. Through effects on chromatin-associated processes and stress-responsive transcriptional programs, SLFN11 can modulate cellular sensitivity to agents that induce DNA lesions. Altered SLFN11 expression or function has been studied in the context of tumor biology and mechanisms that underlie resistance phenotypes in DNA damage–targeting research models.

Slfn11 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 SLFN11 upregulation across a broader range of human cell types.

Slfn11 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 SLFN11 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Slfn11 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SLFN11 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.