Slfn5 Lentiviral Activation Particles (h): sc-408333-LAC

Human SLFN5 encodes Schlafen family member 5 (Slfn5), an interferon-stimulated protein implicated in regulating transcriptional programs that shape cell-cycle progression, DNA damage responses, and innate immune signaling. Slfn5 has been linked to modulation of type I interferon/JAK–STAT pathway outputs and broader chromatin-associated control of gene expression, influencing cellular proliferation and differentiation states. Dysregulated SLFN5 expression has been reported across multiple cancer contexts and inflammatory signaling states, where it may correlate with altered tumor cell growth, stress responses, and immune-related transcriptional signatures. These features make SLFN5 a useful target for dissecting interferon-driven regulation, proliferation checkpoints, and gene expression networks relevant to disease-associated phenotypes.

Slfn5 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 SLFN5 upregulation across a broader range of human cell types.

Slfn5 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 SLFN5 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Slfn5 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SLFN5 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.