SCD5 Lentiviral Activation Particles (h2): sc-402860-LAC-2

Human SCD5 (stearoyl‑CoA desaturase 5) encodes an endoplasmic reticulum–associated Δ9 desaturase that introduces a cis double bond into saturated fatty acyl‑CoAs, generating monounsaturated fatty acids that shape membrane composition, lipid droplet biology, and phospholipid/triacylglycerol biosynthesis. By regulating the saturated-to-monounsaturated fatty acid ratio, SCD5 influences cellular lipid homeostasis and metabolic signaling pathways linked to ER stress responses and redox balance. Dysregulated SCD5 expression has been implicated in altered lipid metabolism observed in metabolic disorders and in the molecular phenotypes of several cancers, where changes in desaturation can affect proliferation and differentiation programs. Gene editing of SCD5 in human cell models enables mechanistic studies of fatty acid desaturation, lipidomic remodeling, and pathway-level responses to perturbations in membrane lipid saturation.

SCD5 Lentiviral Activation Particles (h2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient SCD5 upregulation across a broader range of human cell types.

SCD5 Lentiviral Activation Particles (h2) 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 SCD5 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous SCD5 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SCD5 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.