FBXO3 Lentiviral Activation Particles (m): sc-425412-LAC

Mouse Fbxo3 encodes FBXO3, an F-box substrate receptor within SCF (SKP1–CUL1–F-box) E3 ubiquitin ligase complexes that confers specificity for ubiquitin-dependent protein turnover. Through regulated degradation of signaling intermediates, FBXO3 can influence inflammatory and innate immune signaling dynamics, cell stress responses, and proteostasis pathways. Altered activity of SCF-associated F-box proteins is frequently linked to dysregulated cytokine signaling, aberrant cell-cycle and stress checkpoints, and broader pathways relevant to inflammatory disease mechanisms. Fbxo3 is therefore a useful node for dissecting ubiquitin–proteasome control of signal transduction and transcriptional programs in mouse cellular models.

FBXO3 Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Fbxo3 upregulation across a broader range of human cell types.

FBXO3 Lentiviral Activation Particles (m) 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 Fbxo3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous FBXO3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Fbxo3 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.