
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FOXI1 Lentiviral Activation Particles (m) | sc-420369-LAC | 200 µl | $455.00 | |||
FOXI1 Lentiviral Activation Particles (m2) | sc-420369-LAC-2 | 200 µl | $455.00 |
Foxi1 encodes the forkhead box transcription factor FOXI1, a sequence-specific DNA-binding regulator that controls epithelial lineage programs and differentiation. In mouse, FOXI1 is integral to ion transport and acid–base homeostasis by governing transcriptional networks in specialized epithelial cells, including those involved in renal and inner ear physiology. FOXI1-linked regulation intersects with developmental transcriptional circuitry and epithelial maturation processes that shape tissue patterning and functional specialization. Dysregulated FOXI1 activity is associated with defects in epithelial development and ion-handling phenotypes, making it a useful node for studying gene regulatory networks underlying organogenesis and homeostatic imbalance.
FOXI1 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 Foxi1 upregulation across a broader range of human cell types.
FOXI1 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 Foxi1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous FOXI1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Foxi1 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.