
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FBL19 Lentiviral Activation Particles (h) | sc-407318-LAC | 200 µl | $455.00 |
FBXL19 (FBL19) encodes an F-box and leucine-rich repeat protein that functions as a substrate-recognition component of SCF (SKP1–CUL1–F-box) E3 ubiquitin ligase complexes, directing specific proteins toward ubiquitination and proteasomal turnover. Through control of protein stability, FBXL19 contributes to regulation of cell-cycle progression, signal transduction, and chromatin-associated processes that shape transcriptional programs. FBXL19 has also been linked to CpG island–associated gene regulation via interactions with chromatin and transcriptional machinery, connecting ubiquitin signaling with epigenetic control. Dysregulated ubiquitin-mediated proteostasis and transcriptional regulation involving FBXL19 are relevant to studies of oncogenic signaling, differentiation, and other disease-associated cellular states.
FBL19 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 FBXL19 upregulation across a broader range of human cell types.
FBL19 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 FBXL19 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous FBL19 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native FBXL19 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.