
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FSTL5 Lentiviral Activation Particles (h) | sc-407972-LAC | 200 µl | $455.00 | |||
FSTL5 Lentiviral Activation Particles (h2) | sc-407972-LAC-2 | 200 µl | $455.00 |
FSTL5 (follistatin-like 5) encodes a secreted extracellular matrix–associated glycoprotein within the SPARC/follistatin-like family that can influence cell–cell and cell–matrix interactions. Through modulation of adhesion and signaling cues in the tissue microenvironment, FSTL5 has been linked to processes such as neuronal connectivity, cellular differentiation, and regulation of migration. Altered FSTL5 expression has been reported across multiple disease contexts, including cancers and neurological disorders, where it is studied as a marker of tumor biology, metastatic potential, or neurodevelopmental state. These features make FSTL5 a relevant target for investigating extracellular signaling networks and transcriptional programs that shape phenotypic plasticity.
FSTL5 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 FSTL5 upregulation across a broader range of human cell types.
FSTL5 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 FSTL5 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous FSTL5 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native FSTL5 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.