
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FGFR-3 Lentiviral Activation Particles (h) | sc-400184-LAC | 200 µl | $455.00 |
FGFR3 encodes fibroblast growth factor receptor 3 (FGFR-3), a receptor tyrosine kinase that regulates cell fate decisions by coupling extracellular FGF ligands to intracellular signaling. Upon activation, FGFR-3 engages adaptor proteins and triggers downstream MAPK/ERK, PI3K/AKT, PLCγ, and STAT pathways to influence proliferation, differentiation, survival, and tissue homeostasis. In human biology, FGFR-3 is a key modulator of skeletal development and epithelial cell behavior, and its dysregulation is implicated in aberrant growth control. Altered FGFR3 activity and signaling output are frequently studied in contexts such as developmental disorders and cancer-associated pathway remodeling.
FGFR-3 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 FGFR3 upregulation across a broader range of human cell types.
FGFR-3 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 FGFR3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous FGFR-3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native FGFR3 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.