Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
PDGF Receptor alpha/PDGFRA Lentiviral Activation Particles (h): sc-400107-LAC
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- PDGF Receptor alpha/PDGFRA Lentiviral Activation Particles (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
- PDGF Receptor alpha/PDGFRA Lentiviral Activation Particles (h) contain the following SAM Activation elements: a deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, an MS2-p65-HSF1 fusion protein and a target-specific 20 nt guide RNA. They also contain the blasticidin, hygromycin and puromycin resistance genes
- Upon transduction, the SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by PDGF Receptor alpha/PDGFRA Lentiviral Activation Plasmid (h) and PDGF Receptor alpha/PDGFRA Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the PDGFRA promoter. One or both designs may be available
- Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: PDGF Receptor alpha/PDGFRA Antibody (C-9): sc-398206
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PDGF Receptor alpha/PDGFRA Lentiviral Activation Particles (h) | sc-400107-LAC | 200 µl | $455.00 |
PDGFRA encodes platelet-derived growth factor receptor alpha (PDGFRα), a receptor tyrosine kinase that binds PDGF ligands to regulate cell proliferation, migration, survival, and mesenchymal lineage programs. Upon activation, PDGFRα signals through canonical MAPK/ERK, PI3K–AKT, and PLCγ pathways and can interface with STAT and Rho-family signaling to coordinate cytoskeletal remodeling and developmental patterning. PDGFRA activity is integral to stromal–epithelial crosstalk, extracellular matrix organization, and tissue repair responses. Dysregulated PDGFRA expression or signaling is associated with oncogenic receptor activation, aberrant fibroblast and pericyte behavior, and disease-relevant remodeling processes in multiple tumor and fibrotic microenvironments.
PDGF Receptor alpha/PDGFRA 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 PDGFRA upregulation across a broader range of human cell types.
PDGF Receptor alpha/PDGFRA 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 PDGFRA transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PDGF Receptor alpha/PDGFRA expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PDGFRA 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.