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 CRISPR Activation Plasmid (h): sc-400107-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PDGF Receptor alpha/PDGFRA CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- PDGF Receptor alpha/PDGFRA CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting 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 CRISPR Activation Plasmid (h) and PDGF Receptor alpha/PDGFRA CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the PDGFRA transcriptional start site. One or both designs may be available
- Following transfection, gene knockout 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 CRISPR Activation Plasmid (h) | sc-400107-ACT | 20 µg | $397.00 | |||
PDGF Receptor alpha/PDGFRA CRISPR Activation Plasmid (h2) | sc-400107-ACT-2 | 20 µg | $397.00 |
PDGFRA encodes platelet-derived growth factor receptor alpha, a receptor tyrosine kinase that binds PDGF ligands to initiate autophosphorylation and downstream signaling through PI3K–AKT, RAS–MAPK, and PLCγ pathways. This signaling regulates cell proliferation, survival, migration, and extracellular matrix remodeling, with prominent roles in mesenchymal and stromal biology during development and tissue homeostasis. Dysregulated PDGFRA activity is implicated in aberrant growth-factor signaling programs observed in multiple cancer-associated contexts and in fibroproliferative and inflammatory microenvironments. As a cell-surface kinase node, PDGFRA is frequently studied for mechanisms controlling receptor trafficking, ligand-dependent signaling kinetics, and pathway crosstalk.
PDGF Receptor alpha/PDGFRA CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PDGFRA expression without altering the underlying DNA sequence.
PDGF Receptor alpha/PDGFRA CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PDGFRA locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the PDGFRA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PDGF Receptor alpha/PDGFRA expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PDGFRA locus and enabling the study of PDGF Receptor alpha/PDGFRA-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PDGF Receptor alpha/PDGFRA pathway restoration in tumor cells with silenced or reduced PDGFRA expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.