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 beta/PDGFRB Double Nickase Plasmid (m): sc-422171-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PDGF Receptor beta/PDGFRB Double Nickase Plasmid (m) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- PDGF Receptor beta/PDGFRB Double Nickase Plasmid (m) and PDGF Receptor beta/PDGFRB Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Pdgfrb. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: PDGF Receptor beta/PDGFRB Antibody (D-6): sc-374573
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PDGF Receptor beta/PDGFRB Double Nickase Plasmid (m) | sc-422171-NIC | 20 µg | $410.00 | |||
PDGF Receptor beta/PDGFRB Double Nickase Plasmid (m2) | sc-422171-NIC-2 | 20 µg | $410.00 |
Mouse Pdgfrb encodes platelet-derived growth factor receptor beta (PDGFRB), a receptor tyrosine kinase that regulates pericyte and vascular smooth muscle cell proliferation, migration, and survival during vessel maturation and tissue remodeling. Upon PDGF ligand binding, PDGFRB activates canonical PI3K–AKT, RAS–MAPK, and PLCγ signaling cascades and coordinates cytoskeletal dynamics and extracellular matrix interactions through downstream adaptor proteins. In the developing and adult vasculature, PDGFRB-mediated signaling supports blood–brain barrier integrity, wound repair, and stromal–immune crosstalk. Dysregulated PDGFRB activity is frequently leveraged as a molecular readout in studies of angiogenesis, fibrosis, inflammatory remodeling, and tumor-associated stromal biology in mouse models.
PDGF Receptor beta/PDGFRB Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Pdgfrb locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Pdgfrb. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt Pdgfrb function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of Pdgfrb-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.