CRP2 Double Nickase Plasmid (h): sc-409601-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CRP2 Double Nickase Plasmid (h) 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
- CRP2 Double Nickase Plasmid (h) and CRP2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CSRP2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CRP2 Double Nickase Plasmid (h) | sc-409601-NIC | 20 µg | $410.00 | |||
CRP2 Double Nickase Plasmid (h2) | sc-409601-NIC-2 | 20 µg | $410.00 |
CSRP2 encodes cysteine and glycine-rich protein 2 (CRP2), a LIM domain-containing actin-binding regulator enriched in smooth muscle and vascular cell types. CRP2 localizes to the cytoskeleton and nucleus, where it coordinates actin dynamics with transcriptional programs that shape cell adhesion, migration, and differentiation. It participates in cytoskeletal remodeling and mechanotransduction pathways, influencing gene expression through interactions with LIM domain partners and transcriptional co-regulators. Altered CSRP2/CRP2 expression has been reported across contexts involving vascular remodeling, fibrosis-associated myofibroblast behavior, and tumor cell motility, supporting its study in disease-relevant cell state transitions.
CRP2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CSRP2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CSRP2. 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 CSRP2 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 CSRP2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.