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.
CRP Double Nickase Plasmid (h): sc-401767-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CRP 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
- CRP Double Nickase Plasmid (h) and CRP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CRP. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CRP Antibody (26D7): sc-69770
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CRP Double Nickase Plasmid (h) | sc-401767-NIC | 20 µg | $410.00 | |||
CRP Double Nickase Plasmid (h2) | sc-401767-NIC-2 | 20 µg | $410.00 |
C-reactive protein (CRP) is a pentraxin family pattern-recognition molecule predominantly produced by hepatocytes in response to pro-inflammatory cytokines, especially IL-6, and circulates as a major acute-phase reactant. CRP binds phosphocholine and other ligands on damaged cells and microbial surfaces, promoting opsonization and activation of the classical complement cascade via C1q. Through these innate immune processes, CRP integrates inflammatory signaling with complement-mediated clearance and modulates interactions with Fcγ receptors on myeloid cells. Genetic variation and dysregulated expression of CRP are widely studied in the context of systemic inflammation and cardiometabolic and autoimmune-associated phenotypes, making it a key molecular readout and regulator in inflammation biology.
CRP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CRP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CRP. 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 CRP 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 CRP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.