AKAP 220 Double Nickase Plasmid (h): sc-405585-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AKAP 220 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
- AKAP 220 Double Nickase Plasmid (h) and AKAP 220 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting AKAP11. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AKAP 220 Double Nickase Plasmid (h) | sc-405585-NIC | 20 µg | $410.00 | |||
AKAP 220 Double Nickase Plasmid (h2) | sc-405585-NIC-2 | 20 µg | $410.00 |
Human AKAP11 encodes A-kinase anchoring protein 220 (AKAP 220), a scaffold that spatially organizes PKA with additional signaling enzymes to shape compartmentalized cAMP responses. By tethering kinase activity to defined subcellular domains, AKAP 220 contributes to phosphorylation-dependent control of cell-cycle progression, cytoskeletal dynamics, and receptor-driven signal integration. Disruption of AKAP11-mediated signaling microdomains has been linked to altered proliferative and stress-response programs in disease-relevant contexts, supporting its use as a mechanistic node in pathways that couple second-messenger signaling to cellular state changes. AKAP11 is therefore frequently investigated for how rewired PKA anchoring influences downstream transcriptional outputs and proteostasis networks in human cells.
AKAP 220 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the AKAP11 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within AKAP11. 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 AKAP11 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 AKAP11-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.