CDK2AP2 Double Nickase Plasmid (h): sc-406842-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CDK2AP2 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
- CDK2AP2 Double Nickase Plasmid (h) and CDK2AP2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDK2AP2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CDK2AP2 Double Nickase Plasmid (h) | sc-406842-NIC | 20 µg | $410.00 | |||
CDK2AP2 Double Nickase Plasmid (h2) | sc-406842-NIC-2 | 20 µg | $410.00 |
CDK2AP2 (cyclin-dependent kinase 2 associated protein 2) is a small regulatory factor implicated in controlling cell-cycle progression through modulation of CDK2 activity and cyclin-dependent checkpoint signaling. By influencing phosphorylation-dependent transitions at the G1/S boundary, CDK2AP2 contributes to proliferation control and maintenance of genome stability. Altered CDK2-associated regulatory networks are frequently studied in the context of oncogenic cell-cycle deregulation and replication stress, making CDK2AP2 a relevant node for mechanistic interrogation of growth control pathways. In human cells, CDK2AP2 perturbation is commonly evaluated alongside readouts such as S-phase entry, DNA damage signaling, and changes in transcriptional programs linked to proliferation.
CDK2AP2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDK2AP2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDK2AP2. 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 CDK2AP2 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 CDK2AP2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.