Cdk2 Double Nickase Plasmid (h): sc-400111-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Cdk2 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
- Cdk2 Double Nickase Plasmid (h) and Cdk2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDK2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Cdk2 Antibody (D-12): sc-6248
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Cdk2 Double Nickase Plasmid (h) | sc-400111-NIC | 20 µg | $410.00 | |||
Cdk2 Double Nickase Plasmid (h2) | sc-400111-NIC-2 | 20 µg | $410.00 |
CDK2 encodes cyclin-dependent kinase 2 (Cdk2), a serine/threonine kinase that partners with cyclins E and A to coordinate G1/S transition and S-phase progression. Cdk2 integrates mitogenic signaling with replication origin firing, centrosome duplication, and cell-cycle checkpoint control through phosphorylation of substrates in the RB–E2F axis and DNA replication machinery. Its activity is regulated by CDK inhibitors such as p21 and p27 and by activating phosphorylation, linking CDK2 to responses to DNA damage and replication stress. Dysregulated CDK2 signaling is frequently associated with proliferative phenotypes and altered genome maintenance observed in cancer biology and related model systems.
Cdk2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDK2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDK2. 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 CDK2 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 CDK2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.