Cdk3 Double Nickase Plasmid (h): sc-400846-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Cdk3 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
- Cdk3 Double Nickase Plasmid (h) and Cdk3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDK3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Cdk3 Antibody (4B6): sc-81836
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Cdk3 Double Nickase Plasmid (h) | sc-400846-NIC | 20 µg | $410.00 | |||
Cdk3 Double Nickase Plasmid (h2) | sc-400846-NIC-2 | 20 µg | $410.00 |
CDK3 encodes cyclin-dependent kinase 3 (Cdk3), a serine/threonine kinase that contributes to cell-cycle control by coordinating cyclin interactions and phosphorylation events linked to G0/G1 exit and early G1 progression. Cdk3 activity intersects with core CDK–cyclin signaling and downstream RB/E2F-regulated transcriptional programs that govern proliferation and checkpoint responses. Dysregulated CDK3 expression or activity has been reported in multiple cancer contexts, where altered kinase signaling can influence growth, migration, and stress-adaptive pathways. As a result, CDK3 is frequently investigated for its role in proliferative signaling networks and the molecular determinants of tumor-associated phenotypes.
Cdk3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDK3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDK3. 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 CDK3 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 CDK3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.