



Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CDKN3 Double Nickase Plasmid (h) | sc-403243-NIC | 20 µg | $410.00 | |||
CDKN3 Double Nickase Plasmid (h2) | sc-403243-NIC-2 | 20 µg | $410.00 |
CDKN3 (cyclin-dependent kinase inhibitor 3) encodes a dual-specificity phosphatase that modulates cell-cycle progression by dephosphorylating CDK1 and CDK2, thereby influencing cyclin-CDK activity and checkpoint control at G1/S and G2/M transitions. Through its impact on mitotic entry, DNA replication timing, and proliferation programs, CDKN3 integrates with core cell-cycle regulatory pathways, including RB/E2F-driven transcriptional control. Dysregulated CDKN3 expression has been reported across multiple cancer contexts and is frequently studied for its association with proliferative signatures, genomic instability, and altered checkpoint fidelity. As a human cell-cycle regulator with phosphatase activity, CDKN3 is also relevant for mechanistic studies of mitotic regulation, stress responses, and pathways that couple phosphoregulation to proliferation.
CDKN3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDKN3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDKN3. 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 CDKN3 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 CDKN3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.