cyclin D2 Double Nickase Plasmid (h): sc-401236-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- cyclin D2 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
- cyclin D2 Double Nickase Plasmid (h) and cyclin D2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CCND2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: cyclin D2 Antibody (B-6): sc-376676
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
cyclin D2 Double Nickase Plasmid (h) | sc-401236-NIC | 20 µg | $410.00 | |||
cyclin D2 Double Nickase Plasmid (h2) | sc-401236-NIC-2 | 20 µg | $410.00 |
CCND2 encodes cyclin D2, a regulatory partner of CDK4/6 that drives G1 phase progression by promoting retinoblastoma protein phosphorylation and E2F-dependent transcription. Cyclin D2 integrates mitogenic cues from pathways such as PI3K–AKT and RAS–MAPK to coordinate cell-cycle entry, proliferation, and context-dependent differentiation programs. Altered CCND2 dosage or control can perturb G1/S checkpoints, influencing genome stability and proliferative capacity. Dysregulation of cyclin D2 signaling has been linked to aberrant growth phenotypes and is studied across cancer biology, developmental disorders, and endocrine and neural lineage models where CDK4/6–RB axis control is critical.
cyclin D2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CCND2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CCND2. 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 CCND2 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 CCND2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.