cyclin C Double Nickase Plasmid (h): sc-402308-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- cyclin C 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 C Double Nickase Plasmid (h) and cyclin C Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CCNC. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
cyclin C Double Nickase Plasmid (h) | sc-402308-NIC | 20 µg | $410.00 | |||
cyclin C Double Nickase Plasmid (h2) | sc-402308-NIC-2 | 20 µg | $410.00 |
CCNC encodes cyclin C, a conserved regulatory cyclin that partners with CDK8 or CDK3 to modulate RNA polymerase II transcription through the Mediator complex and phosphorylation-dependent control of transcriptional programs. Cyclin C influences cell-cycle progression, stress-responsive gene expression, and mitochondrial dynamics, integrating signaling inputs that reshape chromatin and transcriptional output. Dysregulation of the CDK8–cyclin C axis has been linked to altered oncogenic transcriptional circuitry and aberrant proliferation in multiple tumor contexts, and CCNC perturbation is also studied in relation to oxidative stress responses and apoptosis-associated pathways. These functions make CCNC a useful target for dissecting transcriptional control, checkpoint coordination, and stimulus-dependent remodeling of gene expression networks.
cyclin C Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CCNC locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CCNC. 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 CCNC 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 CCNC-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.