KCTD5 Double Nickase Plasmid (m): sc-427353-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KCTD5 Double Nickase Plasmid (m) 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
- KCTD5 Double Nickase Plasmid (m) and KCTD5 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Kctd5. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KCTD5 Double Nickase Plasmid (m) | sc-427353-NIC | 20 µg | $410.00 |
Mouse Kctd5 encodes KCTD5, a BTB/POZ domain–containing protein that functions as an adaptor in cullin-RING E3 ubiquitin ligase complexes, supporting substrate recognition and ubiquitin-dependent protein turnover. Through regulation of proteostasis, KCTD5 can influence cell-cycle progression, signal transduction, and synaptic or neuronal processes by modulating the stability of pathway components. Altered ubiquitin–proteasome pathway activity is broadly relevant to neurodevelopmental phenotypes and cancer-associated signaling rewiring, making Kctd5 a useful node for mechanistic studies of protein quality control. In mouse model systems, perturbation of Kctd5 helps interrogate how ubiquitination interfaces with cellular stress responses and differentiation programs.
KCTD5 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Kctd5 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Kctd5. 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 Kctd5 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 Kctd5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.