KCTD5 Double Nickase Plasmid (h): sc-409961-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KCTD5 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
- KCTD5 Double Nickase Plasmid (h) and KCTD5 Double Nickase Plasmid (h2) 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 (h) | sc-409961-NIC | 20 µg | $410.00 | |||
KCTD5 Double Nickase Plasmid (h2) | sc-409961-NIC-2 | 20 µg | $410.00 |
KCTD5 encodes a BTB/POZ domain–containing protein that functions as an adaptor in Cullin 3 (CUL3)-based E3 ubiquitin ligase complexes, helping confer substrate specificity for ubiquitination and proteasome-dependent turnover. Through modulation of protein stability, KCTD5 contributes to proteostasis and cellular signaling programs that influence proliferation, differentiation, and stress responses. Altered ubiquitin-pathway regulation and BTB–CUL3 adaptor activity are recurrent features of cancer and neurobiological disorders, making KCTD5 a useful node for studying pathway rewiring and context-specific signaling dependencies. Investigating KCTD5 in human cells can clarify how targeted degradation interfaces with transcriptional and post-translational control in disease-relevant states.
KCTD5 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KCTD5 locus in human 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.