KCTD1 Double Nickase Plasmid (h): sc-406758-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KCTD1 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
- KCTD1 Double Nickase Plasmid (h) and KCTD1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KCTD1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KCTD1 Double Nickase Plasmid (h) | sc-406758-NIC | 20 µg | $410.00 | |||
KCTD1 Double Nickase Plasmid (h2) | sc-406758-NIC-2 | 20 µg | $410.00 |
Human KCTD1 (potassium channel tetramerization domain-containing protein 1) is a BTB/POZ domain–containing adaptor protein implicated in protein–protein interactions that influence ubiquitin-mediated proteostasis and transcriptional control. KCTD1 has been linked to modulation of signaling networks that govern cell differentiation and developmental patterning, consistent with roles for BTB-Kelch family–associated complexes in regulating substrate stability and gene expression programs. Genetic variation in KCTD1 is associated with developmental disorders, including scalp–ear–nipple syndrome, supporting its relevance to morphogenesis and ectodermal lineage biology. These features make KCTD1 a useful target for studying pathways connecting regulated protein turnover, transcriptional regulation, and tissue development.
KCTD1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KCTD1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KCTD1. 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 KCTD1 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 KCTD1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.