KLHL9 Double Nickase Plasmid (h): sc-406655-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KLHL9 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
- KLHL9 Double Nickase Plasmid (h) and KLHL9 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KLHL9. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KLHL9 Double Nickase Plasmid (h) | sc-406655-NIC | 20 µg | $410.00 | |||
KLHL9 Double Nickase Plasmid (h2) | sc-406655-NIC-2 | 20 µg | $410.00 |
KLHL9 encodes a BTB–BACK–Kelch family protein that functions as a substrate adaptor within Cullin-3 (CUL3) RING E3 ubiquitin ligase complexes, helping confer specificity to ubiquitin-dependent protein turnover. Through regulated ubiquitination, KLHL9 contributes to cellular proteostasis and influences processes linked to cytoskeletal organization and cell-cycle progression, including mitotic control. Disruption of KLHL9 has been associated with neurodevelopmental and neuromuscular phenotypes, consistent with the importance of balanced ubiquitin signaling in long-lived, excitable tissues. As a human KLHL protein, it is frequently studied in pathways connecting E3 ligase substrate recognition to stress responses and cellular homeostasis.
KLHL9 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KLHL9 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KLHL9. 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 KLHL9 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 KLHL9-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.