KIF3A Double Nickase Plasmid (h): sc-403463-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KIF3A 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
- KIF3A Double Nickase Plasmid (h) and KIF3A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KIF3A. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: KIF3A Antibody (E-5): sc-376680
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KIF3A Double Nickase Plasmid (h) | sc-403463-NIC | 20 µg | $410.00 | |||
KIF3A Double Nickase Plasmid (h2) | sc-403463-NIC-2 | 20 µg | $410.00 |
KIF3A encodes kinesin family member 3A, a core motor subunit of the heterotrimeric kinesin-2 complex that drives anterograde transport along microtubules. KIF3A is essential for intraflagellar transport and primary cilium assembly, linking it to Hedgehog and Wnt pathway signal transduction and broader regulation of cell polarity and mechanosensory signaling. Through its roles in ciliary trafficking and microtubule-dependent cargo movement, KIF3A influences developmental programs and epithelial homeostasis. Altered KIF3A function or expression has been associated with ciliopathy-related phenotypes and has been investigated in airway biology and other disease-relevant contexts where ciliary signaling is perturbed.
KIF3A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KIF3A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KIF3A. 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 KIF3A 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 KIF3A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.