KIF13A Double Nickase Plasmid (h): sc-403751-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KIF13A 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
- KIF13A Double Nickase Plasmid (h) and KIF13A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KIF13A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KIF13A Double Nickase Plasmid (h) | sc-403751-NIC | 20 µg | $410.00 | |||
KIF13A Double Nickase Plasmid (h2) | sc-403751-NIC-2 | 20 µg | $410.00 |
KIF13A encodes a kinesin-3 family microtubule motor that powers plus-end–directed transport of membrane compartments, shaping vesicle trafficking, endosomal dynamics, and polarized delivery of cargo in migrating and differentiating cells. Through coupling microtubules to Rab-associated vesicles and polarity regulators, KIF13A contributes to processes including receptor recycling, membrane remodeling, and cytoskeletal coordination. Perturbation of KIF13A-linked trafficking can alter signaling output and organelle positioning, with relevance to cellular programs such as immune function, neuronal transport, and barrier biology. Genetic and functional studies have connected KIF13A to disease-associated pathways involving intracellular transport and epithelial or immune dysregulation, motivating mechanistic interrogation in human cell models.
KIF13A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KIF13A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KIF13A. 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 KIF13A 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 KIF13A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.