KIF1A Double Nickase Plasmid (h): sc-404497-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KIF1A 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
- KIF1A Double Nickase Plasmid (h) and KIF1A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KIF1A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KIF1A Double Nickase Plasmid (h) | sc-404497-NIC | 20 µg | $410.00 | |||
KIF1A Double Nickase Plasmid (h2) | sc-404497-NIC-2 | 20 µg | $410.00 |
KIF1A encodes a kinesin-3 family microtubule motor that drives ATP-dependent anterograde transport of synaptic vesicle precursors and other membrane cargos along axons. By coupling cargo trafficking to the microtubule cytoskeleton, KIF1A supports neurite outgrowth, synaptic maintenance, and long-range neuronal homeostasis, intersecting with pathways that regulate vesicle dynamics, axonal transport, and neuronal polarity. Altered KIF1A function is linked to neurodevelopmental and neurodegenerative phenotypes associated with impaired axonal cargo delivery and synaptic dysfunction, making it a useful node for studying transport-dependent neuronal biology in human cell systems.
KIF1A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KIF1A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KIF1A. 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 KIF1A 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 KIF1A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.