KIF1C Double Nickase Plasmid (m): sc-421271-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KIF1C Double Nickase Plasmid (m) 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
- KIF1C Double Nickase Plasmid (m) and KIF1C Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Kif1c. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KIF1C Double Nickase Plasmid (m) | sc-421271-NIC | 20 µg | $410.00 | |||
KIF1C Double Nickase Plasmid (m2) | sc-421271-NIC-2 | 20 µg | $410.00 |
Mouse Kif1c encodes KIF1C, a kinesin-3 family microtubule motor that drives plus-end–directed transport of vesicular and protein cargo in polarized cells. KIF1C supports integrin trafficking, membrane dynamics, and cytoskeletal organization, linking microtubule-based motility to cell adhesion and directional migration. Through these processes, KIF1C contributes to immune cell polarization and efficient intracellular distribution of signaling components, making it relevant for studies of motility-dependent pathways and neuroimmune cell biology. Perturbation of KIF1C-dependent transport is associated with defects in axonal and cellular trafficking programs that are often interrogated in models of neurodegeneration and immune dysregulation.
KIF1C Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Kif1c locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Kif1c. 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 Kif1c 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 Kif1c-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.