IFT88 Double Nickase Plasmid (h): sc-404089-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IFT88 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
- IFT88 Double Nickase Plasmid (h) and IFT88 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IFT88. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IFT88 Double Nickase Plasmid (h) | sc-404089-NIC | 20 µg | $410.00 | |||
IFT88 Double Nickase Plasmid (h2) | sc-404089-NIC-2 | 20 µg | $410.00 |
IFT88 encodes intraflagellar transport protein 88, a core component of the IFT-B complex required for anterograde trafficking within primary cilia. By coordinating ciliary axoneme assembly and the movement of signaling receptors, IFT88 supports ciliogenesis and regulates cilia-dependent pathways including Hedgehog signaling and other sensory transduction processes. Disruption of IFT88 compromises primary cilium structure and function, altering developmental and homeostatic signaling programs. Genetic and functional perturbation of IFT88 is widely studied in the context of ciliopathies, including disorders characterized by renal, retinal, and skeletal phenotypes.
IFT88 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IFT88 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IFT88. 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 IFT88 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 IFT88-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.