OFD1 Double Nickase Plasmid (h): sc-410551-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- OFD1 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
- OFD1 Double Nickase Plasmid (h) and OFD1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting OFD1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
OFD1 Double Nickase Plasmid (h) | sc-410551-NIC | 20 µg | $410.00 |
OFD1 encodes a centrosomal and basal body protein required for primary cilium biogenesis and maintenance, where it supports axoneme organization and regulates centriolar satellite composition. Through these functions, OFD1 influences ciliogenesis-dependent signaling pathways including Hedgehog and Wnt, as well as cell-cycle progression and polarized trafficking. Perturbation of OFD1 disrupts ciliary structure and signaling fidelity, linking it to ciliopathy-associated phenotypes such as craniofacial and skeletal anomalies, renal involvement, and neurodevelopmental defects. As a cilia and centrosome regulator, OFD1 is widely studied in models of organogenesis, cell polarity, and stress responses associated with defective ciliary dynamics.
OFD1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the OFD1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within OFD1. 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 OFD1 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 OFD1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.