DNAH17 Double Nickase Plasmid (h): sc-409722-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DNAH17 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
- DNAH17 Double Nickase Plasmid (h) and DNAH17 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DNAH17. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DNAH17 Double Nickase Plasmid (h) | sc-409722-NIC | 20 µg | $410.00 |
DNAH17 encodes dynein axonemal heavy chain 17, a microtubule-based motor ATPase that contributes to the structure and motility of cilia and flagella. As part of the axonemal dynein machinery, DNAH17 supports ATP-driven sliding of microtubule doublets that underlies ciliary beat patterning and sperm flagellar propulsion. This protein functions within cytoskeletal organization and motility-related pathways, including axoneme assembly and ciliary transport processes that coordinate movement and signaling. Genetic perturbation of axonemal dyneins, including DNAH17, is linked to male infertility phenotypes such as asthenozoospermia and broader ciliopathy-relevant defects impacting motile cilia function.
DNAH17 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DNAH17 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DNAH17. 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 DNAH17 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 DNAH17-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.