Gigaxonin Double Nickase Plasmid (h): sc-407001-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Gigaxonin 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
- Gigaxonin Double Nickase Plasmid (h) and Gigaxonin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GAN. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Gigaxonin Antibody (F-3): sc-376173
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Gigaxonin Double Nickase Plasmid (h) | sc-407001-NIC | 20 µg | $410.00 | |||
Gigaxonin Double Nickase Plasmid (h2) | sc-407001-NIC-2 | 20 µg | $410.00 |
GAN encodes gigaxonin, a BTB-Kelch family adaptor for CUL3-based E3 ubiquitin ligase complexes that promotes ubiquitination and proteasomal turnover of specific substrates. Gigaxonin is a key regulator of intermediate filament and microtubule-associated protein homeostasis, supporting axonal cytoskeletal organization and neuronal integrity. Through control of protein quality pathways and cytoskeletal dynamics, gigaxonin influences processes such as axon maintenance, intracellular transport, and stress responses. Loss-of-function variants in GAN are linked to giant axonal neuropathy, a neurodegenerative disorder characterized by abnormal intermediate filament accumulation and axonal pathology.
Gigaxonin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GAN locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GAN. 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 GAN 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 GAN-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.