GDAP1 Double Nickase Plasmid (h): sc-412270-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GDAP1 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
- GDAP1 Double Nickase Plasmid (h) and GDAP1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GDAP1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GDAP1 Double Nickase Plasmid (h) | sc-412270-NIC | 20 µg | $410.00 |
GDAP1 (ganglioside-induced differentiation-associated protein 1) is an outer mitochondrial membrane protein enriched in neurons and is implicated in maintaining mitochondrial morphology, distribution, and redox homeostasis. It interfaces with pathways controlling mitochondrial dynamics and quality control, including processes linked to fission–fusion balance, axonal transport of mitochondria, and cellular responses to oxidative stress. Altered GDAP1 function is strongly associated with inherited peripheral neuropathies, particularly Charcot–Marie–Tooth disease subtypes, where neuronal bioenergetic stress and impaired mitochondrial trafficking are prominent mechanistic themes. As a result, GDAP1 is frequently studied in the context of neurodegeneration-relevant mitochondrial biology and axon maintenance.
GDAP1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GDAP1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GDAP1. 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 GDAP1 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 GDAP1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.