γC-crystallin Double Nickase Plasmid (h): sc-402940-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- γC-crystallin 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
- γC-crystallin Double Nickase Plasmid (h) and γC-crystallin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CRYGC. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
γC-crystallin Double Nickase Plasmid (h) | sc-402940-NIC | 20 µg | $410.00 | |||
γC-crystallin Double Nickase Plasmid (h2) | sc-402940-NIC-2 | 20 µg | $410.00 |
Human CRYGC encodes γC-crystallin, a highly abundant structural protein in the ocular lens that contributes to refractive index, transparency, and long-term fiber cell stability. As a member of the β/γ-crystallin superfamily, γC-crystallin supports tight protein packing and resistance to aggregation, processes central to proteostasis in the largely organelle-free lens fiber cell environment. Perturbations in crystallin folding and solubility intersect with oxidative stress responses and chaperone-dependent maintenance of lens proteins, linking disrupted homeostasis to light-scattering aggregates. Genetic variation or dysregulated stability of γC-crystallin is associated with inherited lens opacity phenotypes, providing a molecular entry point for studying cataract-relevant mechanisms.
γC-crystallin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CRYGC locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CRYGC. 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 CRYGC 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 CRYGC-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.