CHAC1 Double Nickase Plasmid (h): sc-403197-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CHAC1 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
- CHAC1 Double Nickase Plasmid (h) and CHAC1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CHAC1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CHAC1 Double Nickase Plasmid (h) | sc-403197-NIC | 20 µg | $410.00 | |||
CHAC1 Double Nickase Plasmid (h2) | sc-403197-NIC-2 | 20 µg | $410.00 |
CHAC1 (ChaC glutathione specific gamma-glutamylcyclotransferase 1) encodes a cytosolic enzyme that degrades glutathione, thereby influencing redox homeostasis and cellular susceptibility to oxidative stress. It is transcriptionally induced by the integrated stress response, including ATF4/CHOP signaling downstream of endoplasmic reticulum stress and amino acid limitation. Through modulation of glutathione pools, CHAC1 intersects with pathways controlling lipid peroxidation, mitochondrial function, and stress-adaptive cell fate decisions. Dysregulated CHAC1 expression has been associated with conditions characterized by proteostasis imbalance and oxidative injury, supporting its relevance in mechanistic studies of stress-linked pathophysiology.
CHAC1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CHAC1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CHAC1. 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 CHAC1 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 CHAC1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.