IMPDH Double Nickase Plasmid (h): sc-403719-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IMPDH 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
- IMPDH Double Nickase Plasmid (h) and IMPDH Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IMPDH1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IMPDH Double Nickase Plasmid (h) | sc-403719-NIC | 20 µg | $410.00 | |||
IMPDH Double Nickase Plasmid (h2) | sc-403719-NIC-2 | 20 µg | $410.00 |
IMPDH1 encodes inosine monophosphate dehydrogenase, a rate-limiting enzyme in de novo guanine nucleotide biosynthesis that catalyzes the conversion of IMP to XMP and supports GTP pool homeostasis. By controlling nucleotide availability, IMPDH1 influences DNA/RNA synthesis, cell-cycle progression, and metabolic adaptation, linking purine metabolism to proliferative and stress-response programs. Altered IMPDH1 activity has been associated with retinal degeneration phenotypes and can modulate cellular sensitivity to fluctuations in nucleotide demand, making it relevant for studies of metabolic regulation and genome maintenance.
IMPDH Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IMPDH1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IMPDH1. 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 IMPDH1 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 IMPDH1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.