CTPS1 Double Nickase Plasmid (h): sc-403505-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CTPS1 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
- CTPS1 Double Nickase Plasmid (h) and CTPS1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CTPS1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CTPS1 Double Nickase Plasmid (h) | sc-403505-NIC | 20 µg | $410.00 | |||
CTPS1 Double Nickase Plasmid (h2) | sc-403505-NIC-2 | 20 µg | $410.00 |
Human CTPS1 encodes CTP synthase 1, a cytosolic enzyme that catalyzes the ATP-dependent amination of UTP to CTP, a rate-limiting step in de novo pyrimidine nucleotide biosynthesis. By controlling intracellular CTP pools, CTPS1 supports DNA and RNA synthesis, phospholipid production, and metabolic adaptation during cell-cycle progression and proliferative stress. CTPS1 activity interfaces with nucleotide salvage and folate-dependent one-carbon metabolism and can assemble into filamentous cytoophidia linked to regulation of enzymatic output. Dysregulated pyrimidine metabolism and CTPS1 dependence have been associated with altered proliferative capacity in immune and cancer-related contexts, making CTPS1 a useful target for studying nucleotide homeostasis and growth control.
CTPS1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CTPS1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CTPS1. 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 CTPS1 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 CTPS1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.