Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
TIGAR Double Nickase Plasmid (h): sc-401390-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TIGAR 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
- TIGAR Double Nickase Plasmid (h) and TIGAR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TIGAR. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TIGAR Antibody (E-2): sc-166290
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TIGAR Double Nickase Plasmid (h) | sc-401390-NIC | 20 µg | $410.00 | |||
TIGAR Double Nickase Plasmid (h2) | sc-401390-NIC-2 | 20 µg | $410.00 |
Human TIGAR (TP53-induced glycolysis and apoptosis regulator) encodes a fructose-2,6-bisphosphatase–like protein that rewires cellular metabolism by lowering fructose-2,6-bisphosphate, suppressing glycolytic flux, and favoring pentose phosphate pathway activity. Through enhanced NADPH generation, TIGAR supports redox homeostasis and limits reactive oxygen species, linking metabolic control to stress responses, apoptosis, and autophagy programs downstream of p53 signaling. TIGAR has been studied in contexts of metabolic reprogramming and oxidative stress adaptation that are relevant to cancer biology and other disorders where redox balance and bioenergetics influence cell fate. As a nodal regulator at the intersection of p53 signaling, glycolysis, and antioxidant defenses, TIGAR provides a tractable target for dissecting metabolism-dependent phenotypes in human cells.
TIGAR Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TIGAR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TIGAR. 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 TIGAR 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 TIGAR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.