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.
Tafazzin Double Nickase Plasmid (h): sc-403588-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Tafazzin 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
- Tafazzin Double Nickase Plasmid (h) and Tafazzin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TAZ. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Tafazzin Antibody (F-7): sc-365810
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Tafazzin Double Nickase Plasmid (h) | sc-403588-NIC | 20 µg | $410.00 | |||
Tafazzin Double Nickase Plasmid (h2) | sc-403588-NIC-2 | 20 µg | $410.00 |
TAZ encodes tafazzin, a mitochondrial inner membrane–associated acyltransferase that remodels cardiolipin to maintain the proper acyl chain composition required for respiratory chain organization and efficient oxidative phosphorylation. Through cardiolipin maturation, tafazzin supports mitochondrial cristae architecture, membrane dynamics, and the stability of protein supercomplexes involved in electron transport. Disruption of TAZ perturbs phospholipid homeostasis, elevates monolysocardiolipin, and can shift cellular bioenergetics toward stress responses linked to impaired mitochondrial function. TAZ dysfunction is strongly associated with Barth syndrome and is frequently studied in the context of cardiomyopathy, skeletal myopathy, neutropenia, and broader mitochondrial lipid remodeling defects.
Tafazzin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TAZ locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TAZ. 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 TAZ 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 TAZ-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.