TADA3L Double Nickase Plasmid (h): sc-409222-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TADA3L 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
- TADA3L Double Nickase Plasmid (h) and TADA3L Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TADA3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TADA3L Antibody (D-10): sc-166118
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TADA3L Double Nickase Plasmid (h) | sc-409222-NIC | 20 µg | $410.00 |
TADA3 encodes TADA3L, a transcriptional adaptor that functions within histone acetyltransferase complexes such as SAGA/GCN5 to coordinate chromatin remodeling and RNA polymerase II–dependent transcription. By linking sequence-specific transcription factors to acetylation of histone substrates, TADA3L helps regulate gene-expression programs controlling cell-cycle progression, DNA damage responses, and differentiation. Perturbation of this axis can alter epigenetic states and transcriptional fidelity, processes frequently implicated in tumor biology and other disorders driven by dysregulated chromatin and transcription. As a result, TADA3L is commonly studied in pathways connecting transcriptional coactivation with genome maintenance and cellular stress signaling.
TADA3L Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TADA3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TADA3. 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 TADA3 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 TADA3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.