ATXN7L3 Double Nickase Plasmid (h): sc-407817-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATXN7L3 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
- ATXN7L3 Double Nickase Plasmid (h) and ATXN7L3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ATXN7L3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATXN7L3 Double Nickase Plasmid (h) | sc-407817-NIC | 20 µg | $410.00 | |||
ATXN7L3 Double Nickase Plasmid (h2) | sc-407817-NIC-2 | 20 µg | $410.00 |
ATXN7L3 (ataxin 7 like 3) encodes a nuclear component of the SAGA transcriptional coactivator complex, where it supports the deubiquitination module that regulates histone H2B ubiquitination status. By coordinating chromatin accessibility and transcriptional output, ATXN7L3 contributes to RNA polymerase II–dependent gene regulation, enhancer activity, and broader epigenetic control of cell-state programs. Its function intersects with chromatin remodeling, DNA damage-associated transcriptional responses, and differentiation-related gene expression networks. Dysregulation of SAGA-linked epigenetic mechanisms and H2B ubiquitination dynamics is relevant to studies of cancer-associated transcriptional reprogramming and neurobiology, making ATXN7L3 a useful target for mechanistic chromatin research.
ATXN7L3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ATXN7L3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ATXN7L3. 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 ATXN7L3 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 ATXN7L3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.