ATF3 Double Nickase Plasmid (h): sc-416577-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATF3 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
- ATF3 Double Nickase Plasmid (h) and ATF3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ATF3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATF3 Double Nickase Plasmid (h) | sc-416577-NIC | 20 µg | $410.00 | |||
ATF3 Double Nickase Plasmid (h2) | sc-416577-NIC-2 | 20 µg | $410.00 |
ATF3 (activating transcription factor 3) is an immediate-early, stress-inducible bZIP transcription factor that integrates diverse cellular signals including MAPK/JNK, NF-κB, and unfolded protein response pathways. By binding CRE/ATF-like elements and forming homo- or heterodimers with AP-1 family members, ATF3 modulates transcriptional programs controlling inflammation, apoptosis, cell-cycle adaptation, and metabolic rewiring. Its expression is rapidly induced by DNA damage, oxidative stress, cytokines, and ER stress, positioning ATF3 as a key regulator of adaptive transcriptional responses. Dysregulated ATF3 activity has been associated with tumor biology, immune signaling, and tissue injury models, making it useful for dissecting context-dependent stress and inflammatory networks in human cells.
ATF3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ATF3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ATF3. 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 ATF3 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 ATF3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.