ATG7 Double Nickase Plasmid (h): sc-400997-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATG7 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
- ATG7 Double Nickase Plasmid (h) and ATG7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ATG7. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ATG7 Antibody (B-9): sc-376212
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATG7 Double Nickase Plasmid (h) | sc-400997-NIC | 20 µg | $410.00 | |||
ATG7 Double Nickase Plasmid (h2) | sc-400997-NIC-2 | 20 µg | $410.00 |
ATG7 encodes an E1-like activating enzyme that is essential for autophagosome biogenesis by catalyzing ubiquitin-like conjugation reactions in the ATG12–ATG5 system and promoting LC3/ATG8 lipidation through ATG3. Through these activities, ATG7 coordinates macroautophagy and contributes to cellular proteostasis, nutrient stress adaptation, mitochondrial quality control, and modulation of innate and inflammatory signaling. Altered ATG7 function or expression has been linked to dysregulated autophagic flux and cellular stress sensitivity, with relevance to neurodegeneration, cancer biology, metabolic dysfunction, and infection-related host–pathogen interactions. ATG7 is therefore widely used as a genetic handle to interrogate autophagy-dependent phenotypes and pathway crosstalk.
ATG7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ATG7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ATG7. 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 ATG7 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 ATG7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.