Atg2A Double Nickase Plasmid (h): sc-411671-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Atg2A 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
- Atg2A Double Nickase Plasmid (h) and Atg2A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ATG2A. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Atg2A Antibody (G-1): sc-514207
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Atg2A Double Nickase Plasmid (h) | sc-411671-NIC | 20 µg | $410.00 | |||
Atg2A Double Nickase Plasmid (h2) | sc-411671-NIC-2 | 20 µg | $410.00 |
ATG2A encodes Atg2A, a conserved autophagy factor required for autophagosome biogenesis and expansion, supporting lipid transfer at phagophore membranes and coordinating with core ATG machinery. In human cells, Atg2A contributes to autophagic flux, nutrient stress adaptation, and proteostasis by promoting formation of functional autophagosomes that deliver cytoplasmic cargo to lysosomes. Disruption of ATG2A-dependent pathways can alter organelle homeostasis, mitochondrial quality control, and inflammatory signaling, linking autophagy defects to mechanisms relevant to neurodegeneration, cancer cell stress tolerance, and metabolic dysfunction. ATG2A is therefore a useful target for dissecting selective and bulk autophagy programs and their downstream cellular phenotypes.
Atg2A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ATG2A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ATG2A. 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 ATG2A 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 ATG2A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.