Atg9b Double Nickase Plasmid (h): sc-406894-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Atg9b 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
- Atg9b Double Nickase Plasmid (h) and Atg9b Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ATG9B. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Atg9b Double Nickase Plasmid (h) | sc-406894-NIC | 20 µg | $410.00 |
ATG9B encodes Atg9b, a multi-pass transmembrane protein that regulates autophagosome biogenesis by supporting membrane delivery to nascent phagophores and coordinating autophagy machinery at pre-autophagosomal sites. It functions within core macroautophagy pathways and intersects with endomembrane trafficking, lysosomal homeostasis, and nutrient-sensing stress responses. Perturbation of ATG9B can alter autophagic flux, impacting proteostasis, organelle quality control, and inflammatory signaling. These processes are frequently implicated in cancer biology, neurodegeneration, and immune dysregulation, making ATG9B a useful node for pathway-focused mechanistic studies.
Atg9b Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ATG9B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ATG9B. 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 ATG9B 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 ATG9B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.